Exposure Groups Research Articles

Radio frequency electromagnetic radiations interfere with the Leydig cell functions in-vitro.

A growing threat to male infertility has become a major concern for the human population due to the advent of modern technologies as a source of radiofrequency radiation (RFR). Since these technologies have become an integral part of our daily lives, thus, it becomes necessary to know the impression of such radiations on human health. In view of this, the current study aims to focus on the biological effects of radiofrequency electromagnetic radiations on mouse Leydig cell line (TM3) in a time-dependent manner. TM3 cells were exposed to RFR emitted from 4G cell phone and also exposed to a particular frequency of 1800 MHz and 2450 MHz from RFR exposure system. The cells were then evaluated for different parameters such as cell viability, cell proliferation, testosterone production, and ROS generation. A considerable reduction in the testosterone levels and proliferation rate of TM3 cells were observed at 120 min of exposure as compared to the control group in all exposure settings. Conversely, the intracellular ROS levels showed a significant rise at 60, 90 and 120 min of exposure in both mobile phone and 2450 MHz exposure groups. However, RFR treatment for different time durations (15, 30, 45, 60, 90, and 120 min) did not have significant effect on cell viability at any of the exposure condition (2450 MHz, 1800 MHz, and mobile phone radiation). Therefore, our findings concluded with the negative impact of radiofrequency electromagnetic radiations on Leydig cell's physiological functions, which could be a serious concern for male infertility. However, additional studies are required to determine the specific mechanism of RFR action as well as its long-term consequences.

Insights into tissue accumulation, depletion, and health risk assessment of clopidol in poultry

Clopidol is extensively used in livestock farming and residues of this antibiotic can persist in animal tissues, posing a risk to humans and the environment. In this study, we investigated the depletion of clopidol in various edible tissues of chickens (muscle, liver, kidney, fat, and eggs) using liquid chromatography–tandem mass spectrometry after the administration of a clopidol-contaminated diet (at 250 mg kg−1 for the high (1x) dose). After 14 d of exposure, the clopidol concentrations were highest in eggs (median: 9.83 mg/kg), followed by liver (3.56 mg/kg), kidney (3.01 mg/kg), muscle (1.56 mg/kg), and fat (0.727 mg/kg) at low exposure group, indicating that clopidol accumulated primarily in eggs rather than the other edible tissues. In addition, the maternal transfer ratios were estimated, and the transfer efficiencies of clopidol in muscle (egg-to-tissue ratio, ETR:1.81) and fat (2.06–58.2) were higher than those in liver (0.731–31.1) and kidney (0.832–38.9). Furthermore, we conducted a cumulative risk assessment for clopidol in edible chicken tissues using the hazard quotient (HQ) method. This assessment revealed that the exposure levels for Korean consumers pose an acceptable risk. However, for eggs from the 1x dose exposure group, the HQ values were greater than 1 for all age groups, particularly for young children (<18 y), suggesting that the higher daily consumption of eggs combined with the higher clopidol residues in eggs resulted in higher HQ values, which requires further attention. The findings of this study can assist in the management and monitoring of clopidol residues in chicken tissues and eggs

Do lead (Pb) content of lipsticks expose a health risk to children? A risk assessment study.

Lead (Pb) content in lipsticks and potential life-long exposure of which might cause severe effects in consumers are an important concern for public. Thus, studies emphasize that lead exposure has no safe levels. From 10 different brands, in total, 25 solid, gloss and creamy lipsticks are deployed from Turkish markets that are also categorized in two different price ranges. In order to evaluate the blood Pb levels in children, the United States Environmental Protection Agency's 'Exposure Uptake Biokinetic Model' is utilized. To assess the health risk of chronic usage both for children and adults, oral daily systemic exposure levels are calculated with the worst-case scenario and are compared with Maximum Allowable Dose Level for lipsticks. For lifetime risk assessment, exposure is assumed to start by age 7, and four different exposure scenarios have been deployed. The mean lead content of lipsticks shows significant statistical differences between the high- and low-priced lipstick groups. Daily level and total risk for lifetime Pb exposure from deployed lipsticks are below the acceptable risk levels but long-worn usage of products with routine monitoring of metal content is crucial for sensitive and unintended exposure groups.

Association of serum vitamin D and the risk of cardiovascular diseases among diabetic patients: A systematic review and meta-analysis

BackgroundThe emerging role of vitamin D has drawn the attention of researchers around the world, including its involvement in cardiovascular complications among individuals with diabetes. AimThis study aimed to obtain comprehensive evidence on the association between serum vitamin D level and the risk of cardiovascular disease among patients with diabetes. MethodsSystematic search was performed on July 1st, 2023, to identify and screen published literature reporting the association between vitamin D and cardiovascular disease among diabetic patients in six databases. Each eligible study was appraised for its quality using modified Newcastle Ottawa Scale for cross-sectional and cohort studies. Meta-analysis was performed using Dersimonian–Laird random effect model or fix-effect model. The heterogeneity and publication bias were judged based on percentage of I2 and the symmetry of Begg’s funnel plot, respectively. ResultsAs many as 22 studies were found eligible for the systematic review. A meta-analysis from 13 studies comprising of 3850 and 1797 (control and exposure groups, respectively) revealed that serum vitamin D level was significantly lower in patients with diabetes and cardiovascular diseases (Z=4.89; p-total<0.001; SMD=0.68 [95%CI: 0.41–0.95]), yet the heterogeneity was high. Following the adjustment of removing the potential outliers, the same results were still observed (Z=6.19; p-total<0.001; SMD=0.35 [95%CI: 0.24–0.46]). Though decreased, high heterogeneity could not be resolved, resulting in moderate level of this evidence. Another pooled analysis of 7 studies with 4211 patients in control group and 2381 patients in exposure group revealed that lower level of serum vitamin D is a risk factor for cardiovascular disease incidence among diabetic patients (Z=4.89; p-total<0.001; OR: 1.76 [95%CI: 1.4–2.2]). ConclusionSerum vitamin D level status is a risk factor for developing cardiovascular diseases among diabetic patients, hence should be carefully monitored and maintained. PROSPERO registrationCRD42023437698.

Association between radiation dose, thyroid hormone, and IQ levels in children exposed to radiation in utero after the Chernobyl accident.

Few studies have explored the effects of n utero radiation exposure on human health and cognition and none have taken into account thyroid hormone levels (T3), which have shown to affect cognitive performance. We investigated mechanisms of possible radiation effects on IQ in two cohorts of 250 persons each: exposed n utero after the Chernobyl accident: a 'higher exposure group (HEG)', whose mothers resided in more heavily contaminated territories at the time of the Chernobyl accident, and a 'lesser exposure group (LEG)' whose mothers resided in less contaminated areas. The dataset included information on estimated prenatal thyroid radiation dose, gestation week at the time of the accident (ATA); thyroid hormones: T3 (triiodothyronine) and T4 (thyroxine) levels measured at age 11-12 years and general IQ measured at three time points: t1: 6-7 years old; t2: 11-12 years old and t3: 15-16 years old. Descriptive and inference analyses were used to explore the dynamic of changes through time and the associations between key variables at the three time points. Estimated radiation doses to the thyroid gland were substantially higher in the HEG than in the LEG (mean 391 vs 25 mGy respectively). Significant differences in thyroid hormones levels were observed between the two groups, with lower values in T3 (higher in T4) in the LEG. At t1, the general IQ, as well as verbal and non-verbal IQ scores, were lower in the HEG than in the LEG. In the HEG, analyses adjusting simultaneously for radiation dose, gestational week ATA and T3 levels suggest that all three variables are associated with IQ, with the latter being highest among those exposed later during gestation and decreasing with increasing level of dose and of T3. No significant association was observed between IQ and T4 levels. No effect of exposure on IQ was seen in the LEG. Further investigation of this hypothesis will be important to understand the relation between n utero exposure radiation dose to thyroid, thyroid hormone levels and IQ, taking into account effects of potential confounding factors (physiological stress, maternal anxiety related evacuation).

Tea tree oil inhibits hydrogen sulfide-induced oxidative damage in chicken lungs through CYP450s/ROS pathway

A large amount of hydrogen sulfide (H2S) is produced in the process of chicken breeding, which can cause serious inflammation and oxidative damage to the respiratory system of chickens. Tea tree oil (TTO) has antioxidant and anti-inflammatory properties. No studies have been reported on the use of TTO in H2S-induced lung injury in chickens. Therefore, in this study, 240 one-day-old Roman pink laying hens were randomly and equally divided into 3 groups: control group (CON), H2S exposure group (AVG, containing H2S), and TTO treatment group (TTG, containing H2S and 0.02 mL/L TTO) to establish an experimental model of TTO treatment with H2S exposure for a period of 42 d. Hematoxylin and eosin (H&E) staining was used to detect lung histopathology. Gene expression profiles were analyzed using transcriptomics. The underlying mechanism of the amelioration of lung injury by TTO was further revealed by antioxidant enzyme assays and qRT-PCR. The results showed that H2S exposure induced significant gene expression of CYP450s (CYP1B1 and CYP1C1) (P < 0.05), and caused intense oxidative stress, apoptosis and inflammation compared with CON. TTO could reduce ROS production and enhance antioxidant capacity (SOD, CAT, T-AOC, and GSH-PX) by regulating the CYP450s/ROS pathway (P < 0.05). Compared with the control group, the treatment group showed significantly decreased expression of apoptotic (Caspase-8, Caspase-3, Bid and Fas) (P < 0.05) and inflammatory (IL-4, IL-16, NF-κB, TNF-α and IFN-γ) (P < 0.05) factors in the lung. This study revealed that TTO regulated CYP450s/ROS pathway to alleviate H2S-induced lung injury in chickens. These results enrich the theory of the action mechanism of TTO on H2S-exposed chicken lungs and are of great value for the treatment of H2S-exposed animals.

Association between secondhand smoke exposure and rheumatoid arthritis in US never-smoking adults: a cross-sectional study from NHANES

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

Beta-Cyfluthrin-Induced Hepatic Alterations in Zebrafish: Enzymatic Profiles and Oxidative Stress Responses

Beta-Cyfluthrin is a widely used pesticide belonging to class of synthetic pyrethroids which affects the central and peripheral nervous systems. The current study investigates the impact of beta-Cyfluthrin on the biochemical parameters of liver of zebrafish (Danio sp.). Adult zebrafish were exposed to concentrations of 0.25, 0.5, 1.0, 2.0 and 4.0 µg/L of beta-Cyfluthrin for acute (96 hours) and chronic (21 days) exposure periods respectively (n=20). It was observed that exposure to beta-Cyfluthrin led to variations in biochemical markers in both acute and chronic exposure groups. Liver function tests revealed significant elevated activity of alanine transaminase (ALT) and aspartate transaminase (AST) at exposure concentrations of 2.0 and 4.0 µg/L of beta-Cyfluthrin in both acute and chronic groups, while acid phosphatase (ACP) and alkaline phosphatase (ALP) activity decreased significantly at concentrations of 1.0, 2.0 and 4.0 µg/L in the chronic group. Lipid peroxidation exhibited a concentration and time-dependent increase with significant difference at 1.0, 2.0 and 4.0 µg/L in both acute and chronic groups, while superoxide dismutase (SOD) and peroxidase (PER) levels declined significantly in both acute and chronic exposure groups at exposure concentrations of 1.0, 2.0 and 4.0 µg/L for SOD and 2.0 and 4.0 µg/L for PER. Catalase (CAT) initially increased significantly in acute groups of 1.0, 2.0 and 4.0 µg/L but decreased in chronic ones. Glutathione S-transferase (GST) levels exhibited a significant increase at lower concentrations of 0.25 µg/L but a decrease at higher concentrations, 1.0, 2.0 and 4.0 µg/L of beta-Cyfluthrin. The level of significance were considered at p&lt;0.05 and p&lt;0.01. This research suggests that exposure to beta-Cyfluthrin leads to hepatic damage in adult zebrafish. This indicates a potential risk to non-target aquatic fauna, through runoff where beta-Cyfluthrin is used as an agricultural pesticide.

Safety of Combined Statin and Fibrate Therapy: Risks of Liver Injury and Acute Kidney Injury in a Cohort Study from the Shizuoka Kokuho Database.

Statins and fibrates are important means of preventing cardiovascular diseases, particularly when administered in combination as part of various therapeutic strategies. In this study, we explored the risks associated with various combinations of these drugs. We aimed to evaluate the risk of 1-year hospitalization with acute kidney injury, liver injury, pancreatitis, or rhabdomyolysis related to the concurrent administration of statins and fibrates. We performed a retrospective cohort study using data from the Shizuoka Kokuho Database, focusing on patients prescribed statins, fibrates, or a combination. Four drug exposure patterns were evaluated: adding statins to fibrates (exposure 1), switching from fibrates to statins (exposure 2), adding fibrates to statins (exposure 3), and switching from statins to fibrates (exposure 4). Hospitalization for the specified conditions within 1year was the outcome. Propensity score matching was used to create balanced cohorts for comparison. We studied 269,226 statin users and 16,282 fibrate users. After propensity score matching, there were 498 participants in the group of exposure 1, matched with 2988 in the fibrate-only group; 1180 in the group of exposure 2, matched with 7080 in the fibrate-only group; 1183 in group of exposure 3, matched with 11,830 in the statin only group; and 1356 in group of exposure 4, matched with 13,560 in the statin only group. The 1-year hospitalization rate with liver injury was higher in the group of exposure 1 than in the fibrate-only group (1.2% vs 0.3%, p < 0.01), in the group of exposure 2 than in the fibrate-only group (0.9% vs 0.3%, p < 0.01), and in the group of exposure 4 than in the statin-only group (0.6% vs 0.2%, p = 0.02). There was also a higher risk of 1-year hospitalization with acute kidney injury in group of exposure 1 than in the fibrate-only group (1.3% vs 0.3%, p = 0.01) but not in evaluations of exposure 2, 3, and 4. However, there were no differences in the risks of 1-year hospitalization with pancreatitis or rhabdomyolysis among the matched groups. We have demonstrated higher risks of 1-year hospitalization with liver injury or acute kidney injury associated with the use of combinations of statins and fibrates. This underscores the need for a cautious approach to the prescribing of such drug combinations and the importance of monitoring patients for potential adverse events.

Chromium levels in placental tissue and neural tube defects: Association and mechanistic study

Human exposure to chromium (Cr) is common but little is known about its adverse effects on pregnancy outcomes. This study aimed to explore the association between Cr exposure and the risk of neural tube defects (NTDs) and the underlying mechanisms of Cr-induced NTDs. 593 controls and 408 NTD cases with placentas were included in this study. Chromium trichloride (Cr(III)) and potassium dichromate (Cr(VI)) were intragastrically administered to pregnant mice and the number of NTDs was recorded. The odds ratio for total NTDs in the highest exposure group in placenta was 4.18 (95% confidence interval (CI), 1.97–8.84). The incidence of fetal NTDs in mice administered with Cr(III) showed a dose-response relationship. Cr(VI) didn't show teratogenicity of NTDs whereas increased the stillbirth rate. Prenatal exposure to Cr(III) increased levels of oxidative stress and apoptosis in fetal mice. RNA-sequencing results indicated significant enrichment of the MAPK pathway. RT-qPCR and Western blot analysis revealed that Cr(III) induced increased expression of p-JNK, p-P38, and Casp3. Toxicological effects can be partly antagonized by antioxidant supplementation. High chromium exposure was associated with increased human NTD risks. Excessive Cr(III) exposure can induce NTDs in fetal mice by increasing apoptosis through upgrading oxidative stress and then activating JNK/P38 MAPK signaling pathway.

Effects of noise exposure on stress hormone changes during task performance in young Korean men: quasi-experimental study

ABSTRACT Numerous studies have suggested that noise exposure might be associated with changes in stress hormone levels. However, quantitative evidence for these effects in humans is rare and remains controversial. This study aimed to investigate the acute effects of exposure to noise and its different levels on stress hormone changes in task performance. Quasi-experimental noise exposure environment was established for 90 male university student volunteers in their twenties, and each was exposed to different noise levels during task performance. The stress hormones tested included cortisol, adrenocorticotropic hormone (ACTH), adrenaline, and noradrenaline. A one-way ANOVA was performed to investigate differences in hormone levels measured in the three groups according to the noise exposure levels (35, 45, or 75 dB). Analysis of covariance (ANCOVA) was used to adjust for confounding factors that might affect hormone levels. After adjusting for confounders, significant exposure-dependent differences were found in hormone levels in salivary cortisol, serum cortisol, serum ACTH, and serum adrenaline. The amount of hormonal increase in 75 dB exposure group compared to 35 or 45 dB groups was detected. Similar results were also seen in the rate of change analysis. Our findings indicate that short-term noise exposure during task performance elevates stress hormone levels. Further, the extent of stress hormone alterations varies with noise exposure levels. Changes in hormone levels are an objective measure that may be used to identify health effects and stress responses in various noise environments.

Additive Interaction Between Insulin Resistance, Chronic Low-Grade Inflammation and Vitamin D Deficiency on the Risk of Type 2 Diabetes Mellitus: A Cohort Study

Objectives The aim of this study was to explore, on an additive scale, the combined effect of the association between insulin resistance (IR), chronic low-grade inflammation (CLGI) and vitamin D deficiency (VDD) on the risk of type 2 Diabetes Mellitus (T2DM). Methods This is a cohort study, including 1484 non-diabetic subjects, followed for a period of four years. 25 hydroxy-vitamin D (25OHD), hypersensitive C-reactive protein (HsCRP) and triglyceride-glucose index were assessed. Based on VDD and CLGI, the population was subdivided into 4 exposure groups. Analysis was performed both in the case of IR and without IR. Cox proportional regression and additive interaction were applied to explore cumulative effects of exposure. Results At follow-up, 162 newly diagnosed cases of T2DM were identified. TYG index (RR = 4.0[2.8–5.6]), HsCRP (RR = 1.6 [1.4–1.7]) and 25OHD (RR = 0.96 [0.39–0.98]) were all significantly associated with the risk of T2DM (p < 0.01). The highest excess risk was recorded in patients cumulating simultaneously IR, CLGI and VDD (RR= 8.4[3.6–19.8], p < 0.0001). The additive interaction was significant, the excess risk linked to the interaction RERI = 10.5[1.43–19.7], the proportion attributable to the combined effect: AP = 0.61[0.37–0.85], and the interaction was synergistic: synergy index: 2.8[1.42–5.69]. Conclusion Baseline levels of TYG index, 25OHD and HsCRP are strongly predictive of future T2DM, and their joint effects are additive and synergistic. Interventional studies are therefore warranted in order to evaluate whether vitamin D supplementation, combined with appropriate anti-inflammatory therapies, is effective as a preventive strategy to reduce the risk of T2DM.

Expression levels of tam receptors and ligands in the testes of rats exposed to short and middle-term 2100 MHz radiofrequency radiation.

With advances in technology, the emission of radiofrequency radiation (RFR) into the environment, particularly from mobile devices, has become a growing concern. Tyro 3, Axl, and Mer (TAM) receptors and their ligands are essential for spermatogenesis and testosterone production. RFR has been shown to induce testicular cell apoptosis by causing inflammation and disrupting homeostasis. This study aimed to investigate the role of TAM receptors and ligands in the maintenance of homeostasis and elimination of apoptotic cells in the testes (weeks), short-term sham exposure (sham/1 week), and middle-term sham exposure (sham/10 weeks). Testicular morphology was assessed using hematoxylin-eosin staining, while immunohistochemical staining was performed to assess expression levels of TAM receptors and ligands in the testes of all groups. The results showed that testicular morphology was normal in the control, sham/1 week, and sham/10 weeks groups. However, abnormal processes of spermatogenesis and seminiferous tubule morphology were observed in RFR exposure groups. Cleaved Caspase 3 immunoreactivity showed statistically significant difference in 1and 10 weeks exposure groups compared to control group. Moreover, there was no significant difference in the immunoreactivity of Tyro 3, Axl, Mer, Gas 6, and Pros 1 between groups. Moreover, Tyro 3 expression in Sertoli cells was statistically significantly increased in RFR exposure groups compared to the control. Taken together, the results suggest that RFR exposure negatively affects TAM signalling, preventing the clearance of apoptotic cells, and this process may lead to infection and inflammation. As a result, rat testicular morphology and function may be impaired.

Tracking bioaerosol exposure among municipal solid waste workers using hematological and inflammatory biomarkers

High levels of bioaerosols may exist in the air of municipal solid waste (MSW) management facilities, constituting a significant occupational hazard for workers. In this study, we investigated the potential association between exposure to bioaerosols and inflammatory biomarkers among municipal solid waste workers (MSWWs) at both the landfill site and the municipal solid waste transfer station (MSWTS), in comparison to a control group without exposure. Air sampling was conducted at six points around the landfill, two points at the MSWTS, and one point in a public park (as a control area) during the spring and summer of 2019. The results of our study revealed that airborne pathogens were highly prevalent at the sampling points, especially in the active zone and leachate collection pond. Aspergillus species were the predominant fungal species detected in this study, with the highest occurrence observed for Aspergillus flavus (83.3%), Aspergillus niger, and Aspergillus fumigatus (75.0%). Furthermore, Staphylococcus species accounted for over 75% of the total bacterial bioaerosols detected across all study areas. The blood test results of workers revealed a significant increase in platelets (PLT), immunoglobulin G (IgG), white blood cells (WBC), neutrophils, basophils, and high-sensitivity C-reactive protein (hs-CRP) compared to the control group. Conversely, platelet distribution width (PDW), mean platelet volume (MPV), and platelet-large cell ratio (P-LCR) in the exposed subjects exhibited a decreasing trend compared to the control group. These findings suggest a potential association between exposure to bioaerosols, particularly in the vicinity of open dumpsites, and elevated levels of hematologic and inflammatory markers in circulation. Furthermore, the influence of smoking status and confounding factors appears to be significant in both the control and exposure groups.

Antibiotic duration and gastric dysmotility in preterm neonates.

Prolonged antibiotic use after birth is associated with neonatal feeding intolerance and functional gastrointestinal disorders (FGIDs). A gastric dysrhythmia (tachygastria) with frequencies >4-9 cycles per minute, measured by electrogastrography (EGG), is associated with FGIDs. The relationship between prolonged antibiotic use and % time spent in tachygastria is unknown in preterm infants. We aimed to compare weekly changes in % tachygastria between preterm infants receiving long (>48 h) versus short (≤48 h) courses of antibiotics for early onset sepsis evaluation (initiated at <3 days of life). This was a longitudinal, prospective cohort study of 88 preterm infants (<34 weeks' gestation) with weekly EGG recordings from the first week of life until 40 weeks' post-menstrual age, discharge, or death. We calculated % of EGG recording time in tachygastria and determined the mean across weekly sessions. A mixed effects model assessed variance in % tachygastria between the short- and long-antibiotic exposure groups across all weeks. Baseline characteristics were similar between the two groups. There was no difference in % tachygastria between short and long antibiotic exposure groups across nine postnatal weeks (p = 0.08). Early, prolonged antibiotic exposure among preterm infants may not lead to significant gastric dysrhythmia. Future studies including larger sample sizes and a "no antibiotic" exposure arm are essential in elucidating this potential relationship.

De novo transcriptome analysis of Protohermes xanthodes Navás (Megaloptera: Corydalidae) reveling the effects of sublethal chlorpyrifos on the expression of cholinergic neuronal genes

The insect cholinergic neuron system is the target for various pesticides, including organophosphate, carbamate and neonicotinoid pesticides. In this study, we conducted a de novo transcriptome analysis on the aquatic insect Protohermes xanthodes and identified for the first time presenting sixteen genes encoding cholinergic neuronal proteins (PxanChaT, PxanVAChT, PxanmAChR, PxannAChRs, and PxanAChEs), which are candidates for acetylcholine synthesis, transport, reception and degradation in cholinergic synapse. FPKM analysis revealed that these genes are primarily expressed in head and nerve cord of P. xanthodes larvae, and some of them are also abundant in hindgut, malpighian tubules and tracheae. After exposed to different concentrations of sublethal chlorpyrifos (CPF), expression of these cholinergic neuronal genes are generally increased and then decreased with the increase of CPF concentration, except PxannAChRα9 which is increased in both 4.2 and 8.4 μg/L CPF groups. Short-term (96 h) CPF exposure resulted in significant up-regulation of PxanAChE1 expression in P. xanthodes larvae exposed to 0.42 and 4.2 μg/L CPF concentrations, while PxanAChE2 was up-regulated only in 0.42 μg/L CPF group. After long-term (14 d) CPF exposure, PxanAChE1 expression was down-regulated in 0.168 and 0.42 μg/L CPF groups. PxanAChE2 expression was dramatically decreased in all CPF groups. Moreover, acetylcholinesterase (AChE) activity was significantly decreased across all long-term CPF exposure groups. These results suggested that sublethal exposure to CPF can disrupt the expression of cholinergic neuronal genes in P. xanthodes larvae, and implied that long-term sublethal CPF exposure may cause toxic effects on P. xanthodes larvae by inhibiting AChE activity. Furthermore, identification of cholinergic neuronal genes in P. xanthodes provided candidate molecular markers for study the toxic effects of environmental pollutants on the neuron system of an aquatic predatory insect with ecological importance.

Non-allergic eosinophilic inflammation and airway hyperresponsiveness induced by diesel engine exhaust through activating ILCs

Diesel engine exhaust (DEE) is associated with the development and exacerbation of asthma. Studies have shown that DEE can aggravate allergen-induced eosinophilic inflammation in lung. However, it remains not clear that whether DEE alone could initiate non-allergic eosinophilic inflammation and airway hyperresponsiveness (AHR) through innate lymphoid cells (ILCs) pathway. This study aims to investigate the airway inflammation and hyperresponsiveness and its relationship with ILC after DEE exposure. Non-sensitized BALB/c mice were exposed in the chamber of diesel exhaust or filtered air for 2, 4, and 6 weeks (4 h/day, 6 days/week). Anti-CD4 mAb or anti-Thy1.2 mAb was administered by intraperitoneal injection to inhibit CD4+T or ILCs respectively. AHR、airway inflammation and ILCs were assessed. DEE exposure induced significantly elevated level of neutrophils, eosinophils, collagen content at 4, 6 weeks. Importantly, the airway AHR was only significant in the 4weeks-DEE exposure group. No difference of the functional proportions of Th2 cells was found between exposure group and control group. The proportions of IL-5+ILC2, IL-17+ILC significantly increased in 2, 4weeks-DEE exposure group. After depletion of CD4+T cells, both the proportion of IL-5+ILC2 and IL-17A ILCs was higher in the 4weeks-DEE exposure group which induced AHR, neutrophilic and eosinophilic inflammation accompanied by the IL-5, IL-17A levels. Diesel engine exhaust alone can imitate asthmatic characteristics in mice model. Lung-resident ILCs are one of the major effectors cells responsible for a mixed Th2/Th17 response and AHR.

Association between threat-related adverse childhood experiences and chronic lung diseases in a middle and older aged population: A cross-sectional and longitudinal study in China

ObjectivesWe investigated the association between threat-related adverse childhood experiences (ACEs) and the risk of chronic lung diseases (CLDs). MethodsThe data used for this study were extracted from the China Health and Retirement Longitudinal Study (CHARLS), a nationally representative survey of respondents recruited from 450 villages/urban communities in 28 provinces. Threat-related ACEs were constructed using five adverse factors: household substance abuse, physical abuse, domestic violence, unsafe neighbourhood, and bullying). Participants were divided into three groups according to their number of threat-related ACEs at baseline and at follow-up. The association between threat-related ACEs and CLD prevalence in the cross-sectional study was calculated using logistic regression models. The association between threat-related ACEs and CLD onset was evaluated using Cox proportional regression models in the cohort study. Potential confounders were considered in both the cross-sectional and cohort studies. ResultsThe CLD prevalence in the total population, no exposure group, exposure to one threat-related ACE, and exposure to at least two threat-related ACEs were 10.07% (1320/13104), 9.20% (665/7232), 10.89% (421/3865), and 11.66% (234/2007), respectively. Exposure to one threat-related ACE (OR: 1.23, 95% CI: 1.07–1.41) and exposure to at least two threat-related ACEs (OR: 1.31, 95% CI: 1.11–1.55) were significantly associated with higher CLD prevalence rates. The cohort study included 11,645 participants. During the 7-year follow-up, 738 CLD incidents were identified. Similarly, exposure to one threat-related ACE (HR: 1.20, 95% CI: 1.01–1.43) and at least two threat-related ACEs (HR: 1.64, 95% CI: 1.35–2.00) were significantly associated with a higher CLD incidence risk. ConclusionsExposure to threat-related ACEs was significantly associated with a higher CLD prevalence risk and onset. It is crucial to identify individuals who have encountered childhood threats and prioritise the monitoring of their pulmonary function.

LRG1 promotes the apoptosis of pulmonary microvascular endothelial cells through KLK10 in chronic obstructive pulmonary disease.

Cigarette smoking is one of the most important causes of COPD and could induce the apoptosis of pulmonary microvascular endothelial cells (PMVECs). The conditional knockout of LRG1 from endothelial cells reduced emphysema in mice. However, the mechanism of the deletion of LRG1 from endothelial cells rescued by cigarette smoke (CS) induced emphysema remains unclear. This research aimed to demonstrate whether LRG1 promotes the apoptosis of PMVECs through KLK10 in COPD. Nineteen patients were divided into three groups: control non-COPD (n=7), smoker non-COPD (n=7), and COPD (n=5). The emphysema mouse model defined as the CS exposure group was induced by CS exposure plus cigarette smoke extract (CSE) intraperitoneal injection for 28 days. Primary PMVECs were isolated from the mouse by magnetic bead sorting method via CD31-Dynabeads. Apoptosis was detected by western blot and flow cytometry. LRG1 was increased in lung tissue of COPD patients and CS exposure mice, and CSE-induced PMVECs apoptosis model. KLK10 was over-expressed in lung tissue of COPD patients and CS exposure mice, and CSE-induced PMVECs apoptosis model. LRG1 promoted apoptosis in PMVECs. LRG1 knockdown reversed CSE-induced apoptosis in PMVECs. The mRNA and protein expression of KLK10 were increased after over-expressed LRG1 in PMVECs isolated from mice. Similarly, both the mRNA and protein levels of KLK10 were decreased after LRG1 knockdown in PMVECs. The result of co-immunoprecipitation revealed a protein-protein interaction between LRG1 and KLK10 in PMVECs. KLK10 promoted apoptosis via the down-regulation of Bcl-2/Bax in PMVECs. KLK10 knockdown could reverse CSE-induced apoptosis in PMVECs. LRG1 promotes apoptosis via up-regulation of KLK10 in PMVECs isolated from mice. KLK10 promotes apoptosis via the down-regulation of Bcl-2/Bax in PMVECs. There was a direct protein-protein interaction between LRG1 and KLK10 in PMVECs. Our novel findings provide insights into the understanding of LRG1/KLK10 function as a potential molecule in COPD.

Micro-and nano-plastics induce kidney damage and suppression of innate immune function in zebrafish (Danio rerio) larvae

Aquatic environments serve as critical repositories for pollutants and have significantly accumulated micro- and nanoplastics (MNPs) due to the extensive production and application of plastic products. While the disease resistance and immunity of fish are closely linked to the condition of their aquatic habitats, the specific effects of nanoplastics (NPs) and microplastics (MPs) within these environments on fish immune functions are still not fully understood. The present study utilized zebrafish (Danio rerio) embryos and larvae as model organisms to examine the impacts of polystyrene NPs (100 nm) and MPs (5 μm) on fish immune responses. Our findings reveal that NPs and MPs tend to accumulate on the surfaces of embryos and within the intestines of larvae, triggering oxidative stress and significantly increasing susceptibility to Edwardsiella piscicida infection in zebrafish larvae. Transmission electron microscopy examined that both NPs and MPs inflicted damage to the kidney, an essential immune organ, with NPs predominantly inducing endoplasmic reticulum stress and MPs causing lipid accumulation. Transcriptomic analysis further demonstrated that both NPs and MPs significantly suppress the expression of key innate immune pathways, notably the C-type lectin receptor signaling pathway and the cytosolic DNA-sensing pathway. Within these pathways, the immune factor interleukin-1 beta (il1b) was consistently downregulated in both exposure groups. Furthermore, exposure to E. piscicida resulted in restricted upregulation of il1b mRNA and protein levels, likely contributing to diminished disease resistance in zebrafish larvae exposed to MNPs. Our findings suggest that NPs and MPs similarly impair the innate immune function of zebrafish larvae and weaken their disease resistance, highlighting the significant environmental threat posed by these pollutants.