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BACKGROUND: Exposure to environmental chemicals has been associated with an elevated risk of heart failure (HF). However, the impact on early markers of HF, such as left ventricular dysfunction (LVD), remains limited. OBJECTIVE: To establish a foundation of evidence regarding early HF markers and their association with environmental pollutants, a systematic review and meta-analysis was conducted. METHODS: The search, conducted on October 13th, 2023, encompassed PubMed, Embase, and Web of Science without filters, focusing on observational studies reporting myocardial geometrical, structural, or functional alterations in individuals without a history of heart disease. This included the general adult population, workers, young people, and the elderly. The risk of bias was assessed using the ROBINS-I tool at both study and item levels. RESULTS: The systematic review included 17 studies involving 43.358 individuals exposed to air pollution and 2038 exposed to heavy metals. Approximately 41% of the effect measures of associations reported significant abnormalities in myocardial structure or function. The metanalyses by pollutants categories indicated positive associations between LV systolic and diastolic abnormalities and exposure to PM2.5 [-0.069 (-0.104, -0.033); -0.044 (-0.062, -0.025)] and PM10 [-0.055 (-0.087, -0.022); -0.030 (-0.050, -0.010)] and NO2 [-0.042 (-0.071, -0.013); -0.021 (-0.037, -0.004)], as well as positive associations between lead exposure and LV systolic abnormalities [-0.033 (-0.051, -0.016)]. CONCLUSIONS: Existing evidence shows that specific early markers of HF may be associated with exposure to chemical pollutants. It is recommended to include such endpoints in new longitudinal and case-control studies to confirm further risk associations. These studies should consider co-exposures, account for vulnerable groups, and identify cardiotoxic compounds that may require regulation. When examining the link between myocardial abnormalities and environmental exposure, it is also advisable to explore the supportive use of Adverse Outcome Pathway (AOP) approaches to confirm a causal relationship.

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BACKGROUND: Previous studies have shown that ALDH2 and ADH1B genes may be associated with alcohol metabolism and the risk of esophageal squamous cell carcinoma (ESCC), with inconsistent results. This meta-analysis aimed at comprehensively assessing the associations between ALDH2 and ADH1B polymorphisms and the risk of ESCC to synthesize and clarify the evidence. METHODS: We calculated summary estimates of the associations between four genetic variants (rs671 and rs674 in ALDH2, and rs1229984 and rs1042026 in ADH1B) and the ESCC risk across 23 publications in the additive model and allelic model. Venice criteria, Bayesian false discovery probability (BFDP), and false-positive reporting probability (FPRP) were used to assess the strength of epidemiological evidence. Heterogeneity among studies was evaluated by using the Higgin's I2 statistic, and publication bias was assessed by using funnel plots and Begg's test. A Mendelian randomization (MR) analysis was performed to determine the causal association between alcohol intake and esophageal cancer risk. Data from the HaploReg v4.1 and PolyPhen-2 were analyzed for functional annotations. RESULTS: Of the four genetic variants, rs671 of ALDH2 was associated with a significantly reduced risk of ESCC (OR: 0.60, 95% CI: 0.50-0.73), whereas rs1229984 of ADH1B was associated with a significantly increased risk (2.50, 95% CI: 1.70-3.69) in the additive model. In the allelic model, the variant rs1229984 of ADH1B also increased the risk of ESCC (OR: 1.50; 95% CI: 1.21-1.87). The result for the variant rs671 was considered as strong epidemiological evidence. Functional annotations identified that the four variants were related to the enhancer histone marks and motif changes. The other two variants were not associated with the ESCC risk (rs674 of ALDH2 OR: 1.22, 95% CI: 0.71-2.12; rs1042026 of ADH1B OR: 1.28, 95% CI: 0.52-3.14) in the additive model. The MR analysis did not find a causal effect of alcohol on the esophageal cancer risk. CONCLUSIONS: The results showed that ADH1B rs1229984 was significantly associated with an increased the risk of ESCC.

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BACKGROUND: Accumulating epidemiological studies have demonstrated that smoking caused damage to human health. However, these studies almost focused on the individual smoking pattern rather than the toxic ingredients of tobacco smoke. Despite the exact accuracy of cotinine as a smoking exposure biomarker, there were few studies investigating the association between serum cotinine and human health. This study aimed to provide novel evidence about the harmful effect of smoking on systemic health from the perspective of serum cotinine. METHODS: All used data was acquired from 9 survey cycles (2003-2020) of the National Health and Nutrition Examination Survey (NHANES) program. The mortality information of participants was derived from the National Death Index (NDI) website. The disease status of participants, including respiratory, cardiovascular, and musculoskeletal diseases, was obtained from questionnaire surveys. The metabolism-related index, including obesity, bone mineral density (BMD), and serum uric acid (SUA), was obtained from examination data. Multiple regression methods, smooth curve fitting, and threshold effect models were used for association analyses. RESULTS: With a total of 53,837 subjects included, we detected an L-shaped association between serum cotinine and obesity-related index, a negative association between serum cotinine and BMD, a positive association between serum cotinine and nephrolith and coronary heart disease (CHD), a threshold effect of serum cotinine on hyperuricemia (HUA), osteoarthritis (OA), chronic obstructive pulmonary disease (COPD), and stroke, as well as a positive saturate effect of serum cotinine on asthma, rheumatoid arthritis (RA), all-cause, cardiovascular disease (CVD)-cause, cancer-cause, and diabetes-cause mortality. CONCLUSIONS: In this study, we investigated the association between serum cotinine and multiple health outcomes, indicating the systematic toxicity of smoking exposure. These findings provided novel epidemiological evidence about how passive exposure to tobacco smoke affects the health condition of the general US population.

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In the last decade, most of the evidence on the clinical benefits of including cruciferous foods in the diet has been focused on the content of glucosinolates (GSL) and their corresponding isothiocyanates (ITC), and mercapturic acid pathway metabolites, based on their capacity to modulate clinical, biochemical, and molecular parameters. The present systematic review summarizes findings of human studies regarding the metabolism and bioavailability of GSL and ITC, providing a comprehensive analysis that will help guide future research studies and facilitate the consultation of the latest advances in this booming and less profusely researched area of GSL for food and health. The literature search was carried out in Scopus, PubMed and the Web of Science, under the criteria of including publications centered on human subjects and the use of Brassicaceae foods in different formulations (including extracts, beverages, and tablets), as significant sources of bioactive compounds, in different types of subjects, and against certain diseases. Twenty-eight human intervention studies met inclusion criteria, which were classified into three groups depending on the dietary source. This review summarizes recent studies that provided interesting contributions, but also uncovered the many potential venues for future research on the benefits of consuming cruciferous foods in our health and well-being. The research will continue to support the inclusion of GSL-rich foods and products for multiple preventive and active programs in nutrition and well-being.

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Purpose: Based on a large number of systematic reviews and meta-analyses exploring the relationship between psoriasis and various health outcomes, we conducted an comprehensive analysis to assess the strength and evidence for the association between psoriasis and medical end-point ramifications in patients. Methods: We searched related meta-analyses, investigating the links between psoriasis and medical ramifications from three databases. All summary effect sizes, 95% CIs, heterogeneity, and small-study effects in the included meta-analyses were recalculated. We assessed the methodological quality of included articles with the AMSTAR 2 tool and graded the epidemiological evidence. Subgroup analysis based on the severity of psoriasis and study design were also performed. Results: A total of 38 articles comprising 85 unique meta-analyses were included in this study. Although 69 outcomes were statistically significant, only 8 outcomes (nonvascular dementia, ulcerative colitis, pediatric dyslipidemia, gestational diabetes, gestational hypertension, fracture, multiple sclerosis, and schizophrenia) showed a high quality of epidemiological evidence. Conclusion: We found that psoriasis increased the risk of 69 health outcomes, and 8 outcomes were graded as high-quality evidence. No evidence was found that psoriasis was beneficial for any medical end point. However, to verify our results, more large-sample, multi-center prospective cohort studies are needed.

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Environmental causes of cardiovascular diseases (CVDs) are global health issues. In particular, an association between metal exposure and CVDs has become evident but causal evidence still lacks. Therefore, this symposium at the Society of Toxicology 2022 annual meeting addressed epidemiological, clinical, pre-clinical animal model-derived and mechanism-based evidence by five presentations: 1) An epidemiologic study on potential CVD risks of individuals exposed occupationally and environmentally to heavy metals; 2) Both presentations of the second and third were clinical studies focusing on the potential link between heavy metals and pulmonary arterial hypertension (PAH), by presenting altered blood metal concentrations of both non-essential and essential metals in the patients with PAH and potential therapeutic approaches; 3) Arsenic-induced atherosclerosis via inflammatory cells in mouse model; 4) Pathogenic effects on the heart by adult chronic exposure to very low-dose cadmium via epigenetic mechanisms and whole life exposure to low dose cadmium via exacerbating high-fat-diet-lipotoxicity. This symposium has brought epidemiologists, therapeutic industry, physicians, and translational scientists together to discuss the health risks of occupational and environmental exposure to heavy metals through direct cardiotoxicity and indirect disruption of homeostatic mechanisms regulating essential metals, as well as lipid levels. The data summarized by the presenters infers a potential causal link between multiple metals and CVDs and defines differences and commonalities. Therefore, summary of these presentations may accelerate the development of efficient preventive and therapeutic strategies by facilitating collaborations among multidisciplinary investigators.

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There is increasing evidence suggesting that Epstein-Barr virus infection is a causative factor of multiple sclerosis (MS). Epstein-Barr virus (EBV) is a human herpesvirus, Human Gammaherpesvirus 4. EBV infection shows two peaks: firstly, during early childhood and, secondly during the teenage years. Approximately, 90-95% of adults have been infected with EBV and for many this will have been a subclinical event. EBV infection can be associated with significant morbidity and mortality; for example, primary infection in older children or adults is the leading cause of infectious mononucleosis (IM). A disrupted immune response either iatrogenically induced or through genetic defects can result in lymphoproliferative disease. Finally, EBV is oncogenic and is associated with several malignancies. For these reasons, vaccination to prevent the damaging aspects of EBV infection is an attractive intervention. No EBV vaccines have been licensed and the prophylactic vaccine furthest along in clinical trials contains the major virus glycoprotein gp350. In a phase 2 study, the vaccine reduced the rate of IM by 78% but did not prevent EBV infection. An EBV vaccine to prevent IM in adolescence or young adulthood is the most likely population-based vaccine strategy to be tested and adopted. National registry studies will need to be done to track the incidence of MS in EBV-vaccinated and unvaccinated people to see an effect of the vaccine on MS. Assessment of vaccine efficacy with MS being a delayed consequence of EBV infection with the average age of onset being approximately 30 years of age represents multiple challenges.

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Polyphenols are a group of secondary plant metabolites widely present in diets and have antagonistic effects on some chronic metabolic diseases, like type 2 diabetes (T2D) and obesity. We attempt to investigate the effects of polyphenols in fruits and vegetables on reducing the risk of T2D and obesity by collecting epidemiological evidence, including cross-sectional survey (CSS), prospective cohort study (PCS), and randomized controlled trial (RCT). Further, we provide possible mechanisms for the anti-diabetic effects including protecting pancreatic ß-cells, affecting glucose digestion, absorption, and uptake, and activating glucose/lipid metabolism pathways, while improving obesity by reducing lipid accumulation, regulating intestinal microflora, alleviating inflammation, and reducing food intake. Polyphenols also play an important role in the relationship between T2D and obesity. On the one hand, obesity is a low-grade chronic inflammation causing insulin resistance, so polyphenols can reduce T2D risk by improving obesity. On the other hand, obesity decreases the polyphenols bioavailability by disturbing gastrointestinal microflora, thus increasing T2D risk. These are instructive for diets and bring considerable development value. Therefore, we discussed the hotspots of polyphenols exploitation in the food industry, including masking bitter and astringent taste, ensuring stability, and improving the bioavailability, which provides ideas for polyphenols application in anti-diabetics and anti-obesity.

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An extensive multi-country outbreak of multidrug-resistant monophasic Salmonella Typhimurium infection in 10 countries with 150 reported cases, predominantly affecting young children, has been linked to chocolate products produced by a large multinational company. Extensive withdrawals and recalls of multiple product lines have been undertaken. With Easter approaching, widespread product distribution and the vulnerability of the affected population, early and effective real-time sharing of microbiological and epidemiological information has been of critical importance in effectively managing this serious food-borne incident.

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The environmental and health impacts from the massive discharge of chemicals and subsequent pollution have been gaining increasing public concern. The unintended exposure to different pollutants, such as heavy metals, air pollutants and organic chemicals, may cause diverse deleterious effects on human bodies, resulting in the incidence and progression of different diseases. The article reviewed the outbreak of environmental pollution-related public health emergencies, the epidemiological evidence on certain pollution-correlated health effects, and the pathological studies on specific pollutant exposure. By recalling the notable historical life-threatening disasters incurred by local chemical pollution, the damning evidence was presented to criminate certain pollutants as the main culprit for the given health issues. The epidemiological data on the prevalence of some common diseases revealed a variety of environmental pollutants to blame, such as endocrine-disrupting chemicals (EDCs), fine particulate matters (PMs) and heavy metals. The retrospection of toxicological studies provided illustrative clues for evaluating ambient pollutant-induced health risks. Overall, environmental pollution, as the hidden culprit, should answer for the increasing public health burden, and more efforts are highly encouraged to strive to explore the cause-and-effect relationships through extensive epidemiological and pathological studies.

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The toxic effects of per- and polyfluoroalkyl substances (PFASs) on humans are mediated by nuclear hormone receptors (NHRs). However, data on the interaction of PFASs and NHRs is limited. Endocrine Disruptome, an inverse docking tool, was used in this study to simulate the docking of 49 common PFASs with 14 different types of human NHRs. According to the findings, 25 PFASs have a high or moderately high probability of binding to more than five NHRs, with androgen receptor (AR) and mineralocorticoid receptor (MR) being the most likely target NHRs. Molecular docking analyses revealed that the binding modes of PFASs with the two NHRs were similar to those of their corresponding co-crystallized ligands. PFASs, in particular, may disrupt the endocrine system by binding to MR. This finding is consistent with epidemiological research that has linked PFASs to MR-related diseases. Our findings may contribute to a better understanding of the health risks posed by PFASs.

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The use of partially treated and untreated wastewater for irrigation is beneficial in agriculture but may be associated with human health risks. Reports from different locations globally have linked microbial outbreaks with agricultural reuse of wastewater. This article reviews the epidemiological evidence and health risks associated with this practice, aiming toward evidence-based conclusions. Exposure pathways that were addressed in this review included those relevant to agricultural workers and their families, consumers of crops, and residents close to areas irrigated with wastewater (partially treated or untreated). A meta-analysis gave an overall odds ratio of 1.65 (95% CI: 1.31, 2.06) for diarrheal disease and 5.49 (95% CI: 2.49, 12.10) for helminth infections for exposed agricultural workers and family members. The risks were higher among children and immunocompromised individuals than in immunocompetent adults. Predominantly skin and intestinal infections were prevalent among individuals infected mainly via occupational exposure and ingestion. Food-borne outbreaks as a result of crops (fruits and vegetables) irrigated with partially or untreated wastewater have been widely reported. Contamination of crops with enteric viruses, fecal coliforms, and bacterial pathogens, parasites including soil-transmitted helminthes (STHs), as well as occurrence of antibiotic residues and antibiotic resistance genes (ARGs) have also been evidenced. The antibiotic residues and ARGs may get internalized in crops along with pathogens and may select for antibiotic resistance, exert ecotoxicity, and lead to bioaccumulation in aquatic organisms with high risk quotient (RQ). Appropriate mitigation lies in adhering to existing guidelines such as the World Health Organization wastewater reuse guidelines and to Sanitation Safety Plans (SSPs). Additionally, improvement in hygiene practices will also provide measures against adverse health impacts.

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We review the hypotheses concerning the association between the paternal age at childbearing and childhood psychiatric disorders (autism spectrum- and attention deficit/hyperactive disorder) and adult disorders (schizophrenia, bipolar-, obsessive-compulsive-, and major depressive disorder) based on epidemiological studies. Several hypotheses have been proposed to explain the paternal age effect. We discuss the four main-not mutually exclusive-hypotheses. These are the de novo mutation hypothesis, the hypothesis concerning epigenetic alterations, the selection into late fatherhood hypothesis, and the environmental resource hypothesis. Advanced paternal age in relation to autism spectrum disorders and schizophrenia provided the most robust epidemiological evidence for an association, with some studies reporting a monotonic risk increase over age, and others reporting a marked increase at a given age threshold. Although there is evidence for the de novo mutation hypothesis and the selection into late fatherhood hypothesis, the mechanism(s) underlying the association between advanced paternal age and psychiatric illness in offspring remains to be further clarified. © 2016 The Authors. American Journal of Medical Genetics Part B: Neuropsychiatric Genetics Published by Wiley Periodicals, Inc.

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Recently, a series of lawsuits were filed in Korea claiming tort liability against tobacco companies. The Supreme Court has already issued decisions in some cases, while others are still pending. The primary issue in these cases is whether the epidemiological evidence submitted by the plaintiffs clearly proves the causal relationship between smoking and disease as required by civil law. Proving causation is difficult in tobacco lawsuits because factors other than smoking are involved in the development of a disease, and also because of the lapse of time between smoking and the manifestation of the disease. The Supreme Court (Supreme Court Decision, 2011Da22092, April 10, 2014) has imposed some limitations on using epidemiological evidence to prove causation in tobacco lawsuits filed by smokers and their family members, but these limitations should be reconsidered. First, the Court stated that a disease can be categorized as specific or non-specific, and for each disease type, causation can be proven by different types of evidence. However, the concept of specific diseases is not compatible with multifactor theory, which is generally accepted in the field of public health. Second, when the epidemiological association between the disease and the risk factor is proven to be significant, imposing additional burdens of proof on the plaintiff may considerably limit the plaintiff's right to recovery, but the Court required the plaintiffs to provide additional information such as health condition and lifestyle. Third, the Supreme Court is not giving greater weight to the evidential value of epidemiological study results because the Court focuses on the fact that these studies were group-level, not individual-level. However, group-level studies could still offer valuable information about individual members of the group, e.g., probability of causation.

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Recently, a series of lawsuits were filed in Korea claiming tort liability against tobacco companies. The Supreme Court has already issued decisions in some cases, while others are still pending. The primary issue in these cases is whether the epidemiological evidence submitted by the plaintiffs clearly proves the causal relationship between smoking and disease as required by civil law. Proving causation is difficult in tobacco lawsuits because factors other than smoking are involved in the development of a disease, and also because of the lapse of time between smoking and the manifestation of the disease. The Supreme Court (Supreme Court Decision, 2011Da22092, April 10, 2014) has imposed some limitations on using epidemiological evidence to prove causation in tobacco lawsuits filed by smokers and their family members, but these limitations should be reconsidered. First, the Court stated that a disease can be categorized as specific or non-specific, and for each disease type, causation can be proven by different types of evidence. However, the concept of specific diseases is not compatible with multifactor theory, which is generally accepted in the field of public health. Second, when the epidemiological association between the disease and the risk factor is proven to be significant, imposing additional burdens of proof on the plaintiff may considerably limit the plaintiff's right to recovery, but the Court required the plaintiffs to provide additional information such as health condition and lifestyle. Third, the Supreme Court is not giving greater weight to the evidential value of epidemiological study results because the Court focuses on the fact that these studies were group-level, not individual-level. However, group-level studies could still offer valuable information about individual members of the group, e.g., probability of causation.

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BACKGROUND: More than 200 articles have been published in the past 20 years on associations between genetic variants and risk of cervical cancer but the results have generally been inconsistent. OBJECTIVE: To provide a synopsis of the current understanding of the genetic architecture of the risk of cervical cancer by conducting a systematic review and meta-analysis. SEARCH STRATEGY: We conducted a systematic literature search by a two-stage strategy using PubMed and other databases on or before 31 March 2012. SELECTION CRITERIA: Cross-sectional, case-control or cohort studies about the relationship between genetic variants and cervical cancer were included. DATA COLLECTION AND ANALYSIS: Study outcomes were presented as odds ratios (ORs) with a 95% confidence interval.We did the meta-analysis for genetic variants which had at least three data sources and for which the significant associations were assessed using the Venice criteria. MAIN RESULTS: A total of 5605 publications were screened, of which 286 were eligible. Meta-analysis was conducted for 58 variants in 25 genes or loci. Fourteen variants in 11 genes or loci could increase the risk of cervical cancer and five variants in three genes or loci could decrease the risk. The epidemiological evidence of the association was graded as strong for four variants in CTLA4 and HLA DQB1, moderate for five variants in IL-1B, IL-10, XRCC3 and HLA DQA1, and weak for 10 variants. CONCLUSIONS: Many genetic variants were associated with the risk of cervical cancer as supported by the epidemiological evidence in this meta-analysis.

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