Disparities in the incidence, prevalence and outcomes of multiple sclerosis (MS) exist in the USA, often to the detriment of Black and Hispanic people. Despite the common misconception that MS is a disease of white people, the incidence is highest in Black people. Disability accumulates faster and at younger ages in Black and Hispanic people with MS than in their white counterparts, and MS-related mortality in early and mid-adulthood is highest in Black people. These differences are often erroneously interpreted as evidence of innate racial or ethnic variations. In this Perspective, we demonstrate how race and ethnicity - social constructs with a limited biological basis that are often assigned by systems of power - can influence biology through lived experiences, a phenomenon termed 'embodiment'. We review how downstream consequences of structural racism can lead to biological outcomes strongly associated with MS susceptibility, such as imbalanced immune system development, dysregulated immune responses to the Epstein-Barr virus and childhood obesity. We also consider how inequitable health-care access and quality, combined with the younger age of onset and higher comorbidity burdens, might explain racial and ethnic disparities in MS prognosis. Our proposed conceptual model offers a roadmap for generating knowledge and implementing interventions to narrow racial and ethnic disparities in MS susceptibility and outcomes.

Nicotine use, including from non-tobacco sources, is associated with impaired wound healing and increased surgical complications. This study evaluated the impact of nicotine and non-tobacco nicotine use on postoperative outcomes in hallux valgus (HV) surgeries.

Using the TriNetX Global Health Research Network, we analyzed adult patients aged 18 and older undergoing HV correction. Cohorts included nicotine users, non-tobacco nicotine users, and controls, matched using propensity score matching (PSM). Postoperative complications were assessed within 90 days.

Both nicotine and non-tobacco nicotine cohorts demonstrated increased postoperative complications compared to the control cohort, notably infections, wound disruption, stroke, pneumonia, and renal failure. Also, both nicotine and non-tobacco nicotine users showed elevated healthcare utilization, including emergency department visits and opioid-related disorders.

Nicotine and non-tobacco nicotine use significantly increase the risk of postoperative complications following HV surgery, emphasizing the importance of mitigating these risks through further research and preoperative strategies.

Level III, Retrospective Comparative Study.

Substance use disorders (SUDs) are a significant public health concern across the United States and may pose a risk to achieving sustained viral suppression (SVS) in people with HIV (PWH). This study aims to examine the association between SUDs and SVS among PWH.

Using electronic health records from the South Carolina Department of Health, we conducted a retrospective study of adults with HIV who were diagnosed between January 2006 and December 2019.

The impact of SUDs on SVS was assessed using generalized linear mixed model. Potential confounders included age, sex, chronic diseases history, etc. Stepwise selection was performed to decide the confounders included in the final model, and the optimal correlation structure was determined by Akaike information criterion.

Of the 9412 eligible participants, 7481 (79.48%) had reached SVS status during their follow-up periods. SUDs related to alcohol [adjusted odds ratio (AOR) = 1.70, 95% confidence interval (CI): 1.46-1.98], cannabis (AOR = 1.62, 95% CI: 1.35-1.95), cocaine (AOR = 1.95, 95% CI: 1.60-2.37), opioid (AOR = 1.91, 95% CI: 1.13-3.23), and tobacco (AOR = 1.80, 95% CI: 1.69-1.92) were negatively associated with SVS. Individuals with chronic conditions such as cardiovascular disease (AOR = 0.31, 95% CI: 0.29-0.33), diabetes (AOR = 0.49, 95% CI: 0.41-0.59), and cancer (AOR = 0.47, 95% CI: 0.38-0.58) showed a higher likelihood of maintaining SVS.

This large cohort study of PWH with extended follow-up highlights the negative impact of SUDs on maintaining SVS. Long-term strategies for reducing substance use could support SVS in PWH.

To track the level of serum antibodies in Fuzhou residents and analyze the possible influencing factors of serum antibodies, so as to provide a scientific basis for the adjustment of population immunity and prevention and control strategies.

Residents in the Fuzhou community who had symptoms of covid-19 infection or who had tested positive for nucleic acid or antigen since December 2022 were selected for the questionnaire survey and their sera were collected to analyze the trend of antibody changes, the antibody level was divided into high antibody group and low antibody group according to the literature data. The possible influencing factors of serum antibody level was analyzed by multivariate logistic regression model.

A total of 2,521 Fuzhou residents were adopted in the study, including 223 in the high antibody group and 194 in the low antibody group. A univariate analysis showed that, there were significant differences in age (Z=-4.028, P<0.00), occupation (χ2 = 18.591, P=0.005), typical symptoms after the first infection (χ2 = 9.784, P=0.002), history of surgery (χ2 = 29.542, P<0.001), symptoms lasting more than 2 weeks after the first infection (χ2 = 4.887, P=0.027), smoking (χ2 = 18.524, P<0.001) and drinking (χ2 = 19.578, P<0.001) between the high antibody group and the low antibody group. Multivariate regression models show that, age (OR= 1.011, 95%CI: 1.002~1.020, P=0.017), history of surgery (OR=4.956,95%CI: 2.606~9.423, P<0.001),smoking (OR=2.089, 95%CI: 1.002~4.355, P=0.049), drinking (OR=2.214, 95%CI: 1.066~4.600, P=0.033) were the risk factors affecting antibody level. Typical symptoms after the first infection (OR=0.224, 95%CI: 0.086~0.579, P=0.002) and symptoms lasting more than 2 weeks after the first infection (OR=0.432, 95%CI: 0.258~0.723, P=0.001) were protective factors. By observing the trend of antibody changes in 3, 6 and 9 months, we found that the level of IgG antibody showed a decreasing trend.

The high level of protection was more likely to occur in young adults, people without operation history, people without smoking history, people without drinking history, people with typical symptoms after the first infection and symptoms lasting more than 2 weeks after the first infection. The level of IgG antibody was decreased in general, so it is necessary to strengthen immunization.

The pathogenesis and pathophysiology of rheumatic diseases is complex and relies on the interaction of different factors. The common view is that the pathological autoimmunity develops in genetically predisposed individuals upon exposure to an environmental trigger. This highlights the importance of recognizing and deconstructing the effects of environmental agents in rheumatic diseases. Several factors have been identified in the last decades, with detrimental or protective effects, impacting not only on disease onset, but also on its natural history. Cigarette smoking has been identified as one of the strongest environmental risk factors, being associated with disease development and severity for several rheumatic diseases, including rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), and spondyloarthropathies. Moreover, other airborne pollutants, such as silica, solvents, asbestos and metals are recognized risk factors for rheumatic diseases. The effect of some other agents is however not straightforward, of which a remarkable example is alcohol consumption. Alcohol has been associated with both pro- and anti-inflammatory effects, exerting a variable effect on rheumatic diseases depending on quantity and frequency of consumption, as well as sex and ethnicity. Similarly, ultraviolet light exposure has been associated with a higher risk of SLE but lower risk of RA. The relationship between microbial exposure and autoimmunity is also complex: while some infectious agents increase the risk of rheumatic diseases, it is widely accepted that less exposure to microbial agents, particularly during immune system development, increases the risk of autoimmunity. Furthermore, in recent years the spotlight has switched to the human microbiome, as alterations in organ-specific microbiome composition are anticipated to be early participants in the onset of immune-mediated illnesses. The aim of this review is to highlight the most relevant environmental factors and their role in Rheumatology, with a specific focus on proposed pathophysiological effect and correlation with clinical outcomes.

Accumulating evidence suggest that Epstein-Barr virus (EBV) is crucial in the development of multiple sclerosis (MS), with inadequate infection control possibly contributing to disease onset. Past infectious mononucleosis (IM) has been found to interact with smoking, obesity, and sun exposure. We aimed to investigate potential interactions between a history of IM and the following risk factors for MS: passive smoking, alcohol consumption, fish consumption, vitamin D status, adolescent sleep duration and sleep quality.

We analyzed data from a Swedish population-based case-control study (3128 cases and 5986 controls). Subjects were categorized based on IM status and each exposure variable and compared regarding MS risk by calculating odds ratios (OR) with 95% confidence intervals (CI) using logistic regression models. Additive interaction between aspects of IM status and each exposure was assessed by calculating the attributable proportion due to interaction (AP) with 95% CI.

The OR of developing MS among those who reported a history of IM was 1.86 (95% CI 1.63-2.12), compared with those who had not suffered from IM. We observed synergistic effects between a history of IM and each exposure variable with respect to risk of MS, with significant APs ranging between 0.20 and 0.35.

The concept of EBV infection as a crucial factor for MS gains further support from our findings suggesting that MS risk factors synergize with a history of IM in disease development. Targeting modifiable MS risk factors that impede effective immune regulation of the virus holds promise for preventive interventions.

Tobacco smoke may affect atopic dermatitis (AD) because of its known effects on humoral and cellular immunity, but prior studies lack data on disease severity and biomarkers over time.

We investigated the association between passive and active tobacco smoke exposure (TSE) during childhood and adolescence and the activity and severity of AD.

A birth cohort of 10,521 individuals was followed through adolescence as part of the Avon Longitudinal Study of Parents and Children. We used mixed-effect models to determine the risk of AD (based on repeated assessments) with passive smoke exposure during childhood, active TSE during adolescence, and using a serum biomarker of tobacco exposure (cotinine) at 3 time points.

After adjusting for confounding factors, there was no evidence of a relationship between passive TSE and concurrent AD activity in childhood (adjusted odds ratio, 0.95; 95% confidence interval, 0.83, 1.07) or of an increased risk between active smoking and AD activity in adolescence (adjusted odds ratio, 0.57; 95% confidence interval, 0.44, 0.75). Secondary analyses demonstrated no dose-response relationship and no increased severity of AD with passive or active TSE. Furthermore, we found no increased risk of AD with a cumulative measure of passive TSE across childhood (adjusted relative risk ratio, 0.98; 95% confidence interval, 0.96, 1.00).

Neither active nor passive TSE was associated with AD during childhood and adolescence.

The influence of environmental factors on the severity of early inflammatory bowel disease (IBD), including ulcerative colitis (UC) and Crohn's disease (CD), is unclear. Herein, we aimed to investigate the role of environmental factors in the initial phenotype, activity, and severity of IBD.

Copenhagen IBD Inception Cohort is a prospective population-based cohort of patients with newly diagnosed IBD between May 2021 and May 2023. Data on environmental factors were captured at IBD diagnosis using International Organisation of IBD (IOIBD) and HeartDiet questionnaires. Environmental factors' influence on outcome was analyzed and odds ratios (aOR) were adjusted for age, gender, and disease characteristics (adjusted OR, aOR [95% confidence interval]).

In total, 208 and 128 patients with incident UC and CD, respectively, were included. Active smoking was associated with increased risk of CD-related hospitalization (aOR = 2.84 [1.03; 7.88]) and stricturing phenotype (aOR = 5.28 [1.76; 15.85]) but lower risk of severe UC course (aOR = 0.28 [0.08; 0.95]). Further, previous smoking was not associated with negative effects in patients with CD in terms of early need for biologics, surgery, or hospitalization. In terms of diets, daily consumption of fruits (aOR = 0.27 [0.07; 0.99]) or vegetables (aOR = 0.27 [0.09; 0.80]) was inversely associated with stricturing CD, whereas whole meal bread was associated with reduced risk of severe CD activity (aOR = 0.40 [0.16; 0.98]).

This prospective population-based study highlighted several environmental factors associated with the initial severity and activity of IBD, emphasizing their pivotal role in the initial disease burden and giving guidance to personalized patient counseling.

Background and Objectives: The aims of this study were to assess the impact of smoking on cervical histopathology in women with high-risk HPV types 16 and 18 (the most common types) utilizing comprehensive clinical data and to conduct a risk analysis based on smoking pack-years. Materials and Methods: Between 2022 and 2024, 1048 high-risk HPV-positive women aged 25 to 65 years were categorized into two groups: smokers and non-smokers. Data acquired from a histopathological examination of samples collected during a colposcopic evaluation of these women were compared individually regarding clinical and demographic factors, specifically age, gravida, parity, and alcohol consumption. Subsequently, the impact of prolonged and excessive smoking on histopathological cellular changes was assessed in women with the same characteristics. A case-control study was performed on 312 smokers and 312 non-smokers following mutual matching. Results: The women were matched one-to-one regarding gravida, parity, and alcohol consumption. Subsequently, they were paired within a ±2-year age range. The mean age of the smoker group was 47.1 ± 8.8, while that of the non-smoker group was 47.2 ± 8.5 (p: 0.904). In all cases of high-risk HPV positivity, the rate of normal cervical cytological results was 14% in women who smoked and 29% in women who did not smoke. The LGSIL, HGSIL, ASC-H, and AGC-NOS rates were elevated in the smoker group, and a statistically significant difference was observed between the two groups in terms of abnormal cervical cytological results (p < 0.001). After a colposcopic biopsy, the smoker group exhibited higher rates of HGSILs, LGSILs, AGC-NOS, and CIS pathological lesions (28% vs. 23%), whereas the non-smoker group exhibited higher rates of chronic cervicitis (23% vs. 16%). However, no statistically significant difference was found between the two groups (p: 0.092). In a comparison of endocervical curettage (ECC) samples, it was observed that the HGSIL, CIS, and AGC-FN rates in the smoker group were almost the same as those in the non-smoker group. However, the LGSIL histopathology results (32% vs. 18%) were higher, and the rate of negativity with no pathology was higher in the non-smoker group (72% vs. 59%). A statistically significant difference in ECC histopathology was noted between the two groups (p < 0.001). An ROC analysis conducted between smoking pack-years and the colposcopic and endocervical curettage biopsy results revealed that the cutoff value for the colposcopic abnormal histopathological results increased, with 40% sensitivity and 76% specificity above 20 pack-years (AUC: 0.592 and p: 0.025). Additionally, the abnormal histopathology rates for endocervical curettage exhibited 81% sensitivity and 32% specificity above 13 pack-years (AUC: 0.586 and p: 0.008). The rate of abnormalities in the colposcopic biopsy results was 2.19 times higher for individuals with over 20 pack-years, and the rate of abnormalities in the ECC results was 2.08 times higher for those with over 13 pack-years; additionally, statistically significant results were obtained (p-values of 0.027 and 0.008, respectively). Conclusions: The most important cause of neoplastic changes in the cervix uteri is high-risk HPV infection, with evidence indicating that prolonged excessive smoking significantly exacerbates the persistence and progression of HPV infection, thereby influencing neoplastic changes in the cervix uteri. It is crucial for women to cease smoking in order to eradicate HPV infection from the body.

Eosinophilic granulomatosis with polyangiitis (EGPA), as a heterogeneous component of antineutrophil cytoplasmic antibody-associated vasculitis, may be induced by a series of environmental and genetic factors, involved with a variety of immune cells and immune components, and presented with various clinical manifestations, with multiple organs and systems (respiratory, skin, heart, kidney, nerve, etc.) involved. The choice of glucocorticoid (GC) dosage and immunosuppressant in traditional treatment strategies varies greatly from individual to individual and is not universally applicable in all the EGPA phenotype spectrum, especially in relapsing or refractory diseases. With the understanding of the heterogeneity of EGPA, a variety of therapeutic approaches are emerging and improving the traditional treatment model. In this review, we summarized the heterogeneity of EGPA etiology and pathogenesis. Clinical and pathological manifestations of the same organ involved also show significant differences and there are even gender differences. Biological treatments that mainly target type 2 inflammatory pathways are widely used in clinical practice for remission induction and maintenance of EGPA. Targeted biological therapy has shown excellent performance in reducing GC dosage and controlling symptoms and recurrence. However, a large number of high-quality randomized controlled studies are still under research for relapsing or refractory EGPA with special organ involvement. We believe that EGPA has a highly heterogeneous phenotype spectrum, and the treatment patterns targeting key molecules in the pathogenesis are of great value for individual treatment of EGPA.

The role of the immune system in cancer defense is likely underappreciated. While there has been longstanding interest in the role of atopic diseases in cancer, only a few studies have tested this hypothesis.

We analyzed data from 202,055 women participating in the Nurses' Health Study (NHS) and the Nurses' Health Study II (NHS II) to explore whether asthma is associated with breast cancer. We used Cox proportional hazards models to link physician-diagnosed asthma with subsequent incidence of breast cancer.

Across the two cohorts, we identified 18,403 cases of physician-diagnosed asthma. During 4,393,760 person-years of follow-up, 11,096 incident cases of breast cancer were diagnosed. In NHS, women with asthma had a covariate-adjusted hazard ratio of 0.92 (95% CI: 0.86-0.99) to develop breast cancer compared to women without asthma; the respective HR in NHS II was 0.93 (0.84-1.03), and 0.92 (0.87-0.98) in the pooled analysis. Among never-smokers, the HR for breast cancer was 0.91 (0.81-1.02) in NHS, 0.81 (0.70-0.93) in NHS II, and 0.86 (0.77-0.97) combined. In two large prospective cohorts of women, participants with asthma had a somewhat lower risk of breast cancer. An active immune system may provide protection from breast cancer.

In these longitudinal studies, women with asthma had a somewhat lower risk of breast cancer. This association was most pronounced among never smokers. An active immune system may provide protection from breast cancer.

Immunosenescence, the age-related decline in immune function, is a complex biological process with profound implications for health and longevity. This phenomenon, characterized by alterations in both innate and adaptive immunity, increases susceptibility to infections, reduces vaccine efficacy, and contributes to the development of age-related diseases. At the cellular level, immunosenescence manifests as decreased production of naive T and B cells, accumulation of memory and senescent cells, thymic involution, and dysregulated cytokine production. Recent advances in molecular biology have shed light on the underlying mechanisms of immunosenescence, including telomere attrition, epigenetic alterations, mitochondrial dysfunction, and changes in key signaling pathways such as NF-κB and mTOR. These molecular changes lead to functional impairments in various immune cell types, altering their proliferative capacity, differentiation, and effector functions. Emerging research suggests that lifestyle factors may modulate the rate and extent of immunosenescence at both cellular and molecular levels. Physical activity, nutrition, stress management, and sleep patterns have been shown to influence immune cell function, inflammatory markers, and oxidative stress in older adults. This review provides a comprehensive analysis of the molecular and cellular mechanisms underlying immunosenescence and explores how lifestyle interventions may impact these processes. We will examine the current understanding of immunosenescence at the genomic, epigenomic, and proteomic levels, and discuss how various lifestyle factors can potentially mitigate or partially reverse aspects of immune aging. By integrating recent findings from immunology, gerontology, and molecular biology, we aim to elucidate the intricate interplay between lifestyle and immune aging at the molecular level, potentially informing future strategies for maintaining immune competence in aging populations.

Cigarette smoking is a recognized risk factor for orthopedic disorders, particularly intervertebral disc (IVD) degenerative disease. However, the IVD pathophysiology, especially the spatial-temporal remodeling progression in the context of cigarette smoking, remains unclear. This study aimed to address this knowledge gap through a quantitative assessment of IVD structural composition and diffusion properties using a Sprague-Dawley rat model.

Twenty-four rats were divided into control and smoke exposure cohorts, each with two sub-groups of six rats. One smoke exposure sub-group was sacrificed after 2 months of daily cigarette smoke exposure in a custom smoking apparatus, while the other was sacrificed after an additional 5 months of smoke cessation. The control groups were age-matched to the smoke exposure groups. A fluorescent recovery after photobleaching (FRAP) technique was used to determine solute diffusivities and multi-photon excitation (MPE) imaging was performed to characterize structural changes in the annulus fibrosus (AF), nucleus pulposus (NP), and cartilage endplate (CEP).

A decrease in diffusivity was observed in the CEP and the AF (radial direction only) after 2 months of smoke exposure. MPE imaging showed aberrant CEP calcification and reduced AF radial collagen fiber bundle diameter, suggesting that the IVD exhibits regionally dependent structural remodeling due to smoke exposure. Furthermore, the smoke cessation group showed deteriorating alterations of structure and diffusivities in all three-disc regions, including the NP, indicating that five-month smoke cessation alone didn't reverse the progression of IVD degenerative remodeling during aging.

This study advances the understanding of IVD pathophysiology in the context of cigarette smoke exposure and cessation, laying the groundwork for potential earlier diagnosis and optimized interventions.

Macrophages in smoking environment exhibit a distinct immunosuppressive phenotype, but the mechanisms that allow nicotine to "educate" macrophages are incompletely understood. Here, we identified that nicotine transiently activates and subsequently deactivates monocytes, leading to reduced anti-infective capability of macrophages. This deactivation results in a suppression of IL-17-producing cell expansion through decreased IL-1β production. Mechanistically, nicotine induces the expression of IRAK-M in macrophages, which inhibits NF-κB signaling and restrains NLRP3 inflammasome-mediated IL-1β production. Moreover, the induction of IRAK-M by nicotine is mediated through α7 nAChR binding, which activates downstream STAT3 and AKT signaling pathways. Targeting the interaction between nicotine and α7 nAChR can decrease IRAK-M expression and restore LPS-mediated NLRP3 inflammasome-driven IL-1β production. Collectively, these findings elucidate how nicotine modulates macrophage function through complex signaling mechanisms, ultimately impacting their anti-infective responses and inflammatory processes.

High-risk human papillomavirus infection (HR-HPV) is necessary but not the only factor needed to develop cervical cancer. It is essential to estimate cervical cancer development risk in the population of high-risk HPV-positive women and to avoid unnecessary examinations and treatment in low-risk individuals. The study aimed to identify associations between different personal factors, vaginal microflora, sexually transmitted, high-risk HPV infection, and various degrees of cervical precancerous lesions. A study was performed in 2016-2020. The study group consisted of 112 patients with abnormal cervical cytology results referred for colposcopic examination. 120 women who came for a routine gynecological check-up were included in the control group. Material from the cervix and upper vaginal fornix was taken for pH measurement, wet mount microscopy, testing the six most common high-risk HPV DNA types (16/18, 31, 33, 45, 58), HPV E6/E7 mRNA, and 7 genital infections-C. trachomatis, N. gonorrhea, T. vaginalis, M. hominis, M. genitalium, U. urealyticum, U. parvum. Results showed that women with all grades of cervical intraepithelial neoplasia (CIN) more often were smokers, had increased vaginal pH levels, and had positive HR-HPV DNA and HR HPV E6/E7 mRNA expression. Abnormal vaginal microflora, especially types associated with aerobic vaginitis, and M. hominis were significantly more often found in women with CIN2+. The presence of C.trachomatis, U. parvum, and U.urealyticum did not differ between the groups. The most important factors independently associated with CIN2+ were positive high-risk HPV E6/E7 mRNA expression (OR 59.4, 95% CI 14.84-237.51), and positive high-risk HPV DNA (OR 3.9, 95% CI 1.16-13.23). Higher education level was associated with reduced risk of CIN2+ (OR 0.2, 95% CI 0.07-0.71). In conclusion, this study reports HR-HPV DNA of the most common six types and E6/E7 mRNA positivity as the most significant factors associated with CIN2+ lesions and higher education related to lower risk of high-grade cervical lesions.

Background. Causing approximately 8 million deaths each year, tobacco smoking represents a significant public health concern. Evidence shows that smoking significantly impairs antibody production and immune cell activity following vaccination. Objectives. This review aims to provide a comprehensive overview of the literature regarding how smoking reduces the effectiveness of active immunization by affecting vaccine-induced immune response. Methods. This study was performed according to the PRISMA guidelines, and the protocol was registered on the PROSPERO platform (ID: CRD42024582638). PubMed, Scopus and Web of Science were consulted as bibliographic and citation databases. Studies published in Italian and English and that aimed to investigate the effects of exposure to active and passive tobacco smoking on vaccine-induced immune response were included. Results. Thirty-four studies were selected. Overall, a decrease in antibody levels and avidity and in immune cell production were observed in individuals exposed to smoke. The meta-analysis showed a weighted mean difference between smokers and non-smokers equal to 0.65 (95% CI: 0.10-1.19, p = 0.02) for vaccinations against COVID-19, influenza, pneumococcus, HBV, HPV, tetanus, pertussis, polio, haemophilus influenzae type b, measles-mumps-rubella, and recurrent urinary tract infections. Conclusions. Smoking cessation campaigns should be considered in order to increase the effectiveness of vaccination programs. Furthermore, the opportunity to adopt different vaccine dosing schemes for smokers and non-smokers, especially in acute epidemics, should be considered.

Transcriptome-wide association studies (TWAS) have provided valuable insight in identifying genes that may impact cigarette smoking. Most of previous studies, however, mainly focused on European ancestry. Limited TWAS studies have been conducted across multiple ancestries to explore genes that may impact smoking behaviors. In this study, we used cis-eQTL data of cerebral cortex from multiple ancestries in MetaBrain, including European, East Asian, and African samples, as reference panels to perform multi-ancestry TWAS analyses on ancestry-matched GWASs of four smoking behaviors including smoking initiation, smoking cessation, age of smoking initiation, and number of cigarettes per day in GWAS & Sequencing Consortium of Alcohol and Nicotine use (GSCAN). Multiple-ancestry fine-mapping approach was conducted to identify credible gene sets associated with these four traits. Enrichment and module network analyses were further performed to explore the potential roles of these identified gene sets. A total of 719 unique genes were identified to be associated with at least one of the four smoking traits across ancestries. Among those, 249 genes were further prioritized as putative causal genes in multiple ancestry-based fine-mapping approach. Several well-known smoking-related genes, including PSMA4, IREB2, and CHRNA3, showed high confidence across ancestries. Some novel genes, e.g., TSPAN3 and ANK2, were also identified in the credible sets. The enrichment analysis identified a series of critical pathways related to smoking such as synaptic transmission and glutamate receptor activity. Leveraging the power of the latest multi-ancestry GWAS and eQTL data sources, this study revealed hundreds of genes and relevant biological processes related to smoking behaviors. These findings provide new insights for future functional studies on smoking behaviors.

Removal of hardware (HR) following a fracture is a frequent question from patients. The incidence of this kind of intervention remains very variable depending on the healthcare systems and its interest is debated in view of the benefits and associated risks that remain poorly defined. Mandatory preoperative information cannot be given optimally in this context.

To determine the rate of complications (major and minor) after non-compulsory planned hardware-removal following a limb fracture.

The rate of major complications was greater than 1%.

A 10-year retrospective single-center study included 1990 patients who had undergone routine HR. Analysis of medical records, with a minimum of one year of follow-up, allowed us to collect: patient data, the type and anatomical location of the osteosynthesis material, as well as the occurrence of a postoperative complication, categorized as a major complication (resulting in either a new surgical procedure, re-hospitalization, or lasting functional impairment) or a minor complication.

Overall, 4.1% (79/1990) of patients experienced postoperative complications, including 1.56% (31/1990) major complications and 21 surgical revisions (1.06%). The time to onset of complications was 9.1 +/- 8.4 days. The most common complications were deep infections and impaired skin healing with superficial infection (55/79, 69.6%). Locations "around the knee" and "around the ankle" were at higher risk of complications (p < 0.01). Smoking was identified as a significant risk factor for complications, particularly deep infection (p = 0.004, OR = 8.7 [1.98; 38.11]).

Non-mandatory routine RH has a significant complication rate even in a healthy population. Preoperative information of the patient and the assessment of the benefit/risk balance are essential in this indication. This study also raises the question of mandatory smoking cessation preoperatively.

IV; retrospective study.

Cigarette smoking exacerbates respiratory diseases, while plant-derived polyphenols offer antioxidant and anti-inflammatory benefits. This study exploresd the effects of Rhoifolin (ROF), a polyphenol from Jordanian Teucrium polium, on lung health in rats exposed to tobacco smoke. Male rats were divided into two groups: one exposed to cigarette smoke (CS), and the other to ROF treatment alongside smoke exposure (CS/ROF). ROF was administered orally for 21 days before smoke exposure. Results showed smoke-induced lung inflammation and oxidative stress, mitigated by ROF treatment. Histological examination revealed smoke-related morphological changes in lung tissue. ROF treatment reduced oxidative stress and inflammation, as evidenced by decreased proinflammatory cytokines. In silico docking demonstrated ROF's potential as an inhibitor of proinflammatory cytokines. This study demonstrates the therapeutic potential of ROF and similar polyphenols in mitigating the harmful effects of cigarette smoke on lung health.

Hepatobiliary and pancreatic diseases, such as cirrhosis, hepatocellular carcinoma, cholelithiasis, and pancreatitis, are major global health challenges. Lifestyle factors like smoking, alcohol consumption, and coffee intake are commonly studied for their health impacts. However, observational studies often face issues with confounding factors and reverse causality, making it difficult to establish causal relationships.

This research uses Mendelian randomization (MR) to investigate the causal effects of smoking, alcohol use, and coffee intake on 10 hepatobiliary and pancreatic diseases. Genetic data from the Sequencing Consortium of Alcohol and Nicotine Use (GSCAN) and self-reported GWAS were used to derive instrumental variables (IVs). The outcomes were obtained from the FinnGen and UK Biobank cohorts. Univariable and multivariable MR analyses were conducted to assess the associations.

Genetic predisposition to tobacco use was associated with increased risks of acute pancreatitis, alcoholic hepatitis, chronic pancreatitis, cirrhosis, gallstones, liver cancer, and pancreatic cancer. Alcohol consumption was linked to acute pancreatitis, chronic pancreatitis, alcoholic liver disease, hepatic cancer, and cholangitis. Coffee intake showed minimal associations, with a slight protective effect against non-alcoholic steatohepatitis.

This study confirms the harmful effects of inhaling tobacco and consuming alcohol on hepatobiliary and pancreatic diseases. It highlights the need for public health strategies to reduce tobacco use and heavy alcohol consumption. Coffee intake showed minimal effects, suggesting further research is needed to understand its relationship with hepatobiliary health.

The human microbiome, comprising trillions of microorganisms, significantly influences human health and disease. During critical periods like the perinatal phase, the microbiome undergoes significant changes, impacting lifelong health. Tobacco smoke, a known environmental pollutant, has adverse effects on health, particularly during pregnancy. Despite this, its association with the perinatal microbiome remains understudied.

We conducted a systematic review to integrate findings on perinatal tobacco smoke exposure and its association with the maternal and neonatal microbiomes. We conducted a comprehensive literature search in the PubMed, Scopus, and Web of Science databases from January 2000 to February 2024. We selected studies that met predefined inclusion criteria and performed data extraction.

The review included eight studies that revealed diverse associations of perinatal tobacco exposure with the maternal and neonatal microbiome. Active smoking during pregnancy was linked to alterations in microbiome composition and diversity in children. Maternal smoking correlated with increased Firmicutes abundance and decreased Akkermansia muciniphila abundance in offspring. Additionally, exposure to thirdhand smoke in neonatal intensive care units was related to infant microbiome diversity. Infants exposed to tobacco smoke showed various microbial changes, suggesting potential implications for childhood health outcomes, including obesity risk.

Perinatal exposure to tobacco smoke exerts significant influence on the maternal and neonatal microbiomes, with potential implications for long-term health outcomes. Addressing socioeconomic and psychological barriers to smoking cessation, implementing stricter smoking regulations, and promoting public health campaigns are essential steps towards reducing tobacco-related harm during the perinatal period. Further longitudinal studies and standardized assessment methods are needed to validate these findings and guide the development of effective preventive measures.

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.

Rheumatoid arthritis (RA) is a worldwide public health problem. Interventions to delay or prevent the onset of RA have attracted much attention in recent years, and researchers are now exploring various prevention strategies. At present, there is still no unified consensus for RA prevention, but targeting therapeutic windows and implementing interventions for at-risk individuals are extremely important. Due to the limited number of clinical trials on pharmacologic interventions, further studies are needed to explore and establish optimal intervention regimens and effective measures to prevent progression to RA. In this review, we introduce the RA disease process and risk factors, and present research on the use of both Western and Chinese medicine from clinical perspectives regarding RA prevention. Furthermore, we describe several complete and ongoing clinical studies on the use of Chinese herbal formulae for the prevention of RA.

Tobacco use presents increased risks for individuals with weakened immune systems (WIS). We investigated the association between cigarette and electronic nicotine delivery systems (ENDS or e-cigarettes) use and WIS in US adults using data from the 2021-2022 National Health Interview Survey.

Data from 57,133 adults were analyzed, focusing on WIS prevalence due to health conditions, prescriptions, or both. Cigarette and ENDS use were categorized as never, former, or current. Weighted multivariable regression models adjusted for demographics and other health conditions to assess associations between tobacco use and WIS.

Among US adults, 4.3% had prescription-related WIS, 4.6% had health condition-related WIS, and 7% had WIS due to either reason. Adjusted results from multivariable regression models indicated that adults with WIS due to health conditions were more likely to be current (AOR = 1.21, 95%CI: 1.05-1.40) and former (AOR = 1.25, 95%CI: 1.11-1.39) cigarette smokers compared to counterparts without WIS. Adults with WIS due to prescriptions were more likely to be former cigarette smokers (AOR = 1.19, 95%CI: 1.06-1.34). Those with WIS for any reason were more likely to be current (AOR = 1.19, 95%CI: 1.05-1.35) and former (AOR = 1.24, 95%CI: 1.13-1.36) cigarette smokers. Adults with WIS due to health conditions (AOR = 1.23, 95%CI: 1.06-1.41) or any reasons (AOR = 1.19, 95%CI:1.05-1.34) were more likely to be former ENDS users compared to those without WIS.

In this nationally representative study, we found a notable link between cigarette and ENDS use with WIS, particularly among those with health condition-related or prescription-related WIS, underscoring the importance of addressing tobacco use in this vulnerable population.

Although the effects of cigarette smoke (CS) on the development of several intestinal diseases is well documented, the impact of e-cigarette aerosol (e-cig) on digestive health is largely unknown. To compare the effects of e-cig and CS on mouse ileum and colon, animals were chronically exposed for 6 months by nose-only inhalation to e-cig at 18 or 30 W power, or to 3R4F CS. Results showed that e-cig exposure decreased colon cell proliferation. Several other proliferative defects were observed in response to both e-cig and CS exposure, including up- and down-regulation of cyclin D1 protein levels in the ileum and colon, respectively. E-cig and CS exposure reduced myeloperoxidase activity in the ileum. In the colon, both exposures disrupted gene expression of cytokines and T cell transcription factors. For tight junction genes, ZO-1- and occludin-protein expression levels were reduced in the ileum and colon, respectively, by e-cig and CS exposure. The 16S sequencing of microbiota showed specific mild dysbiosis, according to the type of exposure. Overall, e-cig exposure led to altered proliferation, inflammation, and barrier function in both the ileum and colon, and therefore may be a gut hazard on par with conventional CS.

Although smoking is a significant risk factor for osteomyelitis, there is limited experimental evidence that nicotine, a key tobacco constituent, is associated with this condition, leaving its mechanistic implications uncharacterized. This study revealed that nicotine promotes Staphylococcus aureus-induced osteomyelitis by increasing Nrf2 and Slc7a11 expression in vivo and in vitro. Inhibition of Slc7a11 using Erastin augmented bacterial phagocytosis/killing capabilities and fortified antimicrobial responses in an osteomyelitis model. Moreover, untargeted metabolomic analysis demonstrated that Erastin mitigated the effects of nicotine on S. aureus-induced osteomyelitis by altering glutamate/glutathione metabolism. These findings suggest that nicotine aggravates S. aureus-induced osteomyelitis by activating the Nrf2/Slc7a11 signaling pathway and that Slc7a11 inhibition can counteract the detrimental health effects of nicotine.

Nicotine has major side effects on human health through numerous mechanisms, one of which is the alteration of the immune system and its genetic components. Such alteration can be a predisposing factor for autoimmune diseases such as spondyloarthritis (SpA) and rheumatoid arthritis (RA). This review aims to shed light on the effects of nicotine smoking on the pathophysiology, clinical presentation, and management of SpA and RA.

This review looked into the studies, excluding case reports and series, which were cited by PubMed/MEDLINE.

Patients with established autoimmune conditions may have a different underlying pathophysiology and disease course when exposed to nicotine through cigarette smoking. Through the involvement of several cytokines, endothelial dysfunction, and epigenetic mechanisms, the severity of SpA is more prominent in smokers. The global health status, pain, and fatigue are worse in SpA patients. The evidence on the effect of nicotine smoking on the treatment of SpA is still limited. Nicotine can contribute to RA via the disruption of cellular regulatory activity, inflammatory responses, morphological, physiological, biochemical, and enzymatic responses. As such, smokers with RA have higher disease activity and are more likely to be seropositive through the citrullination of peptides. In addition, these patients are at risk of achieving a suboptimal response to tumor necrosis factor inhibitors.

Cigarette smoking can substantially affect the pathophysiology and clinical presentation of patients with SpA and RA. The impact of nicotine on the management of these diseases still needs to be further studied.

Pneumonia and lung cancer are both major respiratory diseases, and observational studies have explored the association between their susceptibility. However, due to the presence of potential confounders and reverse causality, the comprehensive causal relationships between pneumonia and lung cancer require further exploration.

Genome-wide association study (GWAS) summary-level data were obtained from the hitherto latest FinnGen database, COVID-19 Host Genetics Initiative resource, and International Lung Cancer Consortium. We implemented a bidirectional Mendelian randomization (MR) framework to evaluate the causal relationships between several specific types of pneumonia and lung cancer. The causal estimates were mainly calculated by inverse-variance weighted (IVW) approach. Additionally, sensitivity analyses were also conducted to validate the robustness of the causalty.

In the MR analyses, overall pneumonia demonstrated a suggestive but modest association with overall lung cancer risk (Odds ratio [OR]: 1.21, 95% confidence interval [CI]: 1.01 - 1.44, P = 0.037). The correlations between specific pneumonia types and overall lung cancer were not as significant, including bacterial pneumonia (OR: 1.07, 95% CI: 0.91 - 1.26, P = 0.386), viral pneumonia (OR: 1.00, 95% CI: 0.95 - 1.06, P = 0.891), asthma-related pneumonia (OR: 1.18, 95% CI: 0.92 - 1.52, P = 0.181), and COVID-19 (OR: 1.01, 95% CI: 0.78 - 1.30, P = 0.952). Reversely, with lung cancer as the exposure, we observed that overall lung cancer had statistically crucial associations with bacterial pneumonia (OR: 1.08, 95% CI: 1.03 - 1.13, P = 0.001) and viral pneumonia (OR: 1.09, 95% CI: 1.01 - 1.19, P = 0.037). Sensitivity analysis also confirmed the robustness of these findings.

This study has presented a systematic investigation into the causal relationships between pneumonia and lung cancer subtypes. Further prospective study is warranted to verify these findings.

Objective: Smoking is the cause of numerous oral pathologies. The aim of the study was to evaluate the effect of smoking traditional cigarettes, e-cigarettes, and heat-not-burn products on the content of salivary cytokines, chemokines, and growth factors in healthy young adults. Design: Three groups of twenty-five smokers each as well as a control group matched in terms of age, gender, and oral status were enrolled in the study. In unstimulated saliva collected from study groups and participants from the control group, the concentrations of cytokines, chemokines, and growth factors were assessed by Bio-Plex® Multiplex System. Results: We demonstrated that smoking traditional cigarettes is responsible for increasing the level of IFN-γ compared to non-smokers and new smoking devices users in unstimulated saliva in the initial period of addiction. Furthermore, e-cigarettes and heat-not-burn products appear to have a similar mechanism of affecting the immune response system of unstimulated saliva, leading to inhibition of the local inflammatory response in the oral cavity. Conclusion: Smoking traditional cigarettes as well as e-cigarettes and heat-not-burn products is responsible for changes of the local immune response in saliva. Further research is necessary to fill the gap in knowledge on the effect of new smoking devices on the oral cavity immune system.

To examine the association between early-life smoking exposure and later risk of inflammatory bowel disease [IBD].

We followed 115663 participants from the Norwegian Mother, Father and Child [MoBa] and All Babies in Southeast Sweden [ABIS] cohorts from birth [1997-2009] through 2021. IBD was identified through national patient registers. Validated questionnaire data defined maternal smoking during pregnancy, maternal environmental tobacco smoke [ETS] exposure during pregnancy, and child ETS exposure by ages 12 and 36 months. Cox regression was used to estimate adjusted hazard ratios [aHRs] for sex, maternal age, education level, parental IBD, and origin. Cohort-specific estimates were pooled using a random-effects model.

During 1 987 430 person-years of follow-up, 444 participants developed IBD [ABIS, 112; MoBa, 332]. Any vs no maternal smoking during pregnancy yielded a pooled aHR of 1.30 [95% CI = 0.97-1.74] for offspring IBD. Higher level of maternal smoking during pregnancy (compared with no smoking, average ≥6 cigarettes/day: pooled aHR = 1.60 [95% CI = 1.08-2.38]) was associated with offspring IBD, whereas a lower smoking level was not (average 1-5 cigarettes/day: pooled aHR = 1.09 [95% CI = 0.73-1.64]). Child ETS exposure in the first year of life was associated with later IBD (any vs no ETS, pooled aHR = 1.32 [95% CI = 1.03-1.69]). Estimates observed for child ETS exposure by 36 months were similar but not statistically significant.

In this prospective Scandinavian cohort study, children exposed to higher levels of maternal smoking during pregnancy or ETS during the first year of life were at increased risk of later IBD.

The number of smokers worldwide increased greatly during the past decades and reached 1.14 billion in 2019, becoming a leading risk factor for human health. Tobacco smoking has wide effects on human genetics, epigenetics, transcriptome, and gut microbiome. Although many studies have revealed effects of smoking on host transcriptome, research on the relationship between smoking, host gene expression, and the gut microbiome is limited.

We first explored transcriptome and metagenome profile differences between smokers and nonsmokers. To evaluate the relationship between host gene expression and gut microbiome, we then applied bidirectional mediation analysis to infer causal relationships between smoking, gene expression, and gut microbes.

Metagenome and transcriptome analyses revealed 71 differential species and 324 differential expressed genes between smokers and nonsmokers. With smoking as an exposure variable, we identified 272 significant causal relationships between gene expression and gut microbes, among which there were 247 genes that mediate the effect of smoking on gut microbes. Pathway-based enrichment analysis showed that these genes were significantly enriched in heme metabolic pathway, which mainly mediated the changes of Bacteroides finegoldii and Lachnospiraceae bacterium 9_1_43BFAA. Additionally, by performing metabolome data analysis in the Integrated Human Microbiome Project (iHMP) database, we verified the correlation between the intermediate products of the heme metabolism pathway (porphobilinogen, bilirubin, and biliverdin) and gut microbiome.

By investigating the bidirectional interaction between smoking-related host gene expression and gut microbes, this study provided evidence for the mediation of smoking on gut microbes through co-involvement or interaction of heme metabolism.

By comparing the metagenome and transcriptome sequencing profiles between 34 smokers and 33 age- and gender-matched nonsmokers, we are the first to reveal causal relationships among tobacco smoking, host gene expression, and gut microbes. These findings offer insight into how smoking affects gut microbes through host gene expression and metabolism, which highlights the importance of heme metabolism in modulating the effects of smoking on gut microbiome.

While smoking is widely acknowledged as a risk factor for rheumatoid arthritis (RA), the connection between secondhand smoke (SHS) exposure and RA in never-smoking adults remains limited and inconsistent. This study aims to explore and quantify this association using serum cotinine levels. We conducted a cross-sectional study with 14,940 adults who self-report as never smokers, using National Health and Nutrition Examination Survey data from 1999 to 2018. Based on previous literature, SHS exposure was categorized into four groups according to serum cotinine levels. Compared to individuals in the unexposed group (serum cotinine < 0.05 ng/mL), the adjusted odds ratio (OR) for RA was 1.37 (95% CI 1.14-1.64, p = 0.001) in the low exposure group (serum cotinine at 0.05 to 0.99 ng/mL) after adjusting for covariates. However, no significant association was found in the moderate exposure group (serum cotinine at 1 to 10 ng/mL) or the heavy exposure group (serum cotinine ≥ 10 ng/mL). Furthermore, we detected a non-linear, positively saturated correlation between the cotinine levels after log2 transformation and RA, with a turning point at approximately - 2.756 ng/mL (OR = 1.163, 95% CI 1.073-1.261, p = 0.0002). The stability of the results was confirmed by subgroup analysis.

Cancer is a leading cause of death worldwide and insufficient physical activity is a significant risk factor. This study analyzed the tumor prevalence based on sex, age, smoking, BMI, and physical activity level (PAL) in the Spanish people. Data from the Spanish National Health Survey (ENSE) was used, comprising a sample of 17,704 people diagnosed with malignant tumors. The findings revealed compelling associations (P < 0.001) between all variables examined and the prevalence of malignant tumors. Notably, women exhibited a higher prevalence than men (P < 0.05). Furthermore, individuals classified as obese displayed a greater prevalence of tumors than those within the normal weight range (P < 0.05). The analysis also showed that the inactive group had a higher prevalence of malignant tumors than the active group (P < 0.05). This study identified significant dependency relationships (P < 0.001) between PAL and the various population groups examined. Additionally, the general population analyzed in the ENSE2017 study demonstrated a reduced risk of developing malignant tumors among the active (P < 0.05) and very active groups (P < 0.05) compared to the inactive group. This risk reduction was consistently observed across different subgroups, including men, women, specific age groups, smoking, and BMI categories (P < 0.05). This study highlighted the importance of regular physical activity in reducing the risk and prevalence of malignant tumors in the Spanish population. These findings underscore the critical role of engaging in physical activity as a protective measure against cancer. Encouraging individuals to adopt an active lifestyle could significantly contribute to cancer prevention efforts and promote overall well-being.

Electronic nicotine delivery systems (ENDS) - which include electronic cigarettes or e-cigarettes, or simply e-cigs, and marijuana vaping have become increasingly popular. ENDS devices have been established as one of the tobacco quit methods and promoted to be safer compared to traditional tobacco cigarettes. Emerging evidence demonstrates that e-cigarette and marijuana vape use can be harmful, with potential associations with cancer. Herein, we summarize the level of evidence to date for altered immune response, with a focus on cancer risks in the offspring after maternal use of, or aerosol exposures from, ENDS or marijuana vape during pregnancy. From 27 published articles retrieved from PubMed, we sought to find out identified carcinogens in ENDS aerosols and marijuana vapor, which cross the placental barrier and can increase cancer risk in the offspring. Carcinogens in vaping aerosols include aldehydes, metals, tobacco-specific nitrosamines, tobacco alkaloids, polycyclic aromatic hydrocarbons, and volatile organic compounds. Additionally, there was only one passive vaping exposure case study on a human fetus, which noted that glycerol, aluminum, chromium, nickel, copper, zinc, selenium, and lead crossed from the mother to the offspring's cord blood. The carcinogens (metals) in that study were at lower concentrations compared to the mother's biological matrices. Lastly, we observed that in utero exposures to ENDS-associated chemicals can occur in vital organs such as the lungs, kidneys, brain, bladder, and heart. Any resulting DNA damage increases the risk of tumorigenesis. Future epidemiological studies are needed to examine the effects of passive aerosol exposures from existing and emerging electronic nicotine and marijuana products on developing offspring to cancer.

The relationship between smoking and the risk of acute respiratory distress syndrome (ARDS) has been recognized, but the conclusions have been inconsistent. This systematic review and meta-analysis investigated the association between smoking and ARDS risk in adults.

The PubMed, EMBASE, Cochrane Library, and Web of Science databases were searched for eligible studies published from January 1, 2000, to December 31, 2023. We enrolled adult patients exhibiting clinical risk factors for ARDS and smoking condition. Outcomes were quantified using odds ratios (ORs) for binary variables and mean differences (MDs) for continuous variables, with a standard 95% confidence interval (CI).

A total of 26 observational studies involving 36,995 patients were included. The meta-analysis revealed a significant association between smoking and an increased risk of ARDS (OR 1.67; 95% CI 1.33-2.08; P < 0.001). Further analysis revealed that the associations between patient-reported smoking history and ARDS occurrence were generally similar to the results of all the studies (OR 1.78; 95% CI 1.38-2.28; P < 0.001). In contrast, patients identified through the detection of tobacco metabolites (cotinine, a metabolite of nicotine, and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL), a metabolite of tobacco products) showed no significant difference in ARDS risk (OR 1.19; 95% CI 0.69-2.05; P = 0.53). The smoking group was younger than the control group (MD - 7.15; 95% CI - 11.58 to - 2.72; P = 0.002). Subgroup analysis revealed that smoking notably elevated the incidence of ARDS with extrapulmonary etiologies (OR 1.85; 95% CI 1.43-2.38; P < 0.001). Publication bias did not affect the integrity of our conclusions. Sensitivity analysis further reinforced the reliability of our aggregated outcomes.

There is a strong association between smoking and elevated ARDS risk. This emphasizes the need for thorough assessment of patients' smoking status, urging healthcare providers to vigilantly monitor individuals with a history of smoking, especially those with additional extrapulmonary risk factors for ARDS.

Smoking is a risk factor for low back pain (LBP) and rheumatoid arthritis (RA). We aimed to estimate the global health and economic burden of LBP and RA attributable to smoking.

This was a cross-sectional study.

The study was conducted in 192 countries and territories.

Prevalent cases of LBP and RA were used, extracted from the Global Burden of Diseases, Injuries and Risk Factors Study 2019 data repositories.

Smoking-attributable health and economic burden was estimated with the population-attributable fraction method. Smoking-attributable prevalence of LBP and RA and health-care costs were estimated for patients of all ages, whereas years lived with disability (YLDs) and productivity losses due to morbidity were estimated for patients aged 15-84 years. Uncertainty intervals (UIs) of the results were obtained by repeating the analysis with the lower and upper bounds of all input variables.

Globally, smoking accounted for 84.5 million (UI = 56.7-120.2 million) prevalent cases of LBP, 1.8 million (UI = 0.5-3.4 million) prevalent cases of RA and 11.3 million (UI = 6.2-18.5 million) YLDs, which represented 1.5% of all-cause YLDs in the working-age population aged 15-84 years in 2019. Health-care costs and productivity losses of smoking-attributable LBP and RA cost the global economy purchasing-power parity $326.0 billion (UI = $184.0-521.4 billion), representing 0.2% of the global gross domestic product. Specifically, smoking accounted for $65.8 billion (UI = $38.0-101.2 billion) in health-care costs world-wide, with more than half [$39.8 billion (UI = $23.1-61.3 billion), 60.6%] borne by the public sector. Smoking also contributed to $260.3 billion (UI = $146.0-420.3 billion) in productivity losses globally. Approximately 60.0% of the global YLDs were observed in middle-income countries, whereas 84.4% of health-care costs and 72.7% of productivity losses were borne by high-income countries.

Globally, in 2019, smoking accounted for more than 11.0 million years lived with disability and purchasing-power parity $326.0 billion in economic losses due to low back pain and rheumatoid arthritis. Middle-income countries suffered more morbidity, whereas high-income countries experienced larger economic losses.

Consensus statement on smoking and vascular risk About 22% of the Spanish population are daily smokers. Men are more likely to smoke than women. In Spain, women between 15-25 years of age smoke as much or more than men. Every smoker should be assessed for: physical dependence on nicotine (Fagerström test), social and psychological dependence (Glover Nilsson test), level of motivation to quit (Richmond test), probability of therapy success (Henri-Mondor and Michael-Fiore tests), and stage of behavioral change development (Prochaska and DiClementi). Advice on smoking cessation is highly cost-effective and should always be provided. Smoking is an enhancer of cardiovascular risk because it acts as a pathogen agent in the development of arteriosclerosis and is associated with ischemic heart disease, stroke, and peripheral artery disease. Smoking increases the risk of chronic lung diseases (COPD) and is related to cancers of the lung, female genitalia, larynx, oropharynx, bladder, mouth, esophagus, liver and biliary tract, and stomach, among others. Combined oral contraceptives should be avoided in women smokers older than 35 years of age due to the risk of thromboembolism. In smoking cessation, the involvement of physicians, nurses, psychologists, etc. is important, and their multidisciplinary collaboration is needed. Effective pharmacological treatments for smoking cessation are available. Combined treatments are recommended when smoker's dependence is high. For individuals who are unable to quit smoking, a strategy based on tobacco damage management with a total switch to smokeless products could be a less dangerous alternative for their health than continuing to smoke.

Influenza A(H7N9) virus showed high pathogenicity in humans when it emerged in 2013. Cigarette smoke (CS) causes pulmonary diseases including bronchitis, emphysema, and lung cancer. Although habitual smoking is thought to increase the risk of severe seasonal influenza virus infection, its effect on A(H7N9) virus infection is poorly understood. Here, we employed a mouse model of long-term exposure to CS to investigate the effect of CS on the pathogenicity of A(H7N9) virus infection. Unexpectedly, body weight loss for mice exposed to CS was milder than that for mock-treated mice upon A(H7N9) virus infection. CS exposure improved the survival rate of A(H7N9) virus-infected mice even though virus titers and pathological changes in the lungs were not significantly different between CS-exposed and control mice. Microarray analysis showed that CS-exposure activates cytokine/chemokine activity, immune response, and cell cycle activities that resemble reactivities against A(H7N9) virus infection. Therefore, under conditions where cytokine and chemokine expression in the lungs is already high due to CS exposure, the enhanced expression of cytokines and chemokines caused by A(H7N9) virus infection might be less harmful to the organs compared to the rapid increase in cytokine and chemokine expression in the air-exposed mice due to the infection. CS may thus induce immunoregulatory effects that attenuate severe pulmonary disease during A(H7N9) virus infection. However, these findings do not support CS exposure due to its many other proven negative health effects.

The emerging use of biomarkers in research and tailored care introduces a need for information about the association between biomarkers and basic demographics and lifestyle factors revealing expectable concentrations in healthy individuals while considering general demographic differences.

A selection of 47 biomarkers, including markers of inflammation and vascular stress, were measured in plasma samples from 9876 Danish Blood Donor Study participants. Using regression models, we examined the association between biomarkers and sex, age, Body Mass Index (BMI), and smoking.

Here we show that concentrations of inflammation and vascular stress biomarkers generally increase with higher age, BMI, and smoking. Sex-specific effects are observed for multiple biomarkers.

This study provides comprehensive information on concentrations of 47 plasma biomarkers in healthy individuals. The study emphasizes that knowledge about biomarker concentrations in healthy individuals is critical for improved understanding of disease pathology and for tailored care and decision support tools.