Effects Of Environmental Risk Factors Research Articles

DNA methylation levels of the serotonin transporter gene are not associated with the outcome of highly standardized one-session exposure-based fear treatment

Epigenetic alterations are regarded as a potential mechanism mediating the effects of environmental risk factors on vulnerability for a range of mental health problems. Recent studies have addressed the question whether DNA methylation patterns predict the outcome of psychological interventions and whether treatment effects might be associated with changes of DNA methylation. We assessed phobic fear symptoms, treatment-relevant traits and treatment response in 308 adults free of psychotropic medication - highly fearful of either spiders, blood-injury-injections, dental-treatments or heights - all subjected to highly standardized exposure-based one-session fear treatment. DNA methylation level of the promotor region of the serotonin transporter gene (SLC6A4) was assessed in either saliva samples (spider and dental treatment fear cohorts) or oral mucosa (BII, heights) to check whether possible effects are independent of the surrogate tissue examined. Moreover, in order to examine possible DNA methylation by genotype effects, patients were assessed for genetic variation of the serotonin transporter-linked polymorphic region (5-HTTLPR). DNA methylation levels were neither associated with pre-treatment fear levels, treatment relevant traits or treatment outcome data even when allelic variation of the 5HTTLPR was considered. Overall DNA methylation levels were higher in saliva samples compared to buccal samples. In saliva samples there was a small pre- to post-treatment increase in DNA methylation, which, however, was also not associated with the investigated phenotypes. We conclude that DNA methylation of SLC6A4 is no suitable biomarker for response efficacy to highly standardized one-session exposure-based fear treatments.

Human herpesvirus 6A and axonal injury before the clinical onset of multiple sclerosis.

Recent research indicates that multiple sclerosis is preceded by a prodromal phase with elevated levels of serum neurofilament light chain (sNfL), a marker of axonal injury. The effect of environmental risk factors on the extent of axonal injury during this prodrome is unknown. Human herpesvirus 6A (HHV-6A) is associated with an increased risk of developing multiple sclerosis. The objective of this study was to determine if HHV-6A serostatus is associated with the level of sNfL in the multiple sclerosis prodrome, which would support a causative role of HHV-6A. A nested case-control study was performed by crosslinking multiple sclerosis registries with Swedish biobanks. Individuals with biobank samples collected before the clinical onset of multiple sclerosis were included as cases. Controls without multiple sclerosis were randomly selected, matched for biobank, sex, sampling date and age. Serostatus of HHV-6A and Epstein-Barr virus was analysed with a bead-based multiplex assay. The concentration of sNfL was analysed with single molecule array technology. The association between HHV-6A serology and sNfL was assessed by stratified t-tests and linear regressions, adjusted for Epstein-Barr virus serostatus and sampling age. Within-pair ratios of HHV-6A seroreactivity and sNfL were calculated for each case and its matched control. To assess the temporal relationship between HHV-6A antibodies and sNfL, these ratios were plotted against the time to the clinical onset of multiple sclerosis and compared using locally estimated scatterplot smoothing regressions with 95% confidence intervals (CI). Samples from 519 matched case-control pairs were included. In cases, seropositivity of HHV-6A was significantly associated with the level of sNfL (+11%, 95% CI 0.2-24%, P = 0.045) and most pronounced in the younger half of the cases (+24%, 95% CI 6-45%, P = 0.007). No such associations were observed among the controls. Increasing seroreactivity against HHV-6A was detectable before the rise of sNfL (significant within-pair ratios from 13.6 years versus 6.6 years before the clinical onset of multiple sclerosis). In this study, we describe the association between HHV-6A antibodies and the degree of axonal injury in the multiple sclerosis prodrome. The findings indicate that elevated HHV-6A antibodies both precede and are associated with a higher degree of axonal injury, supporting the hypothesis that HHV-6A infection may contribute to multiple sclerosis development in a proportion of cases.

Impact of air pollution on cardiovascular aging

The world population is aging rapidly, and by some estimates, the number of people older than 60 will double in the next 30 years. With the increase in life expectancy, adverse effects of environmental exposures start playing a more prominent role in human health. Air pollution is now widely considered the most detrimental of all environmental risk factors, with some studies estimating that almost 20% of all deaths globally could be attributed to poor air quality. Cardiovascular diseases are the leading cause of death worldwide and will continue to account for the most significant percentage of non-communicable disease burden. Cardiovascular aging with defined pathomechanisms is a major trigger of cardiovascular disease in old age. Effects of environmental risk factors on cardiovascular aging should be considered in order to increase the health span and reduce the burden of cardiovascular disease in older populations. In this review, we explore the effects of air pollution on cardiovascular aging, from the molecular mechanisms to cardiovascular manifestations of aging and, finally, the age-related cardiovascular outcomes. We also explore the distinction between the effects of air pollution on healthy aging and disease progression. Future efforts should focus on extending the health span rather than the lifespan.

The synergistic effect of genetic and environmental factors in the development of attention-deficit/hyperactivity disorder symptoms in children and adolescents

Gene-environment interactions (GxE) have been increasingly explored in psychiatry but with low replication rates. Attention-deficit/hyperactivity disorder (ADHD) is a suitable candidate for studying GxE due to its high heritability and well-defined environmental risk factors. Here, we explored GxE using polygenic risk score (PRS) to represent the genetic liability to ADHD (ADHD-PRS) and environmental risk score (ERS) to represent the combined effects of environmental risk factors. We analyzed longitudinal data of 2,046 individuals (6-14 years of age at baseline and 14-23 at the last follow-up) from the Brazilian High-Risk Cohort Study for Psychiatric Disorders. Psychiatric evaluation included the Child Behavior Checklist and the Strength and Difficulties Questionnaire. Statistical analyses were performed using mixed-effects models. We observed statistically significant interactions between ADHD-PRS and ERS, suggesting that environmental and genetic factors act synergistically in the development of ADHD symptoms. These effects were not present for depression or anxiety symptoms. No evidence of GxE correlation was detected. Mechanistically, our findings suggest that environmental stressors modulate the genetic risk for ADHD. Future studies should investigate whether the reduction of environmental risks can prevent the development of symptoms of ADHD, especially in children with a family history of the disorder.

DNA methylation profiling reveals novel pathway implicated in cardiovascular diseases of diabetes.

Epigenetics was reported to mediate the effects of environmental risk factors on disease pathogenesis. We intend to unleash the role of DNA methylation modification in the pathological process of cardiovascular diseases in diabetes. We screened differentially methylated genes by methylated DNA immunoprecipitation chip (MeDIP-chip) among the enrolled participants. In addition, methylation-specific PCR (MSP) and gene expression validation in peripheral blood of participants were utilized to validate the DNA microarray findings. Several aberrantly methylated genes have been explored, including phospholipase C beta 1 (PLCB1), cam kinase I delta (CAMK1D), and dopamine receptor D5 (DRD5), which participated in the calcium signaling pathway. Meanwhile, vascular endothelial growth factor B (VEGFB), placental growth factor (PLGF), fatty acid transport protein 3 (FATP3), coagulation factor II, thrombin receptor (F2R), and fatty acid transport protein 4 (FATP4) which participated in vascular endothelial growth factor receptor (VEGFR) signaling pathway were also found. After MSP and gene expression validation in peripheral blood of participants, PLCB1, PLGF, FATP4, and VEGFB were corroborated. This study revealed that the hypomethylation of VEGFB, PLGF, PLCB1, and FATP4 might be the potential biomarkers. Besides, VEGFR signaling pathway regulated by DNA methylation might play a role in the cardiovascular diseases' pathogenesis of diabetes.

Determining the ergonomic risk factors affecting the musculoskeletal disorders of traffic enforcers in Manila City, Philippines.

Traffic enforcers are vulnerable to work accidents, injuries, and illnesses because they are commonly exposed to ergonomic risk factors while performing their tasks. The purpose of this study is to determine the effects of environmental risk factors and postural risk factor to the prevalence of musculoskeletal disorders (MSDs) among traffic enforcers in Manila City, Philippines using binary logistic regression analysis. A total of 120 participants were included in the study. The Nordic Musculoskeletal Questionnaire (NMQ) and Rapid Entire Body Assessment (REBA) were utilized. In addition, several devices such as a noise dosimeter, digital air thermometer, and IAQ sensors were also utilized to measure the environmental exposure of enforcers during their work shift. The prevalence of MSDs among traffic enforcers was high, with 71% of the respondents reporting symptoms of MSDs in more than one part of the body for the past 7 days. The body part that has highest prevalence was upper back, followed by lower back, and legs/ankles. Logistic regression analysis revealed that awkward work posture (OR = 4.61, 95% CI = 2.17, 9.83), noise exposure (OR = 1.42, 95% CI = 1.11, 1.82), heat exposure (OR = 0.53, 95% CI = 0.85, 1.05), and pollution exposure (OR = 0.94, 95% CI = 0.85, 1.05) were significant contributors for the prevalence of MSDs among traffic enforcers in Manila City. The prevalence of MSDs among traffic enforcers is caused by their work posture and exposure to psychosocial factors such as noise, heat, and poor air quality. Thus, to minimize the risk of MSDs, it is suggested to provide administrative controls, such as job rotation or shifting, and introduce frequent rest breaks. It is also recommended to provide enforcers with appropriate personal protective equipment, such as cooling vests, noise-canceling earplugs and N95 facemasks. This would help in uplifting musculoskeletal health for traffic enforcers and other workers in a similar field.

Highlights of Cardiovascular Disease Prevention Studies Presented at the 2022 European Society of Cardiology Congress.

Focused review of select studies presented at the 2022 European Society of Cardiology Congress. Included studies assessed the effects of aspirin and omega-3 fatty acid supplements on heart failure (ASCEND study); the impact of icosapent ethyl on ST-elevation MI incidence (REDUCE-IT); air temperature's effect on cardiovascular mortality (EXHAUSTION project); LVEF outcomes after troponin-guided neurohormonal blockade for the prevention of anthracycline toxicity; efficacy of routine stress testing after high-risk PCI (POST-PCI trial); influenza vaccine among patients with acute coronary syndromes (VIP-ACS trial); empagliflozin in patients with acute myocardial infarction (EMMY); effects of comprehensive imaging-based cardiovascular screening on death and cardiovascular events (DANCANVAS); safety of long-term evolocumab in patients with established atherosclerotic cardiovascular disease (FOURIER-OLE); and use of a cardiovascular polypill as a global strategy to improve secondary prevention (SECURE). Research presented at the 2022 ESC Congress highlighted many novel applications of preventative and treatment strategies in cardiology, including the effects of environmental risk factors on the incidence of cardiovascular disease.

Exposure to Particulate Matter as a Potential Risk Factor for Attention-Deficit/Hyperactivity Disorder in Korean Children and Adolescents (KNHANES 2008-2018).

Many epidemiological studies have suggested that air pollution adversely affects neurodevelopment in children; however, evidence is still lacking. This study aimed to determine the association between particulate matter (PM) exposure and attention-deficit/hyperactivity disorder (ADHD) in children and adolescents. Data were obtained from the Korean National Health and Nutrition Examination Survey 2008-2018. Outcomes were defined from parental reports of ever doctor-diagnosed ADHD, and ADHD cases were matched to non-cases with 1:10 age-sex matching. Individual exposure levels were assigned according to each study participant's administrative address during the year of diagnosis. Multivariate logistic regression models were used to estimate odds ratios (ORs) and 95% confidence intervals (CIs). After age-sex matching at a 1:10 ratio, the final study participants comprised 1,120 children aged 6-19 years old. A unit increase in the PM10 concentration was significantly associated with ADHD (OR, 1.44; 95% CI, 1.02-2.02 per 10 µg/m3). The association with ADHD was stronger at higher quartiles than in the lower quartiles of PM10 exposure; however, it was not statistically significant. Our results suggested that long-term PM10 exposure was associated with increased ADHD in children and adolescents. Children diagnosed with ADHD suffer from a variety of social activity and have a significant economic burden. Therefore, it is considered an important role to find out the effects of environmental risk factors, including air pollution, on children and adolescents. This may also help to increase the body of knowledge in this field and to stimulate further research.

Early Noise-Induced Hearing Loss Accelerates Presbycusis Altering Aging Processes in the Cochlea.

Several studies identified hearing loss as a risk factor for aging-related processes, including neurodegenerative diseases, as dementia and age-related hearing loss (ARHL). Although the association between hearing impairment in midlife and ARHL has been widely documented by epidemiological and experimental studies, the molecular mechanisms underlying this association are not fully understood. In this study, we used an established animal model of ARHL (C57BL/6 mice) to evaluate if early noise-induced hearing loss (NIHL) could affect the onset or progression of age-related cochlear dysfunction. We found that hearing loss can exacerbate ARHL, damaging sensory-neural cochlear epithelium and causing synaptopathy. Moreover, we studied common pathological markers shared between hearing loss and ARHL, demonstrating that noise exposure can worsen/accelerate redox status imbalance [increase of reactive oxygen species (ROS) production, lipid peroxidation, and dysregulation of endogenous antioxidant response] and vascular dysfunction [increased expression of hypoxia-inducible factor-1alpha (HIF-1α) and vascular endothelial growth factor C (VEGFC)] in the cochlea. Unveiling the molecular mechanisms underlying the link between hearing loss and aging processes could be valuable to identify effective therapeutic strategies to limit the effect of environmental risk factors on age-related diseases.

Environmental Risk Factors and Their Different Effects in Depressive Symptoms of Left-Behind Children in Rural China Compared with Non-Left-Behind Children.

In China, 61 million children were left behind in rural areas as a result of massive urbanization and migration of parents from the countryside to the cities in search of economic opportunities. This study explores the effects of environmental risk factors (i.e., peer victimization, perceived discrimination, and stressful life events) on depressive symptoms of left-behind children (LBC) and examines whether these risk factors have a higher impact on LBC compared with that of non-left-behind children (NLBC). Data collected involve 1548 first and second-year middle school students. Logistic regressions were conducted to examine the associations between environmental risk factors and LBC’s depressive symptoms, the moderating effect of the parental separation duration on these associations, and to compare if the risk factors had a higher impact on LBC’s depressive symptoms than on those of NLBC. Peer victimization is associated with an increased likelihood of depressive symptoms for LBC who were left behind for more than five years. Finally, stressful life events have a higher impact on LBC’s depressive symptoms, while peer victimization has a higher impact on NLBC’s depressive symptoms. The results suggest that stressful life events are an important risk factor that puts LBC at a disadvantage in terms of their mental health.

Impact of MicroRNAs in Interaction With Environmental Factors on Autism Spectrum Disorder: An Exploratory Pilot Study.

Background: This study aimed to explore the main effects of environmental risk factors as well as their interaction effects with miRNA on the risk of autism spectrum disorder (ASD).Methods: One hundred fifty-nine ASD children (ASD group) and 159 healthy children (control group), aged 2–6 years, were included in this study. ASD diagnoses were based on DSM-5 criteria. The extensive medical and demographic characterization of the two groups were recorded. MicroRNAs (miRNAs) in serum were detected by qRT-PCR.Results: Compared with the control group, the ASD group had significantly higher rates of maternal stress during pregnancy (p < 0.001), maternal drinking during pregnancy (p = 0.006), threatened abortion (p = 0.011), pregnancy-induced hypertension (p = 0.032), gestational diabetes (p = 0.039), maternal anemia during pregnancy (p < 0.001), umbilical cord knot (p < 0.001), neonatal jaundice (p < 0.001), family psychiatric history (p = 0.001), and much lower birth weight (p = 0.012). Furthermore, the ASD group had much lower expression levels of hsa-miR-181b-5p (p < 0.001) and hsa-miR-320a (p < 0.001) and significantly higher levels of hsa-miR-19b-3p (p < 0.001). The interactions of hsa-miR-320a and maternal stress during pregnancy (OR = 39.42, p < 0.001), hsa-miR-19b-3p and neonatal jaundice (OR = 2.44, p < 0.001), and hsa-miR-181b-5p and family psychiatric history (OR = 8.65, p = 0.001) could increase ASD risk.Conclusions: The dysregulation of hsa-miR-181b-5p, hsa-miR-320a, and hsa-miR-19b-3p could interact with environmental factors, such as maternal stress during pregnancy, neonatal jaundice, and family psychiatric history, to impact the risk of ASD.

Disentangling heterogeneity of psychosis expression in the general population: sex-specific moderation effects of environmental risk factors on symptom networks.

Psychosis expression in the general population may reflect a behavioral manifestation of the risk for psychotic disorder. It can be conceptualized as an interconnected system of psychotic and affective experiences; a so-called 'symptom network'. Differences in demographics, as well as exposure to adversities and risk factors, may produce substantial heterogeneity in symptom networks, highlighting potential etiological divergence in psychosis risk. To explore this idea in a data-driven way, we employed a novel recursive partitioning approach in the 2007 English National Survey of Psychiatric Morbidity (N = 7242). We sought to identify 'network phenotypes' by explaining heterogeneity in symptom networks through potential moderators, including age, sex, ethnicity, deprivation, childhood abuse, separation from parents, bullying, domestic violence, cannabis use, and alcohol. Sex was the primary source of heterogeneity in symptom networks. Additional heterogeneity was explained by interpersonal trauma (childhood abuse and domestic violence) in women and domestic violence, cannabis use, ethnicity in men. Among women, especially those exposed to early interpersonal trauma, an affective loading within psychosis may have distinct relevance. Men, particularly those from minority ethnic groups, demonstrated a strong network connection between hallucinatory experiences and persecutory ideation. Symptom networks of psychosis expression in the general population are highly heterogeneous. The structure of symptom networks seems to reflect distinct sex-related adversities, etiologies, and mechanisms of symptom-expression. Disentangling the complex interplay of sex, minority ethnic group status, and other risk factors may help optimize early intervention and prevention strategies in psychosis.

Maternal diet as a modifier of environmental risk factors for child neurodevelopmental outcomes: Existing evidence and future directions

BACKGROUND AND AIM: Emerging work suggests diet may modify the effects of environmental risk factors for neurodevelopmental outcomes like autism spectrum disorder (ASD). The goal of this symposium presentation is to summarize evidence for such interactions, highlight opportunities for future work, and discuss preliminary findings for dietary factors and pesticides in association with ASD-related outcomes. METHODS: Participants (n=154) for analyses of joint effects of pesticides and diet on ASD were drawn from the Early Autism Risk Longitudinal Investigation (EARLI), a high-familial risk prospective cohort. Autism diagnosis and ASD-related traits, measured according to the Social Responsiveness Scale (SRS), were captured at 36 months. Levels of organochlorine pesticides, including hexachlorobenzene, transnonachlor, and p,p’-DDE, were measured in maternal mid-pregnancy serum samples. Associations between pesticides and SRS scores and ASD diagnosis were examined using linear and logistic regression respectively, adjusted for maternal characteristics, demographic confounders, and dietary factors like folate and vitamin D, and also stratified by key dietary factors and sources of pesticides. RESULTS:No significant associations were observed with SRS scores, though patterns differed when stratified by vegetable intake, folate, and vitamin D, with increases in SRS scores among those with higher pesticide exposure and lower intake of these factors. Increased odds of ASD was also observed for those with higher levels of transnonachlor, and this association became stronger when stratified by vegetable intake (low intake AOR for interquartile range increase =3.12, 95% CI 1.01, 9.66; high intake AOR=1.03, 95% CI 0.19, 5.55). CONCLUSIONS:Certain dietary factors like vegetable intake, or nutrients within it, may mitigate adverse effects of pesticides on ASD-related outcomes. Future work should further consider these and other joint effects, targeting nutrients and chemicals that act in key pathways like inflammation and oxidative stress, to present opportunities for mitigation and intervention. KEYWORDS: autism, pesticides, diet, interactions

Socioeconomic deprivation and genetic ancestry interact to modify type 2 diabetes ethnic disparities in the United Kingdom.

BackgroundType 2 diabetes (T2D) is a complex common disease that disproportionately impacts minority ethnic groups in the United Kingdom (UK). Socioeconomic deprivation (SED) is widely considered as a potential explanation for T2D ethnic disparities in the UK, whereas the effect of genetic ancestry (GA) on such disparities has yet to be studied.MethodsWe leveraged data from the UK Biobank prospective cohort study, with participants enrolled between 2006 and 2010, to model the relationship between SED (Townsend index), GA (clustering principal components of whole genome genotype data), and T2D status (ICD-10 codes) across the three largest ethnic groups in the UK – Asian, Black, and White – using multivariable logistic regression.FindingsThe Asian group shows the highest T2D prevalence (17·9%), followed by the Black (11·7%) and White (5·5%) ethnic groups. We find that both SED (OR: 1·11, 95% CI: 1·10–1·11) and non-European GA (OR South Asian versus European: 4·37, 95% CI: 4·10–4·66; OR African versus European: 2·52, 95% CI: 2·23–2·85) are significantly associated with the observed T2D disparities. GA and SED show significant interaction effects on T2D, with SED being a relatively greater risk factor for T2D for individuals with South Asian and African ancestry, compared to those with European ancestry.InterpretationThe significant interactions between SED and GA underscore how the effects of environmental risk factors can differ among ancestry groups, suggesting the need for group-specific interventions.FundingThis work was supported by the National Institutes of Health (NIH) Distinguished Scholars Program (DSP) to LMR and the Division of Intramural Research (DIR) of the National Institute on Minority Health and Health Disparities (NIMHD) at NIH.

Gene-Environment Interactions in Multiple Sclerosis: A UK Biobank Study.

ObjectiveWe sought to determine whether genetic risk modifies the effect of environmental risk factors for multiple sclerosis (MS). To test this hypothesis, we tested for statistical interaction between polygenic risk scores (PRS) capturing genetic susceptibility to MS and environmental risk factors for MS in UK Biobank.MethodsPeople with MS were identified within UK Biobank using ICD-10–coded MS or self-report. Associations between environmental risk factors and MS risk were quantified with a case-control design using multivariable logistic regression. PRS were derived using the clumping-and-thresholding approach with external weights from the largest genome-wide association study of MS. Separate scores were created including major histocompatibility complex (MHC) (PRSMHC) and excluding (PRSnon-MHC) the MHC locus. The best-performing PRS were identified in 30% of the cohort and validated in the remaining 70%. Interaction between environmental and genetic risk factors was quantified using the attributable proportion due to interaction (AP) and multiplicative interaction.ResultsData were available for 2,250 people with MS and 486,000 controls. Childhood obesity, earlier age at menarche, and smoking were associated with MS. The optimal PRS were strongly associated with MS in the validation cohort (PRSMHC: Nagelkerke's pseudo-R2 0.033, p = 3.92 × 10−111; PRSnon-MHC: Nagelkerke's pseudo-R2 0.013, p = 3.73 × 10−43). There was strong evidence of interaction between polygenic risk for MS and childhood obesity (PRSMHC: AP = 0.17, 95% CI 0.06–0.25, p = 0.004; PRSnon-MHC: AP = 0.17, 95% CI 0.06–0.27, p = 0.006).ConclusionsThis study provides novel evidence for an interaction between childhood obesity and a high burden of autosomal genetic risk. These findings may have significant implications for our understanding of MS biology and inform targeted prevention strategies.

Edaphic and climatic factors influence on the distribution of soil transmitted helminths in Kogi East, Nigeria

The need for a reliable risk map in the control of soil-transmitted helminths (STHs) in Kogi East, North Central Nigeria is very important. This study was carried out to determine the effect of environmental risk factors on geospatial distribution of STHs. Epidemiological data were obtained from a district-wide survey conducted in 2018 in Kogi East. Edaphic and climatic factors were downloaded as spatial layers from international recognised health data resources centres. A total of 24 environmental factors were used in determining the risk map of STHs using MaxEnt tool. The predicted high-risk areas of A. lumbricoides, hookworms and S. stercoralis were the central part of Kogi East covering parts of Dekina, Ofu, Igalamela-Odolu, Olamaboro and Omala LGAs with probability of 0.8 to 1.00. Among the factors investigated; Temperature [mean diurnal temperature range (BIO2), temperature annual range (BIO7) and maximum temperature of the warmest month (BIO5)], precipitation [precipitation of the wettest quarter (BIO16)], and soil clay contents were the five factors that exerted most significant influence on the geospatial distribution of STHs in Kogi East, Nigeria. Public health control programmes on STHs should target high-risk areas by including them in mass drug administration, health education as well as provision of water, sanitation and hygiene infrastructures.

Sex-specific associations of basal steroid hormones and neuropeptides with Conduct Disorder and neuroendocrine mediation of environmental risk

Conduct Disorder (CD) is characterized by severe aggressive and antisocial behavior. The stress hormone system has frequently been investigated as a neurobiological correlate of CD, while other interacting neuroendocrine biomarkers of sex hormone or neuropeptide systems have rarely been studied, especially in females. We examined multiple basal neuroendocrine biomarkers in female and male adolescents with CD compared to healthy controls (HCs), and explored whether they mediate effects of environmental risk factors on CD. Within the FemNAT-CD study, salivary cortisol, alpha-amylase, testosterone, dehydroepiandrosterone-sulfate (DHEA-S), estradiol, progesterone, oxytocin, and arginine-vasopressin were measured under basal conditions in 166 pubertal adolescents with CD, and 194 sex-, age-, and puberty-matched HCs (60% females, 9–18 years). Further, environmental risk factors were assessed. Single hormone analyses showed higher DHEA-S, and lower estradiol and progesterone levels in both females and males with CD relative to HCs. When accounting for interactions between neuroendocrine systems, a male-specific sex hormone factor (testosterone/DHEA-S) predicted male CD, while estradiol and a stress-system factor (cortisol/alpha-amylase) interacting with oxytocin predicted female CD. Estradiol, progesterone, and oxytocin partly explained associations between early environmental risk and CD. Findings provide evidence for sex-specific associations between basal neuroendocrine measures and CD. Especially altered sex hormones (androgen increases in males, estrogen reductions in females) robustly related to CD, while basal stress-system measures did not. Early environmental risk factors for CD may act partly through their effects on the neuroendocrine system, especially in females. Limitations (e.g., basal neuroendocrine assessment, different sample sizes per sex, pubertal participants, exploratory mediation analyses) are discussed.

Assessing the impacts of ALAN and noise proxies on sleep duration and quality: evidence from a nation-wide survey in Israel

ABSTRACT Sleep is a reversible state that sustains physiological and psychological processes in humans. As well established, individual-level factors, such as stress, smoking, drugs, and caffeine intake, reduce sleep duration and quality. However, studies of the effect of environmental risk factors, such as artificial light at night (ALAN) and noise, on sleep have been infrequent. Using records obtained from the 2017 Social Survey of Israel and combined with ALAN satellite data and various proxies for traffic noise, the present study aimed to determine how the combination of ALAN and traffic noise impact sleep duration and quality in urban areas. The increase of road density at the place of residence reduces average sleep duration by ~4.5% (~18 min.) and increases the frequency of reported sleep difficulties by ~3.5%, all other factors held equal. Similarly, an increase in ALAN exposure reduces average sleep duration by ~3% (~12 min) and increases the frequency of reported sleep difficulties by ~11%. The study also reveals a significant interaction between the two environmental risk factors in question, with the adverse impact of ALAN on sleep quality especially pronounced in high noise exposure areas.

Environmental exposure to urinary Bisphenol-A in North Indian children aged between 6 and 16 years and its association with body mass index.

This study investigates the effect of environmental risk factors among North Indian children aged between 6 and 16 years associated with body mass index by comparing fasting and non-fasting urine Bisphenol-A, urine creatinine, and serum thyroid levels with other potential confounding factors. A total of 301 children were enrolled, and term fasting and non-fasting were used based on the sample collection, either first morning or random. Children were grouped into obese, non-obese, and underweight categories based on age- and gender-specific Centre for Disease Control (CDC) 2000 growth chart and grouped according to their body mass index. The overall mean ± SD (standard deviation) of age (years) was 10.45±2.39 (boys age 10.38±2.38 and girls age 10.45±2.40). Urinary Bisphenol-A concentration (ng/mL ± SD) was higher among obese (2.40±4.70) than non-obese (1.30±1.67) and underweight (1.84±3.46) category children. Higher levels of fasting urinary Bisphenol-A (≥2 ng/mL) and thyroid-stimulating hormone (TSH) (≥12.7 μg/dL) were associated with obesity than those of non-fasting children. Being non-fasting among girls at quartile 4 (obese, >2.1800 ng/mL; underweight, >2.1325 ng/mL) had higher odds (obese adjusted odds ratio (aOR) 7.72 (95% CI 0.08-1368.52), underweight adjusted odds ratio (aOR) 12.45 (95% CI 1.55-171.24)] than fasting children. We recommend awareness programs and policy guidelines by engaging teachers and parents for the physical assessment of the presence of Bisphenol-A in food packaging materials to reduce the potential exposure to other chemical migrations sources. Graphical abstract.

Socioeconomic Deprivation and Genetic Ancestry Interact to Modify Type 2 Diabetes Ethnic Disparities in the United Kingdom

Background: Type 2 diabetes (T2D) is a complex common disease that disproportionately impacts minority ethnic groups in the United Kingdom (UK). Socioeconomic deprivation (SED) is widely considered to be a risk factor for T2D ethnic disparities in the UK, whereas the effect of genetic ancestry (GA) on such disparities has yet to be studied. Methods: We leveraged data from the UK Biobank to model the relationship between SED (Townsend index), GA (clustering principal components of whole genome genotype data), and T2D status (ICD-10 codes) across the three largest ethnic groups in the UK – Asian, Black, and White. Findings: The Asian group shows the highest T2D prevalence (17·9%), followed by the Black (11·7%) and White (5·5%) ethnic groups. We find that both SED (OR: 1·11, 95% CI: 1·10-1·11) and non-European GA (OR South Asian versus European: 4·37, 95% CI: 4·10-4·66; OR African versus European: 2·52, 95% CI: 2·23-2·85) are significantly associated with the observed T2D disparities, with GA showing a stronger effect than SED in the overall population. GA and SED show significant interaction effects on T2D, with SED being a greater risk factor for T2D for individuals with South Asian and African ancestry, compared to those with European ancestry. Interpretation: The significant interaction between SED and GA underscore how the effects of environmental risk factors can differ among ancestry groups, suggesting the need for group-specific interventions. Funding: Applied Bioinformatics Laboratory. National Institutes of Health (NIH) Distinguished Scholars Program, Division of Intramural Research, National Institute on Minority Health and Health Disparities. Declaration of Interests: The author have no competing interests.