Oxide Exposure Research Articles

Association between ethylene oxide exposure and osteoarthritis risk mediated by oxidative stress: evidence from NHANES 2013-2020.

Ethylene oxide is extensively used for sterilizing medical equipment, and its carcinogenicity has been well documented. Furthermore, the onset of multiple diseases, including diabetes and hypertension, has been demonstrated to be associated with exposure to this compound. However, its association with osteoarthritis risk remains elusive. The study analyzed data from the National Health and Nutrition Examination Survey from 2013-2020, which included 6088 American adults, among whom 763 (12.5%) were diagnosed with osteoarthritis. We utilized a weighted generalized linear model to assess the correlation between ethylene oxide exposure levels and osteoarthritis risk. This study used mediation analysis to assess the functions of indicators of oxidative stress (γ-glutamyl transferase) and inflammation (alkaline phosphatase, white blood cell count, neutrophil count, and lymphocyte count) as mediators of how ethylene oxide affects osteoarthritis. The analysis revealed that elevated levels of ethylene oxide were correlated with a higher risk of osteoarthritis, even when controlling for other variables. The odds of developing osteoarthritis were 1.86 times higher in the fourth quartile than in the first quartile (95% confidence interval: 1.20-2.88, P = 0.0097, P for trend = 0.0087). Subgroup analyses indicated consistency across different cohorts. Mediation analysis revealed that oxidative stress (γ-glutamyl transferase), not inflammation, was the mediator linking ethylene oxide levels to the risk of osteoarthritis. This finding in a sample of American adults revealed a direct relationship between exposure to ethylene oxide and increased osteoarthritis risk. Oxidative stress has been suggested as a possible biological explanation for osteoarthritis caused by ethylene oxide.

The novel secretome ST266 activates Akt and protects against oxidative stress-mediated injury in human RPE and Müller cells

Oxidative stress-mediated retinal pigment epithelial (RPE) cell damage is associated with age-related macular degeneration (AMD). ST266 is the biological secretome produced by a novel population of amnion-derived multipotent progenitor cells. Herein, we investigated the effect of ST266 on RPE cell injury induced by hydroquinone (HQ), a cigarette smoke related oxidant, hydrogen peroxide (H2O2) and all-trans retinal (atRal), a pro-oxidant component of the retinoid cycle. We additionally investigated its effect on Müller cell injury induced by H2O2.Cultured human RPE cells were pre-treated for 1 hour in the presence or absence of MK-2206, a protein kinase B (Akt) inhibitor, then treated with varying concentrations of HQ, H2O2, or atRal for 1.5 hours. Cultured human Müller cells (MIO-M1) were pre-treated for 1 hour in the presence or absence of MK-2206, then treated with varying concentrations of H2O2 for 1.5 hours. Media were then replaced with STM100 (control media into which the ST266 secretome proteins were collected) or ST266 at various times. Cell viability was determined with WST-1 reagent. Mitochondrial membrane potential (Δψm) was quantified by a fluorescence plate reader. The protein phosphorylation levels of Akt, glycogen synthase kinase 3 beta (GSK-3β), and p70 ribosomal S6 kinase (p70S6K) were measured by Western blot.ST266 significantly improved RPE and MIO-M1 cell viability that was reduced by oxidant exposure and improved oxidant-disrupted Δψm. In both cell types, ST266 induced phosphorylation of Akt, GSK-3β, and p70S6K. MK-2206 significantly eliminated ST266-mediated protein phosphorylation of Akt, GSK-3β, and p70S6K and abolished the ST266-protective effect on cell viability. In conclusion, ST266 activates Akt, protects against oxidative stress-mediated cell injury in an Akt-dependent manner, and improves Δψm, suggesting a potential role for ST266 therapy in treating retinal diseases such as AMD.

Molecular Mechanisms of Polyphenols in Management of Skin Aging.

The natural process of skin aging is influenced by a variety of factors, including oxidative stress, inflammation, collagen degradation, and UV radiation exposure. The potential of polyphenols in controlling skin aging has been the subject of much investigation throughout the years. Due to their complex molecular pathways, polyphenols, a broad class of bioactive substances present in large quantities in plants, have emerged as attractive candidates for skin anti-aging therapies. This review aims to provide a comprehensive overview of the molecular mechanisms through which polyphenols exert their anti-aging effects on the skin. Various chemical mechanisms contribute to reducing skin aging signs and maintaining a vibrant appearance. These mechanisms include UV protection, moisturization, hydration, stimulation of collagen synthesis, antioxidant activity, and anti-inflammatory actions. These mechanisms work together to reduce signs of aging and keep the skin looking youthful. Polyphenols, with their antioxidant properties, are particularly noteworthy. They can neutralize free radicals, lessening oxidative stress that might otherwise cause collagen breakdown and DNA damage. The anti-inflammatory effects of polyphenols are explored, focusing on their ability to suppress pro-inflammatory cytokines and enzymes, thereby alleviating inflammation and its detrimental effects on the skin. Understanding these mechanisms can guide future research and development, leading to the development of innovative polyphenol-based strategies for maintaining healthy skin.

Spatially Precise Light-Activated Dedoping in Wafer-Scale MoS2 Films.

2D materials, particularly transition metal dichalcogenides (TMDCs), have shown great potential for microelectronics and optoelectronics. However, a major challenge in commercializing these materials is the inability to control their dopingat a wafer scale with high spatial fidelity. Interface chemistry is used with the underlying substrate oxide and concomitant exposure to visible light in ambient conditions for photo-dedoping wafer scale MoS2. It is hypothesized that the oxide layer traps photoexcited holes, leaving behind long-lived electrons that become available for surface reactions with ambient air at sulfur vacancies (defect sites) resulting in dedoping. Additionally, high fidelity spatial control is showcased over the dedoping process, by laser writing, and fine control achieved over the degree of doping by modulating the illumination time and power density. This localized change in MoS2 doping density is very stable (at least 7 days) and robust to processing conditions like high temperature and vacuum. The scalability and ease of implementation of this approach can address one of the major issues preventing the "Lab to Fab" transition of 2D materials and facilitate its seamless integration for commercial applications in multi-logic devices, inverters, and other optoelectronic devices.

Identification of Specific Hemoglobin Adduct Patterns in Users of Different Tobacco/nicotine Products by Nontargeted GC-MS/MS Analysis.

Tobacco smoke contains several electrophilic constituents which are capable of forming adducts with nucleophilic sites in DNA and proteins like hemoglobin (Hb) and albumin. New nicotine and tobacco products are discussed as less harmful forms of tobacco use compared to smoking combustible cigarettes (CC) due to reduced exposure to harmful constituents. Hence, the adduct profile in users of various tobacco/nicotine products is expected to differ characteristically. In this article, we present a novel nontargeted screening strategy using GC-MS/MS for Hb adducts based on the analysis of the respective derivatized N-terminal valine adducts after modified Edman degradation. We analyzed blood samples from a clinical study with habitual users of CCs, electronic cigarettes, heated tobacco products (HTPs), oral tobacco, nicotine replacement therapy products and nonusers of any tobacco/nicotine products. Our nontargeted approach revealed significant differences in the Hb adduct profiles of the investigated tobacco/nicotine product user groups. Adduct identification was performed by means of an internal database, retention time estimations based on the theoretical boiling points, as well as in-house synthesized reference compounds. Several chemicals that form adducts with Hb could be identified: methylating and ethylating agents, ethylene oxide, acrylonitrile, acrylamide, glycidamide and 4-hydroxybenzaldehyde. Levels were elevated in smokers compared to all other groups for Hb adducts from methylating agents, ethylene oxide, acrylonitrile, acrylamide and glycidamide. Our approach revealed higher concentrations of Hb adducts formed by ethylation, acrylamide and glycidamide in users of HTPs compared to nonusers. However, concentrations for the latter two were still lower than in smokers. Due to their long half-lives, Hb adducts related to acrylonitrile, acrylamide (glycidamide), and ethylene oxide exposure may be useful for the biochemical verification of subjects̀ compliance in longitudinal and cross-sectional studies with respect to smoking and HTP use/abstinence.

Proteomics Analysis on the Effects of Oxidative Stress and Antioxidants on Proteins Involved in Sterol Transport and Metabolism in Human Telomerase Transcriptase-Overexpressing-Retinal Pigment Epithelium Cells.

Age-related macular degeneration (AMD) is the most prevalent ocular disease in the elderly, resulting in blindness. Oxidative stress plays a role in retinal pigment epithelium (RPE) pathology observed in AMD. Tocopherols are potent antioxidants that prevent cellular oxidative damage and have been shown to upregulate the expression of cellular antioxidant proteins. Here, we determined whether oxidative stress and tocopherols, using either normal cellular conditions or conditions of sublethal cellular oxidative stress, alter the expression of proteins mediating sterol uptake, transport, and metabolism. Human telomerase transcriptase-overexpressing RPE cells (hTERT-RPE) were used to identify differential expression of proteins resulting from treatments. We utilized a proteomics strategy to identify protein expression changes in treated cells. After the identification and organization of data, we divided the identified proteins into groups related to biological function: cellular sterol uptake, sterol transport and sterol metabolism. Exposure of cells to conditions of oxidative stress and exposure to tocopherols led to similar protein expression changes within these three groups, suggesting that α-tocopherol (αT) and γ-tocopherol (γT) can regulate the expression of sterol uptake, transport and metabolic proteins in RPE cells. These data suggest that proteins involved in sterol transport and metabolism may be important for RPE adaptation to oxidative stress, and these proteins represent potential therapeutic targets.

Ethylene oxide exposure, inflammatory indicators, and depressive symptoms: a cross-sectional study and mediation analysis based on a non-institutionalized American population.

Ethylene oxide (EO) is a volatile compound positively correlated with respiratory and cardiovascular diseases. Currently, evidence suggests that environmental exposure may contribute to depressive symptoms. This study evaluated the correlation between EO exposure and depressive symptoms and investigated whether inflammatory indicators had a mediation effect on this correlation. Patients were enrolled from the National Health and Nutrition Examination Survey during 2013-2016, and 2,764 (49.67% male and 50.33% female) participants were ultimately included. EO exposure was determined by measuring hemoglobin-EO adduct (Hb-EO) concentration due to its long half-life, which was log2-transformed. Depressive symptoms were assessed using the Patient Health Questionnaire-9. Multivariable logistic regression analysis was performed to identify any correlations before and after covariate adjustment. Sensitivity analysis, subgroup analyses, and interaction tests were performed to further evaluate identified correlations. Mediation analysis was conducted to reveal whether specific inflammatory indicators mediated the correlation. A high prevalence of depressive symptoms was observed in quartiles with increased levels of EO exposure, and male individuals exhibiting higher Hb-EO levels than female individuals. A positive correlation was observed between EO exposure and depressive symptoms (odds ratio [OR]: 1.439, 95% confidence interval [CI]: 1.310, 1.581), which remained stable even after covariate adjustment (OR: 1.332, 95% CI: 1.148, 1.545). Interaction tests showed significant effects of sex (p < 0.001) and thyroid diseases (p = 0.048) on this correlation. In the mediation analysis, white blood cell (p = 0.010) and neutrophil counts (p = 0.010) exerted a mediating effect, accounting for 13.6 and 11.9%, respectively. Increased exposure to EO is associated with an elevated risk of depressive symptoms, where white blood cell and neutrophil counts exert a significant mediating effect. Further prospective studies are required to investigate the potential link among EO, other environmental pollutants, and human mental health.

Ascorbic Acid and Graphene Oxide Exposure in the Model Organism Acheta domesticus Can Change the Reproduction Potential.

The use of nanoparticles in the industry carries the risk of their release into the environment. Based on the presumption that the primary graphene oxide (GO) toxicity mechanism is reactive oxygen species production in the cell, the question arises as to whether well-known antioxidants can protect the cell or significantly reduce the effects of GO. This study focused on the possible remedial effect of vitamin C in Acheta domesticus intoxicated with GO for whole lives. The reproduction potential was measured at the level of Vitellogenin (Vg) gene expression, Vg protein expression, hatching success, and share of nutrition in the developing egg. There was no simple relationship between the Vg gene's expression and the Vg protein content. Despite fewer eggs laid in the vitamin C groups, hatching success was high, and egg composition did not differ significantly. The exceptions were GO20 and GO20 + Vit. C groups, with a shift in the lipid content in the egg. Most likely, ascorbic acid impacts the level of Vg gene expression but does not affect the production of Vg protein or the quality of eggs laid. Low GO concentration in food did not cause adverse effects, but the relationship between GO toxicity and its concentration should be investigated more thoroughly.

Association Between Ethylene Oxide Exposure and Cognitive Function in US Older Adults: NHANES 2013-2014.

Ethylene oxide (EO) is a common organic compound associated with many adverse health outcomes. However, studies exploring the association between EO exposure and cognitive function are limited. This study aims to examine this relationship between EO exposure and cognition in older adults. This study enrolled 438 older adults from the National Health and Nutrition Examination Survey (NHANES) 2013-2014 cycle. EO exposure was quantified by the measurements of blood hemoglobin adducts of ethylene oxide (HbEO) concentrations. Cognitive function was measured by the Consortium to Establish a Registry for Alzheimer's Disease battery (CREAD), the Animal Fluency test (AFT), and the Digit Symbol Substitution Test (DSST). Linear regression model, generalized additive model, and smooth curve fitting were applied to examine the linear and nonlinear relationship between EO exposure and cognitive function. We used a two-piecewise linear regression model to detect the threshold effect of EO exposure on cognitive function. Participants with higher HbEO levels had lower AFT and DSST scores than those with lower HbEO levels. After adjusting for all confounding factors, log2-transformed HbEO levels were negatively associated with AFT score. The smooth curve fitting demonstrated the nonlinear relationship between EO exposure and DSST scores. When log-2 transformed HbEO levels >4.34 pmol/g Hb, EO exposure was negatively associated with DSST score. This study indicated that high levels of HbEO were associated with cognitive decline in US older adults. Future cohort studies are needed to verify our findings.

A comprehensive evaluation of enhanced temperature influence on gas and aerosol chemistry in the lamp-enclosed oxidation flow reactor (OFR) system

Abstract. Oxidation flow reactors (OFRs) have been extensively utilized to examine the formation of secondary organic aerosol (SOA). However, the UV lamps typically employed to initiate the photochemistry in OFRs can result in an elevated reactor temperature when their implications are not thoroughly evaluated. In this study, we conducted a comprehensive investigation into the temperature distribution within an Aerodyne potential aerosol mass OFR (PAM-OFR) and then examined the subsequent effects on flow and chemistry due to lamp heating. A lamp-induced temperature increase was observed, which was a function of lamp-driving voltage, number of lamps, lamp types, OFR residence time, and positions within the PAM-OFR. Under typical PAM-OFR operational conditions (e.g., &lt; 5 d of equivalent atmospheric OH exposure under low-NOx conditions), the temperature increase typically ranged from 1–5 °C. Under extreme (but less frequently encountered) conditions, the heating could reach up to 15 °C. The influences of the increased temperature over ambient conditions on the flow distribution, gas, and condensed-phase chemistry within PAM-OFR were evaluated. Our findings indicate that the increase in temperature altered the flow field, resulting in a diminished tail on the residence time distribution and corresponding oxidant exposure due to faster recirculation. According to simulation results from a radical chemistry box model, the variation in absolute oxidant concentration within PAM-OFR due to temperature increase was minimal (&lt; 5 %). The temperature influences on seed organic aerosol (OA) and newly formed secondary OA were also investigated, suggesting that an increase in temperature can impact the yield, size, and oxidation levels of representative biogenic and anthropogenic SOA types. Recommendations for temperature-dependent SOA yield corrections and PAM-OFR operating protocols that mitigate lamp-induced temperature enhancement and fluctuations are presented. We recommend blowing air around the reactor's exterior with fans during PAM-OFR experiments to minimize the temperature increase within PAM-OFR. Temperature increases are substantially lower for OFRs utilizing less powerful lamps compared to the Aerodyne version.

Oxidative Gaseous Air Pollutant Exposure Interacts with PNPLA3 Genotype to Influence Liver Fat Fraction and Multi-Omics Profiles in Young Adults

Oxidative Gaseous Air Pollutant Exposure Interacts with PNPLA3 Genotype to Influence Liver Fat Fraction and Multi-Omics Profiles in Young Adults

Involvement of ahr-dependent Cyp1a detoxification activity, oxidative stress and inflammatory regulation in response to graphene oxide exposure in rainbow trout (Oncorhynchus mykiss)

Graphene oxide (GO) is a very attractive material for use in a vast number of applications. However, before its widespread use, it is important to consider potential issues related to environmental safety to support its safe application. The aim of this study was to investigate effects on fish (rainbow trout) following GO exposure. Using both an in vitro approach with the RTL W1 rainbow trout liver cell line, and in vivo exposures, following OECD TG 203, disturbances at the cellular level as well as in the gills and liver tissue of juvenile trout were assessed. In RTL W1 cells, a time and concentration-dependent loss in cell viability, specifically plasma membrane integrity and lysosomal function, was observed after 96 h of exposure to GO at concentrations ≥18.75 mg/L. Additionally, increased reactive oxygen species (ROS) levels were evidenced at concentrations ≥18.75 mg/L, and an enhancement of metabolic activity was noted with concentrations ≥4.68 mg/L. In vivo exposures to GO did not provoke mortality in rainbow trout juveniles following 96 h exposure but led to histological alterations in gills and liver tissues, induction of enzymatic detoxification activities in the liver, as well as aryl hydrocarbon receptor (ahr)–cytochrome P450 1a (cyp1a) gene expression downregulation, and upregulation of pro-inflammatory cytokines il1b and il8 at GO concentrations ≥9.89 mg/L.

The Effects of Oxidative Stress on RNA Editing with Insight into the Relationship Between Air Pollution and Alzheimer's Disease

Human interactions with the environment today add pressure on the world’s resources and ecosystems, which in turn harm human health. Many anthropogenic environmental changes, including climate change, biodiversity loss, and pollution, have accelerated morbidity and mortality. Research across multiple countries have found correlations between anthropogenic air pollution exposure and neurological degeneration, particularly with Alzheimer’s disease (AD). RNA editing induced by oxidative stress is one possible mechanism in which air pollution increases the risk of AD. To study this further, RNA adenosine-to-inosine (A-to-I) alterations were analyzed to identify a mechanism linking air pollution to neurological degeneration. These alterations occur in RNA, most prevalently in the central nervous system (CNS). Adenosine deaminase acting on RNA (ADAR) enzymes mediate A-to-I alterations and are essential for mammalian development and survival. ADAR mediated alterations have been associated with AD and the A-to-I occurrence frequency may increase in polluted environments that trigger increased oxidative stress. To test this possibility, wildtype (WT) and ADAR knockout (adr-2(-) Caenorhabditis elegans in their first larval (L1) developmental stage were exposed to juglone solution for 0, 15, and 60 minute experimental settings. For the two worm strains, WT and adr-2(-), the 0 minute treatment was the control, the 15 minute treatment represented acute oxidative stress exposure, and the 60 minute treatment represented chronic exposure. RNA was extracted from both groups and quantitative Real Time PCR (qRT-PCR) was used to measure the expression of gst-4, an Alzheimer’s associated gene (sel-12), and adr-2 normalized to the expression of gpd-3, the housekeeping gene that corrected for systemic errors. The gst-4 gene expression confirmed that oxidative stress occurred. Lack of adr-2 gene significantly decreased sel-12 expression at acute exposure, but adr-2 gene expression in WT worms did not significantly change across treatments. It remains to be determined whether oxidative stress impacts RNA editing of target mRNAs. Future studies are needed to explore the role of adr-2 in promoting sel-12 expression.

Association between air pollution and bone mineral density: a Mendelian randomization study.

The association of air pollution with bone mineral density (BMD) has attracted increasing attention. However, establishing a causal relationship remains uncertain. We conducted a Mendelian randomization (MR) study employing PM2.5, PM2.5-10, PM10, nitrogen dioxide, and nitrogen oxides as exposures and BMD as the outcome to explore the causality between air pollution and the occurrence of decreased BMD. By employing the IVW method, we identified a negative causality between air pollution (PM2.5, PM10, and nitrogen oxides) and BMD. Our findings demonstrate that PM2.5, PM10 and nitrogen oxides exposure may contribute to decreased BMD.

Associations between Ethylene Oxide Exposure and Liver Function in the US Adult Population.

Ethylene oxide, a reactive epoxy compound, has been widely used in various industries for many years. However, evidence of the combined toxic effects of ethylene oxide exposure on the liver is still lacking. We analyzed the merged data from the National Health and Nutrition Examination Survey (NHANES) from 2013 to 2016. Ultimately, 4141 adults aged 18 and over were selected as the sample. We used linear regression to explore the association between blood ethylene oxide and LFT indicators. The weighted linear regression model showed that HbEO is positively correlated with ALP (β = 2.61, 95% CI 1.97, 3.24, p < 0.0001), GGT (β = 5.75, 95% CI 4.46, 7/05, p < 0.0001), ALT (β = 0.50, 95% CI 0.09, 0.90, p = 0.0158), and AST (β = 0.71, 95% CI 0.44, 0.98, p < 0.0001) and negatively correlated with TBIL (β = -0.30, 95% CI -0.43, -0.16, p < 0.0001). Ethylene oxide exposure is significantly associated with changes in liver function indicators among adults in the United States. Future work should further examine these relationships.

Metabolomics analysis of human spermatozoa reveals impaired metabolic pathways in asthenozoospermia.

Infertility is a major health issue, affecting 15% of reproductive-age couples with male factors contributing to 50% of cases. Asthenozoospermia (AS), or low sperm motility, is a common cause of male infertility with complex aetiology, involving genetic and metabolic alterations, inflammation and oxidative stress. However, the molecular mechanisms behind low motility are unclear. In this study, we used a metabolomics approach to identify metabolic biomarkers and pathways involved in sperm motility. We compared the metabolome and lipidome of spermatozoa of men with normozoospermia (n = 44) and AS (n = 22) using untargeted LC-MS and the metabolome of seminal fluid using 1H-NMR. Additionally, we evaluated the seminal fluid redox status to assess the oxidative stress in the ejaculate. We identified 112 metabolites and 209 lipids in spermatozoa and 27 metabolites in the seminal fluid of normozoospermic and asthenozoospermic men. PCA analysis of the spermatozoa's metabolomics and lipidomics data showed a clear separation between groups. Spermatozoa of asthenozoospermic men presented lower levels of several amino acids, and increased levels of energetic substrates and lysophospholipids. However, the metabolome and redox status of the seminal fluid was not altered inAS. Our results indicate impaired metabolic pathways associated with redox homeostasis and amino acid, energy and lipid metabolism in AS. Taken together, these findings suggest that the metabolome and lipidome of human spermatozoa are key factors influencing their motility and that oxidative stress exposure during spermatogenesis or sperm maturation may be in the aetiology of decreased motility in AS.

Analysis of Risk Factors and The Impact of Nitric Oxide (NO) and Carbon Monoxide (CO) Levels on Lung Function: A Comparative Study of Palm Oil Factory Workers and the Community in Kuantan Mudik District, Riau, Indonesia

Background: Air pollution, particularly from industrial sources like palm oil factories, poses a significant risk to respiratory health. This study aimed to investigate the impact of nitric oxide (NO) and carbon monoxide (CO) exposure on lung function in palm oil factory workers and compare it to the lung function of individuals in the surrounding community. Methods: A cross-sectional study was conducted in Kuantan Mudik District, Riau, Indonesia. One hundred palm oil factory workers with a minimum of two years of employment and 100 community members not occupationally exposed to NO and CO were recruited. Lung function was assessed using spirometry, and NO and CO levels were measured using specialized analyzers. Participants completed the European Community Respiratory Health Survey (ECRHS) questionnaire, and demographic and clinical data were collected. Statistical analyses included univariate, bivariate, and multivariate logistic regression. Results: Factory workers exhibited significantly higher levels of NO (p=0.000) and a higher prevalence of restrictive lung function (17%) compared to the community members (3%). Multivariate analysis identified NO exposure as the most significant risk factor for restrictive lung function (p=0.005). Each unit increase in NO was associated with a 1.12-fold increased risk of restrictive lung function. CO exposure, age, gender, smoking history, and the use of personal protective equipment (PPE) were not significantly associated with lung function impairment in this study. Conclusion: Occupational exposure to NO in palm oil factories is a significant risk factor for restrictive lung function impairment. Regular monitoring of NO levels and the implementation of effective control measures are crucial to protect the respiratory health of palm oil factory workers.

Ethylene Oxide Hemoglobin Adducts in Cord Blood and Offspring's Size at Birth: The NewGeneris European Cohort Study.

Prenatal ethylene oxide exposure may have adverse effects on fetal development. We examined the relationships between ethylene oxide hemoglobin (Hb) adduct levels and offspring's size at birth in a prospective European mother-child study. This study included 1106 singletons from the NewGeneris project (2006-2010) with ethylene oxide Hb adducts measured in cord blood. We examined the relationships between adduct levels and offspring's size at birth among all infants and separately among infants of nonsmokers, using linear regression models for birth weight and birth head circumference and logarithmic binomial regression models for small for gestational age. We examined potential interactions between CYP2E1 single nucleotide polymorphisms in cord blood and the effects of ethylene oxide Hb adduct levels on offspring birth size. Higher quartiles of adduct levels as a measure of exposure were associated with decreasing birth weight and head circumference in the overall population. Compared to infants in the lowest quartile, those in the highest quartile exhibited lower birth weight (-70.73 g, 95% confidence interval = -141.16, -0.30) and reduced head circumference (-0.30 cm, 95% confidence interval = -0.58, -0.02). We observed similar, albeit less pronounced, patterns among infants of nonsmokers. There was no evidence of an association between ethylene oxide Hb adducts and risk of small for gestational age, nor consistent evidence of an interaction with CYP2E1 polymorphisms on the association between EO Hb adduct levels and offspring's size at birth. Results suggest that higher ethylene oxide Hb adduct levels in cord blood are associated with a reduction in offspring birth size.

Association between oxidative balance score and skeletal muscle mass and strength: NHANES from 2011 to 2018.

Oxidative stress is a risk factor for sarcopenia. The Oxidative Balance Score (OBS) is a widely employed tool for evaluating the oxidative stress-related exposures from dietary and lifestyle factors. In this study, we aimed to conducted to explore the relationship between OBS and skeletal muscle mass and strength. 6,438 subjects from 2011 to 2018 and 5,414 from 2011 to 2014 from the National Health and Nutrition Examination Survey (NHANES) were selected for analysis. The correlations between OBS and skeletal muscle mass and handgrip strength were investigated using multivariate logistic regression and linear regression analysis. Compared with lowest OBS, participants with OBS in the highest quartile had lower risk of low skeletal muscle mass (OR = 0.173 (0.120 ~ 0.248), p < 0.0001) and low handgrip strength (β = 0.173 (0.120 ~ 0.248), p = 0.011). The negative association also were found between dietary/lifestyle OBS and skeletal muscle mass (OR = 0.268 (0.178 ~ 0.404), p < 0.0001; OR = 0.231 (0.130 ~ 0.410), p < 0.0001) and handgrip strength (β = 1.812 (0.555 ~ 3.071), p = 0.008; β = -2.255 (-3.430 ~ -1.079), p < 0.001) independently. The positive association remains significant, especially among men and those with higher education levels by subgroup analysis. All of these results indicated a negative association between OBS and low skeletal muscle mass and handgrip strength. An antioxidant-rich diet and healthy lifestyle are crucial for enhancing skeletal muscle mass and strength.

Associations of ethylene oxide exposure with depression in American adults

Ethylene oxide (EO) is an organic compound known for its high reactivity and negative impact on human health, but its adverse effects on depression remain poorly understood. A cross-sectional study was conducted among 2884 participants from the National Health and Nutrition Examination Survey (NHANES) between 2013 and 2016. Participants were classified into four groups according to quartiles of log10-transformed hemoglobin adducts of EO (HbEO) levels. A logistic regression model was used to estimate the association between EO exposure and the risk of depression. Finally, we evaluated whether the association was mediated by inflammatory factors. Individuals with depression exhibited higher levels of hemoglobin adducts of ethylene oxide (HbEO) compared to those without depression. After adjusting for all covariates, patients in the highest quartile of HbEO (Q4 group) had a higher risk of depression, using the lowest quartile (Q1 group) as the reference group [odds ratio (OR) = 2.21, 95% confidence interval (95% CI): (1.47, 3.40)]. Additionally, the relationship between EO levels and the prevalence of depression followed a non-linear U-shaped pattern. Furthermore, inflammatory cells showed a positive correlation with EO levels. Moreover, white blood cells and neutrophils significantly mediated the relationship between HbEO and the risk of depression with mediated proportions of 14.70 and 12.55%, respectively. Exposure to ethylene oxide increases the risk of depression. Inflammatory factors partially mediated the observed association between EO exposure and depression.