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This study gives an insight into certain systemic conditions and factors such as nutrition, age, hematological disorders, hypertension, smoking, obesity, and metabolic syndrome that have a notable effect on the periodontium. The review highlights the importance of taking these factors into consideration in periodontal therapy and their impact on the prognosis of periodontal therapies. The other systemic factors are discussed in detail elsewhere in the special issue.

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Background: Although there is consistent evidence that smoking is a risk factor associated with tuberculosis (TB), whether smoking cessation improves treatment outcomes and reduces the risk of TB recurrence remains understudied. Methods: We conducted a prospective cohort study with a seven-year follow-up in China. We recruited newly-diagnosed TB patients and classified them as non-smokers, ex-smokers, and current smokers. Current smokers were invited to participate in a smoking cessation intervention programme. We used a Cox proportional hazards model to assess the risk of death among TB patients and the risk of recurrence among successfully treated patients. Results: In total, 634 (79.2%) patients completed anti-TB treatments and 115 (14.4%) patients died. We confirmed the existence of a dose-response relationship between smoking frequency and the risk of TB recurrence (the slope of the fitted line >0; P < 0.05). Compared to those who continued smoking, the risk of death and recurrent TB for the patients who quit smoking during treatment decreased. The HR of mortality for smokers who smoked 30 or more cigarettes was 2.943 (95% confidence interval (CI) = 1.035-8.368), while the HR of mortality for those who smoked 30 or more cigarettes, but quit during treatment was 2.117 (95% CI = 1.157-3.871). However, the risk of recurrence remained high for ex-smokers who had a smoking history of 25 years or more. Conclusions: Our study provides further evidence supporting the World Health Organization's call for co-management of smoking and other risk factors as part of routine TB treatment.

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Background: The study's main objectives were to evaluate the distribution of levels of procrastination and its relationship with sleep quality, smoking status, alcohol consumption, and skipping breakfast, as a proxy measure of an unhealthy dietary pattern, among Italian university students. Methods: A cross-sectional study was conducted at the "Magna Græcia" University of Catanzaro in the Southern part of Italy, using stratified random sampling techniques. Eligible students were sent an anonymous online survey aimed at assessing sociodemographic characteristics, procrastination levels using the Pure Procrastination Scale, sleep quality using Pittsburgh Sleep Quality Index, smoking status, alcohol consumption using WHO's Alcohol Use Disorders Identification Tool, and breakfast habits. Results: The study included 518 participants with a mean age of 23 year. More than half of the sample was enrolled in medicine or life science majors and the procrastination mean score was 15 (±5.9 SD). Being procrastinators was significantly more frequently among students who were poor sleepers, hazardous alcohol consumers and breakfast skippers. When analyzing the clustering of risky behaviors, it was found that as the number of risky behaviors increased, the procrastination score exhibited an exponential increase. Conclusion: The study findings showed that university students who engage in procrastination tend to adopt risky health behaviors. The data gathered could be useful to derive targeted interventions aimed at groups more exposed to harmful health behaviors and to encourage institutional policies to promote healthy lifestyles within universities. Universities can act as hubs for cultivating a culture of well-being and promoting a healthy environment.

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BACKGROUND: Late-onset multiple sclerosis (LOMS), defined as the development of MS after the age of 50, has shown a substantial surge in incidence rates and is associated with more rapid progression of disability. Besides, studies have linked tobacco smoking to a higher chance of MS progression. However, the role of smoking on the risk of developing LOMS remains unclear. This study aims to evaluate the possible association between lifetime exposure to cigarette and waterpipe smoking, drug abuse, and alcohol consumption and the risk of LOMS. METHODS: This population-based case-control study involved LOMS cases and healthy sex and age-matched controls from the general population in Tehran, Iran. The primary data for confirmed LOMS cases were obtained from the nationwide MS registry of Iran (NMSRI), while supplementary data were collected through telephone and on-site interviews. Predesigned questionnaire for multinational case-control studies of MS environmental risk factors was used to evaluate the LOMS risk factors. The study employed Likelihood ratio chi-square test to compare qualitative variables between the two groups and utilized two independent sample t-test to compare quantitative data. Adjusted odds ratio (AOR) for age along with 95% confidence intervals (CI) were calculated using matched logistic regression analysis in SPSS 23. RESULTS: Totally, 83 LOMS cases and 207 controls were included in the analysis. The female to male ratio in the cases was 1.5: 1. The mean ± SD age of 83 cases and 207 controls was 61.14 ± 5.38) and 61.51 ± 7.67 years, respectively. The mean ± SD expanded disability status scale (EDSS) score was 3.68 ± 2.1. Although the results of waterpipe exposure had no significant effect on LOMS development (P-value: 0.066), ever cigarette-smoked participants had a significantly higher risk of developing LOMS than those who never smoked (AOR: 2.57, 95% CI: 1.44-4.60). Furthermore, people with a history of smoking for more than 20 years had 3.45 times the odds of developing MS than non-smokers. Drug and alcohol abuse were both associated with LOMS in our study; of which opioids (AOR: 5.67, 95% CI: 2.05-15.7), wine (AOR: 3.30, 95% CI: 1.41-7.71), and beer (AOR: 3.12, 95% CI: 1.45-6.69) were found to pose the greatest risk of LOMS, respectively. CONCLUSION: For the first time, we identified smoking, drug, and alcohol use as potential risk factors for LOMS development. According to the global increase in cigarette smoking and alcohol use, these findings highlight the importance of conducting interventional approaches for prevention.

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BACKGROUND: Studies have identified individual blood biomarkers associated with chronic obstructive pulmonary disease (COPD) and related phenotypes. However, complex diseases such as COPD typically involve changes in multiple molecules with interconnections that may not be captured when considering single molecular features. METHODS: Leveraging proteomic data from 3,173 COPDGene Non-Hispanic White (NHW) and African American (AA) participants, we applied sparse multiple canonical correlation network analysis (SmCCNet) to 4,776 proteins assayed on the SomaScan v4.0 platform to derive sparse networks of proteins associated with current vs. former smoking status, airflow obstruction, and emphysema quantitated from high-resolution computed tomography scans. We then used NetSHy, a dimension reduction technique leveraging network topology, to produce summary scores of each proteomic network, referred to as NetSHy scores. We next performed a genome-wide association study (GWAS) to identify variants associated with the NetSHy scores, or network quantitative trait loci (nQTLs). Finally, we evaluated the replicability of the networks in an independent cohort, SPIROMICS. RESULTS: We identified networks of 13 to 104 proteins for each phenotype and exposure in NHW and AA, and the derived NetSHy scores significantly associated with the variable of interests. Networks included known (sRAGE, ALPP, MIP1) and novel molecules (CA10, CPB1, HIS3, PXDN) and interactions involved in COPD pathogenesis. We observed 7 nQTL loci associated with NetSHy scores, 4 of which remained after conditional analysis. Networks for smoking status and emphysema, but not airflow obstruction, demonstrated a high degree of replicability across race groups and cohorts. CONCLUSIONS: In this work, we apply state-of-the-art molecular network generation and summarization approaches to proteomic data from COPDGene participants to uncover protein networks associated with COPD phenotypes. We further identify genetic associations with networks. This work discovers protein networks containing known and novel proteins and protein interactions associated with clinically relevant COPD phenotypes across race groups and cohorts.

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Genome wide association studies (GWAS) have associated thousands of loci with quantitative human blood trait variation. Loci and related genes that impact blood trait variation may regulate blood cell-intrinsic biological processes, or alternatively impact blood cell development and function via systemic factors. Clinical observations have linked tobacco or alcohol use with altered blood traits, but these trait relationships have not been systematically explored at the genetic level. Applying a Mendelian randomization (MR) framework to GWAS summary statistics, we explore relationships between smoking and drinking behaviors with 15 quantitative blood traits. We find that the effects of smoking and drinking are confined to red blood cell traits. An instrumental variable (IV) comprised of 113 single nucleotide polymorphisms (SNPs) associated with smoking initiation is associated with decreased hemoglobin (HGB: Effect = -0.07 standard deviation units [95% confidence interval = -0.03 to -0.10 SD units], P = 1x10-4), hematocrit (HCT: Effect = -0.06 [-0.03 - -0.09] SD units, P = 4x10-4), and red blood cell count (RBC: Effect = -0.05 [-0.02 - -0.09] SD units, P = 5x10-3) without impacting platelet count (P = 0.9) or white blood cell count (P = 0.6). Similarly, an IV associated with an increased number of alcoholic drinks consumed per week is associated with decreased HGB (Effect = -0.22 [-0.42 - -0.02] SD units, P = 3x10-2) and RBC (Effect = -0.27 [-0.51 - -0.03] SD units, P = 3x10-2). Using multivariable MR and causal mediation analyses, we find that an increased genetic predisposition to smoking initiation is associated with increased alcohol intake, and that alcohol use mediates the genetic effect of smoking initiation on red blood cell traits. These findings demonstrate a novel role for genetically influenced behaviors on human blood traits, revealing opportunities to dissect related pathways and mechanisms that influence hematopoiesis and blood cell biology.

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Smoking is a leading cause of preventable morbidity and mortality globally. During the COVID-19 pandemic, Smoking Cessation (SC) services faced many challenges, including lockdown and social distancing restrictions. Consequently, SC services had to adapt to the challenges in different ways or halt delivery. This research evaluated the impact of COVID-19 on the delivery and outcomes of SC services. This was achieved by comparing service delivery and outcomes pre-COVID-19 and during the pandemic and drawing insights for the delivery of SC services post-pandemic. Secondary analysis was performed on the data of 11,533 participants who attended the One Life Suffolk (OLS) SC services pre- and during the COVID-19 pandemic. A total of 4923 and 6610 participants attended SC services pre-COVID-19 and during COVID-19 respectively. Fifty-four percent of participants achieved quit status at week-4 while attending the SC services during the COVID-19 pandemic, compared with 46% pre-COVID-19, (X2(1) = 38.2, p-value<0.001). Participants who attended the SC services during the COVID-19 period were 1.7 times more likely to achieve quit status at week-4 than pre-COVID-19. However, the proportion of participants lost-to-follow-up (LTF) was significantly higher during the COVID-19 period (11%) compared to pre-COVID-19 (7%), (X2(1) = 51.4, p-value <0.001). There was an increased participation and quit rate during the pandemic for modified, remotely delivered SC services indicating successful delivery of remote services during the pandemic. Although switching from face-to-face to online helped some smokers to access the service at a time of motivational readiness, despite the COVID-19 restrictions, some smokers could not access or use some aspects of the remote delivery due to a lack of internet access, poor digital literacy, no peer support and no commitment to a group during face-to-face sessions, contributing to an increased rate of LTF. Posing a major challenge to SC services delivery, COVID-19 compelled OLS SC services to adapt and be more innovative in their delivery. SC services need to continue to evolve and adapt by applying the lessons learnt during the pandemic in terms of flexibility and person-centered delivery given what did and did not work well for different demographics within the population.

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Selenium, a crucial antioxidant in the body, has been linked to all-cause and cause-specific mortality. However, the relationship between selenium and mortality in the general population remains unclear. A total of 5449 participants in the National Health and Nutrition Examination Survey (NHANES) (2003-2004, 2011-2016) were analyzed to track participant mortality until December 31, 2019. The COX proportional hazard model, Kaplan‒Meier survival analysis and restricted cubic spline regression analysis were used to investigate the associations. Subgroup analysis was conducted on the basis of age (≤ 60, > 60), sex (male, female), and smoking status (nonsmoker, former smoker, and current smoker). The second quartile was associated with lower all-cause mortality and noncardiovascular mortality (HR and 95% CI 0.61,0.45-0.83;0.59,0.42-0.83, respectively). The third quartile was associated with lower cardiovascular-related mortality (HR and 95% CI 0.49, 0.32-0.76). Elevated serum selenium concentrations were associated with lower all-cause mortality, noncardiovascular mortality (range ≤ 129.82 µg/L), and cardiovascular mortality (range ≤ 129.08 µg/L). Subgroup analysis revealed a positive correlation between the serum selenium concentration (range ≥ 129.82 µg/L) and all-cause mortality among the subgroup of current smokers (p < 0.001). This study indicates that the protective effect of the serum selenium concentration on cause-specific mortality decreases beyond a certain range in the general population, potentially increasing the risk of death among current smokers.

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The WHO recently published a Tobacco Knowledge Summary (TKS) synthesizing current evidence on tobacco and COPD, aiming to raise awareness among a broad audience of health care professionals. Furthermore, it can be used as an advocacy tool in the fight for tobacco control and prevention of tobacco-related disease. This article builds on the evidence presented in the TKS, with a greater level of detail intended for a lung-specialist audience. Pulmonologists have a vital role to play in advocating for the health of their patients and the wider population by sharing five key messages: (1) Smoking is the leading cause of COPD in high-income countries, contributing to approximately 70% of cases. Quitting tobacco is an essential step toward better lung health. (2) People with COPD face a significantly higher risk of developing lung cancer. Smoking cessation is a powerful measure to reduce cancer risk. (3) Cardiovascular disease, lung cancer and type-2 diabetes are common comorbidities in people with COPD. Quitting smoking not only improves COPD management, but also reduces the risk of developing these coexisting conditions. (4) Tobacco smoke also significantly impacts children's lung growth and development, increasing the risk of respiratory infections, asthma and up to ten other conditions, and COPD later in life. Governments should implement effective tobacco control measures to protect vulnerable populations. (5) The tobacco industry's aggressive strategies in the marketing of nicotine delivery systems and all tobacco products specifically target children, adolescents, and young adults. Protecting our youth from these harmful tactics is a top priority.

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INTRODUCTION: To assess nicotine-containing products (NCPs; heated tobacco products and/or electronic cigarettes) use in relation to conventional smoking. METHODS: "LOST IN ITALY" ("LOckdown and Lifestyles IN ITALY") and "LOST IN TOSCANA" cross-sectional surveys estimated lifestyles changes before, during, and after the lockdown in a representative sample of the Italian population. A Poisson regression model was used to estimate prevalence ratios of NCP use according to socio-demographic, mental distress, and smoking variables. RESULTS: The prevalence of conventional cigarette smokers did not decrease, remaining stable at 23%. Exclusive conventional cigarette smokers decreased from 21% before the lockdown in 2020 to 15% in 2023 but dual users, representing the large majority of NCP users, increased by 4 times, and exclusive NCP users decreased from 7% in 2020 to 5% in 2023. CONCLUSIONS: NCPs are mostly accompanying instead of replacing conventional cigarettes. A targeted campaign should be developed in Italy to raise awareness on that.

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Sex and gender differences play a crucial role in health and disease outcomes. This study used data from the National Health and Nutrition Examination Survey to explore how environmental exposures affect health-related traits differently in males and females. We utilized a sex-stratified phenomic environment-wide association study (PheEWAS), which allowed the identification of associations across a wide range of phenotypes and environmental exposures. We examined associations between 272 environmental exposures, including smoking-related exposures such as cotinine levels and smoking habits, and 58 clinically relevant blood phenotypes, such as serum albumin and homocysteine levels. Our analysis identified 119 sex-specific associations. For example, smoking-related exposures had a stronger impact on increasing homocysteine, hemoglobin, and hematocrit levels in females while reducing serum albumin and bilirubin levels and increasing c-reactive protein levels more significantly in males. These findings suggest mechanisms by which smoking exposure may pose higher cardiovascular risks and greater induced hypoxia for women, and greater inflammatory and immune responses in men. The results highlight the importance of considering sex differences in biomedical research. Understanding these differences can help develop more personalized and effective health interventions and improve clinical outcomes for both men and women.

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As the heritability of abdominal aortic aneurysm (AAA) is high and AAA partially shares genetic architecture with other cardiovascular diseases, genetic information could help inform AAA screening strategies. Exploiting pleiotropy and meta-analysing summary data from large studies, we construct a polygenic risk score (PRS) for AAA. Leveraging related traits improves PRS performance (R2) by 22.7%, relative to using AAA alone. Compared with the low PRS tertile, intermediate and high tertiles have hazard ratios for AAA of 2.13 (95%CI 1.61, 2.82) and 3.70 (95%CI 2.86, 4.80) respectively, adjusted for clinical risk factors. Using simulation modelling, we compare PRS- and smoking-stratified screening with inviting men at age 65 and not inviting women (current UK strategy). In a futuristic scenario where genomic information is available, our modelling suggests inviting male current smokers with high PRS earlier than 65 and screening female smokers with high/intermediate PRS at 65 and 70 respectively, may improve cost-effectiveness.

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This study aimed to analyze patterns and predictors of secondhand smoke (SHS) exposure among adolescents (12-16 years old) in Bahrain, Kuwait, Oman, Qatar, Saudi Arabia, and the United Arab Emirates. Nationally representative data from the most recent Global Youth Tobacco Survey in each country were analyzed (N = 17,220). SHS exposure at home, in public places, and at school was assessed. Descriptive statistics summarized exposure prevalence overall and by sex. Multivariable logistic regression examined factors associated with each SHS exposure's outcome. The results showed that SHS exposure was high overall, with exposure at home and school ranging from 12.7 to 20.7%, respectively, in Oman to 39.4% and 36.7%, respectively, in Kuwait. Almost half of the adolescents reported exposure to SHS in public places, with a prevalence of 40.8% in Saudi Arabia to 65.9% in Kuwait. The prevalence of exposure varied between countries, with the highest rates occurring in Kuwait. Girls had higher exposure at home, while boys had higher exposure in public and at school. Factors associated with higher exposure included parental smoking, friend smoking, and tobacco advertising. The belief that SHS is harmful was associated with lower home exposure. In conclusion, adolescents in the Gulf Cooperation Council countries are exposed to concerning levels of SHS, especially in public places. These findings underscore the urgent need for stronger tobacco control policies, including comprehensive smoke-free laws covering all public venues, to protect youth from SHS exposure. Additionally, the results support the development of targeted interventions promoting smoke-free homes and social norms against smoking.

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OBJECTIVE: Evidence from low- and middle-income countries regarding the effect of smoking in people with diabetes is lacking. Here, we report the association of smoking with mortality in a large cohort of Mexican adults with diabetes. METHODS: Participants with diabetes mellitus (self-reported diagnosis, use of antidiabetic medications or HbA1c ≥ 6.5%) aged 35-74 years when recruited into the Mexico City Prospective Study were included. Cox regression confounder-adjusted mortality rate ratios (RRs) associated with baseline smoking status were estimated. RESULTS: Among 15,975 women and 8225 men aged 35-74 years with diabetes but no other comorbidities at recruitment, 2498 (16%) women and 2875 (35%) men reported former smoking and 2753 (17%) women, and 3796 (46%) men reported current smoking. During a median of 17 years of follow-up there were 5087 deaths at ages 35-74 years. Compared with never smoking, all-cause mortality RR was 1.08 (95%CI 1.01-1.17) for former smoking, 1.11 (95%CI 1.03-1.20) for current smoking, 1.09 (95%CI 0.99-1.20) for non-daily smoking, 1.06 (95%CI 0.96-1.16) for smoking < 10 cigarettes/day (median during follow-up 4 cigarettes/day), and 1.28 (95% CI 1.14-1.43) for smoking ≥ 10 cigarettes/day (median during follow-up 15 cigarettes/day). Mortality risk among daily smokers was greatest for COPD, lung cancer, cardiovascular diseases, and acute diabetic complications. CONCLUSION: In this cohort of Mexican adults with diabetes, low-intensity daily smoking was associated with increased mortality, despite observing smoking patterns which are different from other populations, and over 5% of total deaths were associated with smoking.

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Background: Chronic obstructive pulmonary disease (COPD), usually caused by long-term tobacco smoking, is independently associated with systemic inflammation. However, little is known about the systemic inflammatory status of patients with early-stage COPD (classified as GOLD 1) and long-term smokers with normal lung function (LF). Here, we characterised the early changes in the associated inflammatory state in patients with GOLD 1 and in long-term smokers with normal LF. Methods: Fresh blood samples from 27 patients with GOLD 1, 27 long-term smokers and 14 non-smokers were analysed. Results: Ex vivo blood analysis revealed greater leucocyte-platelet adhesion to TNFα-stimulated pulmonary endothelium in patients with GOLD 1 than in smokers and non-smokers. In addition, platelet reactivity (platelet count and activation, and fibrinogen levels) and the frequency of leucocyte-platelet aggregates were higher in the GOLD 1 group than in the other groups. Some of these findings correlated with the severity of lung dysfunction, while platelet hyperactivity correlated positively with leucocyte-platelet adhesion. The GOLD 1 group also had a higher Th17/Treg ratio and higher circulating levels of IL-17C and C-reactive protein than the other groups. However, long-term smokers also had higher leucocyte counts and activation, and higher plasma levels of TNFα and IL-6 than non-smokers. Conclusion: Our data suggest that the altered inflammatory parameters in long-term smokers may represent early biomarkers of COPD. Accordingly, peripheral immune monitoring based on the above parameters may be useful to prevent disease progression in long-term smokers with normal LF and early COPD.

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BACKGROUND: Smoking is an important risk factor for various metabolic and cardiovascular disorders, and smoking cessation reduces the risk of these conditions. However, weight gain is commonly observed when individuals quit smoking, which often leads to hesitation in pursuing smoking cessation. Weight gain increases the risk of metabolic syndrome (MS). However, previous studies that investigated the relationship between smoking cessation and MS have yielded inconsistent results. Therefore, we conducted a meta-analysis to evaluate the association between smoking cessation and MS. METHODS: Medline, Embase, Cochrane Library and CINAHL databases, were comprehensively searched from inception to April 2023, to identify relevant studies examining the relationship between smoking cessation and MS, comparing such relationship to that with active smoking. The methodological quality of the selected studies was assessed using the Newcastle-Ottawa Quality Assessment Scale. A random-effects model was used for meta-analysis. RESULTS: Of 495 identified studies, 24 were reviewed. The risk of selection bias was identified in all the studies. The overall analysis of 14 studies, including data of combined results for both men and women, revealed an increased risk of MS among ex-smokers compared with that among active smokers (pooled relative risk [RR] 1.18, 95% confidence interval [CI]: 1.08-1.29). From the selected studies, 13 studies analyzing men were extracted for subgroup analysis. Among men, no significant difference in the risk of developing MS was observed between ex-smokers and smokers (pooled RR: 1.05, 95% CI: 0.95-1.17). In men, the risk of MS increased if the cessation period was ≤15 years in men (pooled RR 1.26, 95% CI: 1.01-1.56) and slightly decreased if the cessation period was > 15 years (RR 0.84, 95% CI: 0.70-1.00) in ex-smokers compared with that in current smokers. CONCLUSION: An increased risk of MS was observed in the early stages of smoking cessation compared with current smoking. As the longer duration of smoking cessation, the risk of MS becomes less significant.

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The potential role of smoking as a risk factor for thoracic aortic aneurysm is still a subject of debate. Therefore, it is important to systematically investigate the causal relationship between smoking and thoracic aortic aneurysm using Mendelian randomization methods. Genetic data were obtained from genome-wide association studies using the inverse variance weighting method as the primary approach. A thorough sensitivity analysis was conducted to ensure the reliability of the findings. Instrumental variables were assessed using the F statistic, and meta-analysis was employed to assess the average genetic predictive effect between smoking and thoracic aortic aneurysm. Our Mendelian randomization study found a positive association between smoking and thoracic aortic aneurysm. The odds ratios (OR) in the inverse variance weighting method were OR = 1.23 (95% confidence interval [CI] = 1.00-1.51; P = .053) and OR = 2.07 (95% CI = 1.10-3.91; P = .024). Furthermore, meta-analyses consistently demonstrated a positive causal relationship between ferritin and myocardial infarction, although statistical significance was not observed. The analysis results did not indicate any horizontal pleiotropy. Despite the presence of heterogeneity, the Mendelian randomization analysis still yielded significant results. This study employed Mendelian randomization to establish a positive association between smoking levels and the risk of thoracic aortic aneurysm. The genetic evidence reveals a causal relationship between the two, offering new insights for future interventions targeting thoracic aortic aneurysms.

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SOURCE CITATION: Cinciripini PM, Green CE, Shete S, et al. Smoking cessation after initial treatment failure with varenicline or nicotine replacement: a randomized clinical trial. JAMA. 2024;331:1722-1731. 38696203.

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BACKGROUND: Incarceration is a social determinant of cardiovascular health but is rarely addressed in clinical settings or public health prevention efforts. People who have been incarcerated are more likely to develop cardiovascular disease (CVD) at younger ages and have worse cardiovascular outcomes compared with the general population, even after controlling for traditional risk factors. This study aims to identify incarceration-specific factors that are associated with uncontrolled CVD risk factors to identify potential targets for prevention. METHODS AND RESULTS: Using data from JUSTICE (Justice-Involved Individuals Cardiovascular Disease Epidemiology), a prospective cohort study of individuals released from incarceration with CVD risk factors, we examine the unique association between incarceration-specific factors and CVD risk factor control. Participants (N=471), with a mean age of 45.0±10.8 (SD) years, were disproportionately from racially minoritized groups (79%), and poor (91%). Over half (54%) had at least 1 uncontrolled CVD risk factor at baseline. People released from jail, compared with prison, had lower Life's Essential 8 scores for blood pressure and smoking. Release from jail, as compared with prison, was associated with an increased odds of having an uncontrolled CVD risk factor, even after adjusting for age, race and ethnicity, gender, perceived stress, and life adversity score (adjusted odds ratio 1.62 [95% CI, 1.02-2.57]). DISCUSSION: Release from jail is associated with poor CVD risk factor control and requires tailored intervention, which is informative as states design and implement the Centers of Medicare & Medicaid Services Reentry 1115 waiver, which allows Medicaid to cover services before release from correctional facilities.

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