Search Results (198)

Background: Prostate cancer in the Middle East and North Africa (MENA) region is shaped by a complex interplay of behavioral and environmental risk factors, yet comprehensive estimates of preventable cases remain scarce. To address this gap, we estimated population-attributable fractions (PAFs) for a range of modifiable exposures among men aged 50 years and older and assessed potential reductions in incidence under feasible intervention scenarios. Methods: Regional prevalence data were combined with relative risks from meta-analyses to compute closed-form PAFs for tobacco smoking, obesity, physical inactivity, high dairy and calcium intake, heavy alcohol use, drinking water nitrates, trihalomethanes, arsenic, lead, selenium status, ambient PM_2.5 and NO₂, and occupational diesel exhaust, covering an estimated 47 million men. Estimates were validated using a synthetic cohort simulation of 100,000 individuals, with uncertainty quantified through Monte Carlo sampling. Results: Results showed that drinking water nitrate exposure accounted for the largest single fraction (17.4%), followed by tobacco smoking (9.5%), physical inactivity (6.7%), and trihalomethane exposure (5.0%), while other exposures contributed smaller but meaningful shares. Joint elimination of all exposures projected a 45.5% reduction in incidence, and simultaneous feasible reductions in four targeted exposures yielded a combined potential impact fraction of 12.1%. Conclusions: These findings suggest that integrated water quality management, tobacco control, lifestyle interventions, and targeted environmental surveillance should be prioritized to reduce prostate cancer burden in the MENA region. However, estimates of drinking-water nitrate exposure rely on limited evidence from a single case–control study with a relatively small sample size, and should therefore be considered exploratory and primarily hypothesis-generating. Full article

Acrolein, a highly reactive environmental toxicant widely present in urban air and tobacco smoke, has been implicated in the development of multiple malignancies. In oral tissues, chronic acrolein exposure induces oxidative stress, inflammation, and genetic mutations, all of which are closely linked to the development of oral squamous cell carcinoma (OSCC). Although accumulating evidence indicates a strong association between acrolein exposure and OSCC, its prognostic significance remains poorly understood. In this study, we analyzed transcriptome data to identify differentially expressed genes (DEGs) between tumor and adjacent normal tissues, and screened acrolein-related candidates by intersecting DEGs with previously identified acrolein-associated gene sets. Functional alterations of these genes were assessed using Gene Set Variation Analysis (GSVA), and a protein–protein interaction (PPI) network was constructed to identify key regulatory genes. A prognostic model was developed using Support Vector Machine–Recursive Feature Elimination (SVM-RFE) combined with LASSO-Cox regression and validated in an independent external cohort. Among the acrolein-related DEGs, four key genes (PLK1, AURKA, CTLA4, and PPARG) were ultimately selected for model construction. Kaplan–Meier analysis showed significantly worse overall survival in the high-risk group (p < 0.0001). Receiver operating characteristic (ROC) curve analysis further confirmed the strong predictive performance of the model, with area under the curve (AUC) values of 0.72 at 1 year, 0.72 at 3 years, and 0.75 at 5 years. Furthermore, the high risk score was significantly correlated with a ‘cold’ immune microenviroment, suggesting that acrolein-related genes may modulate the tumor immune microenvironment. Collectively, these findings highlight the role of acrolein in OSCC progression, suggesting the importance of reducing acrolein exposure for cancer prevention and public health, and call for increased attention to the relationship between environmental toxicants and disease initiation, providing a scientific basis for public health interventions and cancer prevention strategies. Full article

Atopic eczema and asthma frequently co-occur, forming a distinct complex phenotype that likely arises from shared genetic pathways and early-life environmental influences. We aimed to investigate whether variants in TNS1 and NRXN1—previously identified in a genome-wide interaction study—influence susceptibility to atopic eczema and the asthma–eczema phenotype and whether early-life environmental tobacco smoke (ETS) exposure modifies these genetic effects. A total of 188 Caucasian children under 2 years at recruitment were prospectively followed up to 6 years of age. Eligibility of all participants for the study or control group was based on a questionnaire and a physician-confirmed diagnosis of eczema and asthma. Early-life ETS exposure was assessed by parental questionnaire. All participants were genotyped for TNS1 and NRXN1 SNPs. The TNS1 rs918949 [T] allele was associated with the combined asthma–eczema phenotype but not with eczema alone. Synergistic gene–environment interactions were identified for both TNS1 and NRXN1, with the highest risk of the combined asthma–eczema phenotype observed among ETS-exposed carriers of risk alleles. Our findings provide the first independent replication of evidence suggesting that TNS1 and NRXN1 may contribute to the asthma–eczema comorbidity through mechanisms that could be substantially modified by early-life ETS exposure. Full article

Background: Vitamin D (VD) plays a central role in calcium homeostasis during pregnancy and has been implicated in redox-related biological processes. While VD deficiency (VDD) has been consistently associated with adverse pregnancy outcomes, the relationships between VD insufficiency (VDI), maternal antioxidant-related biomarkers, and neonatal outcomes remain incompletely characterized, particularly during the third trimester. Objective: To determines the prevalence of VDI in third-trimester pregnant women and to examine its associations with antioxidant-related markers and selected neonatal outcomes. Methods: A cross-sectional study was conducted among pregnant women in the third trimester attending a tertiary referral hospital in Mexico City. Maternal serum 25-hydroxyvitamin D (25-OHD) concentrations were measured, along with a panel of redox-related markers, including 2,2-diphenyl-2-2picrylhydrazyl (DPPH) radical scavenging activity, reduced glutathione (GSH), glutathione S-transferase (GST), glutathione peroxidase (GPx), and oxygen radical absorbance capacity (ORAC). Neonatal anthropometric parameters were recorded at birth. Associations between maternal VD status, redox-related markers, environmental factors, and neonatal outcomes were evaluated using appropriate statistical analyses. Results: A high prevalence of VDI was observed in the study population. Maternal VDI was associated with lower activities of GSH, GST, and GPx. Passive exposure to tobacco smoke and season of sampling were also associated with lower VD concentrations. Neonates born to women with VDI had higher birth weight compared with those born to women with sufficient VD concentrations. Maternal serum 25-OHD concentrations correlated positively with selected antioxidant enzyme activities. Conclusions: In this cohort of third-trimester pregnant women, VDI co-occurred with environmental factors, differences in maternal redox-related markers, and selected neonatal outcomes. These findings support an associative framework in which suboptimal VD status during the third trimester is accompanied by variations in redox-related markers. Longitudinal and mechanistic studies are needed to clarify the temporal sequence and biological relevance of these associations. Full article

(1) Background: Tobacco use constitutes a significant preventable cause of morbidity and mortality on a global scale. It contributes to cumulative exposure to carcinogenic and toxic heavy metals, including cadmium, lead, nickel, and copper. Collectively, these metals promote oxidative stress, multi-organ damage, and an increased risk of cancer, cardiovascular, respiratory, and renal diseases; (2) Methods: The research material comprised 119 tobacco samples. The concentrations of cadmium, lead, copper, and nickel in the samples were subsequently determined. A series of calculations were conducted in order to estimate the non-carcinogenic and carcinogenic health risks associated with the consumption of tobacco products under a variety of exposure scenarios; (3) Results: The concentrations of heavy metals in the tobacco samples ranged as follows, with mean values: Cd: 0.3–8.6 mg/kg (mean 1.0), Cu: 3.4–92.6 mg/kg (mean 12.3), Ni: 1.1–15.4 mg/kg (mean 3.4), and Pb: 0.2–1633.3 mg/kg (mean 46.5). A health risk assessment indicated that exposure through inhalation to cadmium Cd, Ni, and Pb, even in the minimal smoking scenario of one cigarette per day, consistently exceeded internationally established thresholds for carcinogenic risk; (4) Conclusions: The presence of high inter-brand variability and high-risk outliers underscores the necessity for enhanced regulation and monitoring of toxic metals in tobacco products. Full article

Background/Objectives: Thirdhand smoke (THS), residual tobacco pollutants persisting on surfaces, dust, and fabrics, poses specific risks to infants and children, yet its implications for nursing remain underexplored. This scoping review mapped existing evidence on THS in neonatal and pediatric contexts and synthesized nursing implications, focusing on nurses’ knowledge, unintentional environmental contamination, and educational roles. Methods: Following JBI methodology and reported according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines, a three-step search was performed across MEDLINE, CINAHL, Scopus, Web of Science, Cochrane Library, Google Scholar, and OpenGrey. Studies were included if they addressed (1) nurses’ knowledge, beliefs, and attitudes toward THS-related risks in infants and children; (2) nurses’ contribution to unintentional environmental THS contamination; or (3) nurse-led educational or preventive interventions targeting parents or communities. Results: Among 563 records, 8 met inclusion criteria. Four investigated nurses’ awareness and perceptions, revealing limited understanding of THS despite recognition of its harmfulness. One study examined contamination, detecting nicotine residues on nurses’ fingers, suggesting possible in-hospital transmission. No nurse-led interventions specifically targeting THS were found, though broader smoke-exposure education programs showed benefits when supported by nursing staff. Conclusions: Evidence is scarce but underscores significant gaps in nurses’ knowledge, clinical guidance, and educational initiatives concerning THS. Strengthening nursing education and research is essential to mitigate THS exposure in neonatal and pediatric settings and enhance nurses’ preventive and advocacy roles. Full article

White-matter development during fetal life represents one of the most vulnerable processes to environmental disruption, as it relies on the precisely timed proliferation, migration, and differentiation of oligodendrocyte lineage cells. Among environmental threats, exposure to toxic compounds contained in tobacco smoke and vaping aerosols represents a major yet preventable risk during pregnancy. Despite growing awareness, tobacco smoking remains widespread, and a substantial proportion of the population—including pregnant women—continues to perceive electronic nicotine delivery systems (ENDS) as less harmful, a misconception that contributes to persistent prenatal exposure. These products expose the fetus to numerous substances that readily cross the placenta and reach the developing brain, including compounds with endocrine-disrupting activity, where they interfere with white-matter development. Epidemiological and neuroimaging studies consistently reveal microstructural alterations in white matter that correlate with long-term cognitive and behavioral impairments in offspring exposed in utero. These alterations may arise from both nicotine-specific pathways and the actions of other toxicants in cigarette smoke and ENDS aerosols that cross the placenta and disrupt white-matter emergence and maturation. Preclinical research provides mechanistic insight: nicotine acts directly on nicotinic acetylcholine receptors (nAChRs) in oligodendrocyte precursor cells, disrupting calcium signaling and differentiation, while additional constituents of smoke and vaping aerosols also affect astrocyte and microglial function and disturb the extracellular milieu required for proper myelination. Full article

The use of sweeteners in e-cigarette liquids has become increasingly common, aiming to enhance the sensory appeal of vaping products. Compounds like aspartame, saccharin, and sucralose are added to provide a sweet taste without any calories, especially in flavored e-liquids popular among younger users. However, recent studies suggest that these additives may pose significant health risks when vaporized and inhaled. Sucralose, in particular, can break down into potentially harmful chlorinated by-products at high temperatures typical of vaping devices. Moreover, there is growing concern about the synergistic effects of sweeteners like sucralose, one sweetener with another and when combined with other e-liquid components. It has been observed that the presence of sucralose may amplify oxidative stress; genotoxicity, including mutations; and overall toxicity, along with environmental impact. This is not limited to nicotine- and smoke-related harm, as it may strengthen the toxic effect of the substances used in e-liquids that are not present in traditional cigarettes. The combined exposure to these heated compounds can intensify cytotoxicity, potentially increasing the risk of respiratory, cardiovascular, and neurological effects over time. While marketed as safer alternatives to tobacco, e-cigarettes containing sweeteners like sucralose may introduce new and poorly understood toxicological hazards that deserve urgent regulatory attention. Full article

Background: Lung carcinoma remains the leading cause of cancer-related mortality worldwide, with smoking as the primary risk factor and radon exposure as the second, and the first among non-smokers. The combined effect of tobacco smoke and indoor radon increases disease risk up to 2.5 times, emphasizing the need for prevention and environmental risk assessment. Methods: This study analyzed the incidence of lung carcinoma in Bulgaria during 2013–2022 and examined its association with indoor radon exposure across different regions. Annual data were obtained from the National Statistical Institute and the National Survey of Indoor Radon Concentrations in Residential Buildings (2015–2016). Results: The average annual incidence was 43.5 per 100,000 population, showing a 3.4% annual decline, while the average prevalence was 131.7 per 100,000, decreasing by 1.4% per year. Considerable interregional variation was observed, with incidence ranging from 25.5 to 62.4 per 100,000. A moderate positive correlation was found between lung carcinoma incidence and mean indoor radon concentration, and a stronger to very strong correlation with the proportion of dwellings exceeding 300 Bq/m³ and 200 Bq/m³. Conclusions: These findings indicate a positive association between residential radon exposure and lung cancer morbidity and support maintaining the WHO-recommended reference level of 200 Bq/m³. Full article

Developmental programming, shaped by environmental and lifestyle stressors during prenatal life, is increasingly recognized as a major contributor to non-communicable diseases (NCDs) later in life. Oxidative stress, one of key mechanisms linking these stressors to fetal metabolomic reprogramming and disease pathogenesis, leaves measurable metabolomic signatures that reflect disrupted redox balance. Alterations in glucose, lipid, and amino acid metabolism and antioxidant response could reveal the main pathways driving NCD development. This review summarizes epidemiological studies that have investigated biochemical responses of the prenatal exposure to metals, air pollution, and tobacco smoke and e-cigarette vapor in maternal–placental–fetal compartments using a metabolomic approach. Summarized studies indicate that maternal exposure to metals primarily disrupts amino acid pathways related to one-carbon metabolism, glutathione synthesis, and oxidative stress defense, while air pollution, particularly fine particulate matter, mainly affects lipid oxidation, fatty acid β-oxidation, and amino acid and carbohydrate metabolism. Tobacco smoke and e-cigarette vapor induce widespread disturbances involving reduced citric acid cycle intermediates, altered acylcarnitines and phospholipids, and impaired antioxidant capacity, collectively promoting oxidative damage and inflammatory signaling. The identification of these metabolome alterations might contribute to a deeper understanding of the toxicity and biological impact of environmental stressors on offspring health. These results may eventually lead to the identification of early biomarkers and to the development of therapeutic strategies aimed at reducing NCD risk. Full article

Background/Objectives: Lead, a toxic heavy metal, is widely recognized as a hazardous environmental contaminant capable of disrupting physiological homeostasis by altering stress response mechanisms and impairing pulmonary function. A comparable detrimental factor is tobacco smoking, which represents one of the most prevalent addictions worldwide. The presented study aimed to evaluate the combined impact of cigarette smoking and occupational lead exposure on selected oxidative stress biomarkers and pulmonary function parameters. Methods: 453 male employees working in a zinc smelter were recruited for participation in the study. Participants were subsequently divided into two groups: current smokers (n = 209) and former smokers (n = 244). Each group was then further subdivided according to blood lead concentration into subgroups with high (>35 μg/dL) and low (<35 μg/dL) lead levels. Venous blood samples were collected for biochemical analysis of oxidative stress parameters, including total oxidant status (TOS), malondialdehyde (MDA), protein thiol content (PSH), total antioxidant capacity (TAC), and the oxidative stress index (OSI). In addition, spirometric evaluation was conducted. Results: Former smokers demonstrated significantly more favorable oxidative stress profiles and superior spirometric outcomes compared with current smokers. No statistically significant associations were observed between lead exposure levels and either biochemical or spirometric parameters. Conclusions: Cigarette smoking appears to exert a stronger adverse influence on oxidative balance and pulmonary function than occupational lead exposure. Full article

It is well known that environmental factors influence the risk of type 2 diabetes mellitus (T2DM). Several studies have linked the xenobiotics present in tobacco or air pollutants to T2DM development, although the underlying mechanisms remain unclear. Surfactant protein D (SP-D), an immune component released into the bloodstream after lung injury, has been associated with metabolic diseases. The aim of this study was to investigate whether SP-D mediates the effects of smoking or air pollution exposure on T2DM risk in the Spanish adult population. Socio-demographic, lifestyle (including smoking status) and clinical data from 2155 participants from the Di@bet.es cohort were analyzed. Annual concentrations of PM₁₀, PM_2.5, SO₂, CO and NO₂ according to participants’ residential address codes were used to study air pollution exposure. T2DM was diagnosed at baseline and after 7.5 years of follow-up. SP-D serum levels were measured by ELISA and categorized as above or below the 25th percentile. Our results revealed a higher percentage of smokers in the high SP-D category; however, no associations were observed between air pollutants (PM₁₀, PM_2.5, SO₂, CO) and SP-D categories. Both smoking and elevated SP-D levels were found to increase the risk of T2DM independently. Mediation analysis indicated that SP-D mediates 14% of the effect of smoking on T2DM incidence in the Spanish adult population. Full article

Introduction: Cigarette smoking is unquestionably associated with an increase in morbidity and mortality worldwide, exerting significant adverse effects on respiratory health. The impact of tobacco persists in the epigenome long after smoking cessation. Furthermore, the offspring of smokers may also be affected by the detrimental effects of smoking. Material and methods: The modifications made to the body, such as DNA methylation, histone modification, and regulation by non-coding RNAs, do not change the DNA sequence but can influence gene expression. In respiratory disease, multigenerational effects have been reported in humans, with an increased risk of asthma or COPD and decreased lung function in offspring, despite them not being exposed to smoke. Prenatal nicotine exposure leads to pulmonary pathology that persists across three consecutive generations, supported by animal studies conducted by Rehan et al. Significant advances in high-throughput genomic and epigenomic technologies have enabled the discovery of molecular phenotypes. These either reflect or are influenced by them. Due to the hidden environmental effects and the rise of artificial intelligence (AI) in biomedical research, new predictive models are emerging that not only explain complex data but also enable earlier detection and prevention of smoking-related diseases. In this narrative review, we synthesise the latest research on how smoking affects gene regulation and chromatin structure, emphasising how tobacco can increase vulnerability to multiple diseases. Discussion: For many years, it was widely believed that diseases are solely inherited through genetics. However, recent research in epigenetics has led to a significant realisation: environmental factors play a crucial role in an individual’s life. External influences leave a mark on DNA that can influence future health and offer insights into potential illnesses. In this context, it is possible that in the future, doctors might treat people not as a whole but as individual beings, with personalised medication, tests, and other approaches. Conclusions: The accumulated evidence suggests that exposure to various environmental factors is associated with multigenerational changes in gene expression patterns, which may contribute to increased disease risk. The application of artificial intelligence in this domain is currently a crucial tool for researching potential future health issues in individuals, and it holds a powerful prospect that could transform current medical and scientific practice. Full article

Early childhood caries (ECC) remains a significant global health challenge, disproportionately affecting marginalized populations. While traditional research emphasizes behavioral and biological risk factors, emerging evidence highlights the critical role of environmental determinants. This narrative synthesis aims to highlight the role of environmental determinants as a risk factor for ECC pathogenesis. Environmental toxins (e.g., lead, perfluoroalkyl acids, tobacco smoke, air pollution) disrupt enamel development, impair salivary function, and compromise immune responses, directly increasing caries susceptibility. Environmental degradation, including air pollution, reduces ultraviolet B radiation exposure, limiting endogenous vitamin D synthesis that is vital for enamel mineralization and immune regulation. These risks are compounded in low- and middle-income countries, where structural inequities, inadequate sanitation, and climate disruptions exacerbate ECC burdens. We introduce ecovitality—the resilience of ecosystems supporting human health—as a novel framework linking ecological vitality to oral health. Degraded environments limit access to fluoridated water and nutrient-dense foods while promoting sugary diets and endocrine disruptors. A One Health approach is advocated to address interconnected environmental, social, and biological determinants of the risk for ECC. Despite global reductions in tobacco use and lead exposure, the Global Burden of Disease 2021 analysis reports stagnation in ECC prevalence. This underscores the critical need for longitudinal and mechanistic studies to establish causality, quantify the contributions of environmental controls, and explore how mitigating these risks can reduce the global ECC burden. Such evidence may promote interdisciplinary action to align oral health promotion for children with the Sustainable Development Goals. Full article

Asthma is a chronic respiratory disease resulting from a complex interplay of genetic, environmental, and occupational factors. Key environmental risks include exposure to tobacco smoke and respiratory sensitizing agents, many of which are prevalent in workplace settings. In adults, asthma is associated with reduced employment, job instability, and work-related disability, resulting in significant social and economic consequences. This scoping review investigates the role of exposure to respiratory sensitizers in the onset and progression of asthma, considering data from the general population to occupational settings, with a focus on sex and gender as key modifiers of risk, disease severity, and occupational outcomes. Biological studies were also considered to clarify the mechanisms underlying observed sex/gender differences. Epidemiological data indicate that women are disproportionately affected by asthma, experiencing more severe symptoms, higher comorbidity rates, and increased exposure in certain professions such as healthcare, cleaning, and textile work. These disparities are attributed to both sex-related factors (e.g., hormonal influences) and gender-related factors (e.g., occupational roles, smoking habits). Although traditional job roles are changing, women continue to face greater occupational asthma risks. As roles evolve, physiological sex-based differences may become increasingly relevant in shaping asthma susceptibility. This review emphasizes the need for sex- and gender-sensitive strategies in asthma prevention, surveillance, and management, especially in occupational health contexts. Full article