RESUMO
This prospective birth cohort study evaluated the association of exposure to PM2.5 (diameter ≤2.5 µm), PM1-2.5 (1-2.5 µm), and PM1 (≤1 µm) with maternal thyroid autoimmunity and function during early pregnancy. A total of 15,664 pregnant women were included at 6 to 13+6 gestation weeks in China from 2018 to 2020. Single-pollutant models using generalized linear models (GLMs) showed that each 10 µg/m3 increase in PM2.5 and PM1-2.5 was related with 6% (odds ratio [OR] = 1.06, 95% confidence interval [CI]: 1.01, 1.12) and 15% (OR = 1.15, 95% CI: 1.08, 1.22) increases in the risk of thyroid autoimmunity, respectively. The odds of thyroid autoimmunity significantly increased with each interquartile range increase in PM2.5 and PM1-2.5 exposure (P for trend <0.001). PM1 exposure was not significantly associated with thyroid autoimmunity. GLM with natural cubic splines demonstrated that increases in PM2.5 and PM1-2.5 exposure were associated with lower maternal FT4 levels, while a negative association between PM1 and FT4 levels was found when exposure exceeded 32.13 µg/m3. Only PM2.5 exposure was positively associated with thyrotropin (TSH) levels. Our findings suggest that high PM exposure is associated with maternal thyroid disruption during the early pregnancy.
Assuntos
Autoimunidade , Material Particulado , Glândula Tireoide , Humanos , Feminino , Gravidez , Adulto , China , Estudos Prospectivos , Poluentes Atmosféricos , Exposição MaternaRESUMO
Children's exposures to environmental antibiotics are a major public health concern. However, limited data are available on the effects of environmental antibiotic exposures on childhood obesity. Our study aimed to explore this relationship. We conducted a cross-sectional case-control study nested in a population-based survey of primary school students, including 1855 obese and 1875 random selected control children. A total of 10 antibiotics in urine samples were measured by liquid chromatography-tandem mass spectrometry. Multivariable survey logistic regression was used to assess the associations between environmental antibiotics exposures and childhood obesity. After adjusting for potential confounders, increased odds of obesity were observed in children exposed to tetracycline (OR = 1.31, 95% CI: 1.09-1.57) and sulfamonomethoxine (OR = 1.43, 95% CI: 1-2.05). Comparing none (Assuntos
Antibacterianos
, Exposição Ambiental
, Obesidade Infantil
, Humanos
, Estudos de Casos e Controles
, Antibacterianos/efeitos adversos
, Masculino
, Criança
, Estudos Transversais
, Feminino
, Exposição Ambiental/estatística & dados numéricos
, Obesidade Infantil/epidemiologia
, Obesidade Infantil/induzido quimicamente
, Poluentes Ambientais/urina
, Modelos Logísticos
RESUMO
Chlorinated polyfluorinated ether sulfonate, commercially known as F-53B, has been associated with adverse birth outcomes. However, the reproductive toxicology of F-53B on the placenta remains poorly understood. To address this gap, we examined the impact of F-53B on placental injury and its underlying molecular mechanisms in vivo. Pregnant C57BL/6â¯J female mice were randomly allocated to three groups: the control group, F-53B 0.8⯵g/kg/day group, and F-53B 8⯵g/kg/day group. After F-53B exposure through free drinking water from gestational day (GD) 0.5-14.5, the F-53B 8⯵g/kg/day group exhibited significant increases in placental weights and distinctive histopathological alterations, including inflammatory cell infiltration, heightened syncytiotrophoblast knots, and a loosened trophoblastic basement membrane. Within the F-53B 8⯵g/kg/day group, placental tissue exhibited increased apoptosis, as indicated by increased caspase3 activation. Furthermore, F-53B potentially induced the NF-κB signaling pathway activation through IκB-α phosphorylation. Subsequently, this activation upregulated the expression of inflammatory cytokines and components of the NLRP3 inflammasome, including activated caspase1, IL-1ß, IL-18, and cleaved gasdermin D (GSDMD), ultimately leading to pyroptosis in the mouse placenta. Our findings reveal a pronounced inflammatory injury in the placenta due to F-53B exposure, suggesting potential reproductive toxicity at concentrations relevant to the human population. Further toxicological and epidemiological investigations are warranted to conclusively assess the reproductive health risks posed by F-53B.
Assuntos
Inflamassomos , Camundongos Endogâmicos C57BL , Proteína 3 que Contém Domínio de Pirina da Família NLR , Placenta , Animais , Feminino , Gravidez , Proteína 3 que Contém Domínio de Pirina da Família NLR/metabolismo , Placenta/efeitos dos fármacos , Placenta/patologia , Camundongos , Inflamassomos/efeitos dos fármacos , Inflamação/induzido quimicamente , Inflamação/patologia , Apoptose/efeitos dos fármacos , NF-kappa B/metabolismo , Fluorocarbonos/toxicidade , Transdução de Sinais/efeitos dos fármacosRESUMO
BACKGROUND AND OBJECTIVES: Studies on the effects of airborne particulates of diameter ≤ 1 µm (PM1), airborne particulates of diameter ≤ 2.5 µm (PM2.5) and airborne particulates of diameter ranges from 1 to 2.5 µm (PM1-2.5) on incidence of hyperuricemia are limited. We aimed to investigate the associations between PM1, PM2.5, and PM1-2.5 and hyperuricemia among male traffic officers. METHODS: We conducted a prospective cohort study of 1460 traffic officers without hyperuricemia in Guangzhou, China from 2009 to 2016. Exposures of PM1 and PM2.5 were estimated with a spatiotemporal model. PM1-2.5 concentrations were calculated by subtracting PM1 from PM2.5 concentrations. Cox's proportional hazards regressions models were used to examine the association between PM1, PM2.5, and PM1-2.5 and hyperuricemia, adjusted for potential confounders. Associations between PM1, PM2.5, and PM1-2.5 and serum uric acid (SUA) levels were evaluated with multiple linear regression models. RESULTS: Hazard ratios (HRs) and 95% confidence intervals (CIs) of hyperuricemia associated with 10 µg/m3 increment in PM1, PM2.5, and PM1-2.5 were 1.67 (95% CI:1.30-2.36), 1.49 (95% CI: 1.27-1.75), and 2.18 (95% CI: 1.58-3.02), respectively. The SUA concentrations increased by 12.23 µmol/L (95% CI: 5.91-18.56), 6.93 µmol/L (95% CI: 3.02-10.84), and 8.72 µmol/L (95% CI: 0.76-16.68) per 10 µg/m3 increase in PM1, PM2.5, and PM1-2.5, respectively. Stratified analyses indicated the positive associations of PM2.5 and PM1-2.5 with SUA levels were stronger in non-smokers, and PM1, PM2.5, and PM1-2.5 with SUA levels were stronger in non-drinkers. CONCLUSION: Long-term PM1, PM2.5, and PM1-2.5 exposures may increase the risk of hyperuricemia and elevate SUA levels among male traffic officers, especially in non-smokers and non-drinkers.
Assuntos
Poluentes Atmosféricos , Poluição do Ar , Hiperuricemia , Humanos , Masculino , Material Particulado/toxicidade , Material Particulado/análise , Poluentes Atmosféricos/análise , Hiperuricemia/epidemiologia , Estudos Prospectivos , Ácido Úrico/análise , Exposição Ambiental/efeitos adversos , Exposição Ambiental/análise , China/epidemiologia , Poluição do Ar/análiseRESUMO
Chlorinated polyfluorinated ether sulfonates (Cl-PFESAs) are one kind of replacement chemistry for perfluorooctanesulfonate (PFOS). Recent studies have shown that Cl-PFESAs could interfere with thyroid function in animal models. However, epidemiological evidence on the link between Cl-PFESAs and thyroid function remains scarce. In this study, we focused on two representative legacy perfluoroalkyl substances (PFAS), including PFOS and perfluorooctanoic acid (PFOA), and two PFOS alternatives (6:2 and 8:2 Cl-PFESAs) in the general adult population from a cross-sectional study, the "Isomers of C8 Health Project in China". Three serum thyroid hormones (THs), thyroid stimulating hormone (TSH), free triiodothyronine (FT3), and free thyroxine (FT4), were measured. We fitted generalized linear regression, restricted cubic spline regression, and Bayesian kernel machine regression models to assess associations of individual Cl-PFESAs, legacy PFAS, and PFAS mixtures with THs, respectively. We found individual PFAS and their mixtures were nonlinearly associated with THs. The estimated changes of the TSH level (µIU/mL) at the 95th percentile of 6:2 Cl-PFESA and PFOS against the 5th percentile were -0.74 (95% CI: -0.94, -0.54) and -1.18 (95% CI: -1.37, -0.98), respectively. The present study provided epidemiological evidence for the association of 6:2 Cl-PFESA with thyroid hormone levels in the general adult population.
Assuntos
Ácidos Alcanossulfônicos , Fluorocarbonos , Alcanossulfonatos , Animais , Teorema de Bayes , China/epidemiologia , Estudos Transversais , Éter , Éteres , Fluorocarbonos/análise , Glândula Tireoide , Hormônios Tireóideos , TireotropinaRESUMO
OBJECTIVE: Patients undergoing carotid endarterectomy (CEA) have a significant possibility of developing postoperative cognitive decline (POCD). POCD after surgery could be result from cerebral hypotension induced by cross-clamping or postoperative hyperperfusion. Optic nerve sheath diameter (ONSD) exhibits an excellent correlation with invasive intracranial pressure monitoring, Here, the authors explored the risk factors of POCD in patients undergoing CEA, paying close attention to ONSD to test the hypothesis that decrease of coronal ONSD was related to the incidence of POCD. DESIGN: Observational retrospective review. SETTING: Single tertiary academic center. PARTICIPANTS: One hundred sixteen patients undergoing CEA from January 1, 2019 to December 31, 2019. INTERVENTION: None. MEASUREMENTS AND MAIN RESULTS: A multivariate logistic regression, scatter diagrams, and a receiver operating curve were used to evaluate the ability to predict POCD though the change in coronal ONSD. This study ultimately enrolled 84 patients and the incidence of POCD within postoperative two days was 28.6%. Decrease of coronal ONSD (odds ratio [OR], 0.438; 95% confidence interval [CI] 0.217-0.881; pâ¯=â¯0.021) and total intravenous anesthesia (TIVA) (OR, 25.541, 95% CI 2.100-310.614, pâ¯=â¯0.011) were independent risk factors for POCD. Changes in coronal ONSD had an area under the curve to distinguish POCD of 0.716 (95% CI 0.531-0.902). Using a cutoff of 0.05 cm, changes of coronal ONSD had a sensitivity of 66.7% and specificity of 66.7%. CONCLUSIONS: Decrease of coronal ONSD, measured by ultrasonography and TIVA, were associated with POCD. Change in coronal ONSD was a moderate predictor of incidence of POCD.
Assuntos
Endarterectomia das Carótidas , Hipertensão Intracraniana , Complicações Cognitivas Pós-Operatórias , Endarterectomia das Carótidas/efeitos adversos , Humanos , Pressão Intracraniana , Nervo Óptico/diagnóstico por imagem , Estudos Prospectivos , Estudos Retrospectivos , UltrassonografiaRESUMO
Puerarin has the anti-Alzheimer's disease (AD) activity,which can reverse nerve injury induced by Aßand inhibit neuronal apoptosis.However,its potential pharmacodynamic mechanism still needs to be further researched.The occurrence and development of AD is due to the change of multiple metabolic links in the body,which leads to the destruction of balance.Puerarin may act on multiple targets and multiple metabolic processes to achieve therapeutic purposes.Quantitative proteomic analysis provides a new choice to understand the mechanism as completely as possible.This research adopted SH-SY5Y cells induced by Aß_(1-42)to establish AD cell model,and Aßimmunofluorescence detection showed that Aßdecreased significantly after puerarin intervention.The mechanism of puerarin reversing SH-SY5Y cell injured by Aß_(1-42)was further explored by using label-free non-labeled quantitative technology and Western blot detection based on bioinformatics analysis result.The results showed that most of the differential proteins were related to biological processes such as cellular component organization or biogenesis,cellular component organization and cellular component biogenesis,and they mainly participated in the top ten pathways of P value such as pathogenic Escherichia coli infection,m TOR signaling pathway,regulation of autophagy,regulation of actin cytoskeleton,spliceosome,hepatocellular carcinoma,tight junction,non-small cell lung cancer,apoptosis and gap junction.Annexin V/PI flow cytometry and TUNEL were used to detect apoptosis,and the results showed that Aßdecreased significantly and the rate of apoptosis decreased significantly after puerarin intervention.Western blot analysis found that the protein expression level of autophagy related protein LC3â ¡was up-regulated after Aßinduction,and the degree of this up-regulation was further enhanced in puerarin intervention group.The trend of the ratio of LC3â ¡/LC3â among groups was the same as the protein expression level of LC3â ¡ï¼the protein expression level of p62 in the control group,AD model group and puerarin intervention group decreased successively.Protein interaction network analysis showed that CAP1 was correlated with TUBA1B,HSP90AB2P,DNM1L,TUBA1A and ERK1/2,and the correlation between CAP1 and ERK1/2 was the highest among them.Western blot showed that the expressions of p-ERK1/2,Bax and CAP1 were significantly down-regulated and the protein expression level of Bcl-2 was significantly up-regulated after puerarin intervention.Therefore,puerarin might improve the SH-SY5Y cells injured by Aß_(1-42)through the interaction of multiple biological processes and pathways in cells multiple locations,and CAP1 might play an important role among them.
Assuntos
Carcinoma Pulmonar de Células não Pequenas , Isoflavonas , Neoplasias Pulmonares , Peptídeos beta-Amiloides , Apoptose , Linhagem Celular Tumoral , Humanos , Isoflavonas/farmacologia , ProteômicaRESUMO
There is a large body of evidence linking Environmental Tobacco Smoke (ETS) exposure with impaired lung function. However, it is not known whether exposure to pets modifies this relationship. To investigate if pet ownership changes the association between ETS exposure and lung function, a population-based sample of 7326 children, 7-14 years old, were randomly recruited from 24 districts in northeast China. Lung function including forced vital capacity (FVC), forced expiratory volume in 1 s (FEV1), peak expiratory flow (PEF), and maximal mid-expiratory flow (MMEF) was measured by spirometry, while pet ownership time periods and ETS exposure were collected by questionnaire. Two-level regression analysis was done, with covariates controlled for. The results showed pet exposure in certain early lifetime windows modified the associations of ETS exposure on decreased lung function in children. Among children exposed to current ETS, those exposed to pets in utero had greater reductions in lung function (for instance: OR for reduced FVC (<85% predicted) = 10.86; 95% CI: 3.80-30.97) than those not exposed to pets in utero (OR = 2.32; 95% CI: 1.76-3.05) (pinteraction = 0.005). While, children exposed to current pet ownership reduced the lung function impairment induced by ETS exposure during the first 2 years of life and/or ETS exposure during pregnancy, especially for FVC impairment. For instance, OR (95%CI) for reduced FVC (<85% predicted) was 0.81 (0.56, 1.18) and 1.42 (1.15, 1.74), respectively, for children with or without current pet ownership exposed to ETS during the first 2 years of life (pinteraction = 0.010). Furthermore, pet type or number of pets did not significantly modify associations between ETS exposure and lung function. In conclusion, the timing of pet ownership modified associations between ETS exposure and lung function, pet ownership in utero and during the first 2 years of life significantly worsened the adverse impacts of passive smoking on lung function.
Assuntos
Exposição Ambiental , Pulmão , Animais de Estimação , Poluição por Fumaça de Tabaco , Adolescente , Animais , Criança , China , Estudos de Coortes , Feminino , Volume Expiratório Forçado , Humanos , Pulmão/fisiopatologia , Propriedade , GravidezRESUMO
PURPOSE: To compare the effects of active and passive movements on brain activation in patients with cerebral infarction using fMRI. METHODS: Twenty-four hemiplegic patients with cerebral infarction were evaluated using fMRI. All patients performed active and passive finger opposition movements. Patients were instructed to perform the finger opposition movement for the active movement task. For the passive movement task, the subject's fingers were moved by the examiner to perform the finger opposition movement. Statistical parametric mapping software was used for statistical analyses and to process all data. RESULTS: In the affected hemisphere, sensorimotor cortex (SMC) activation intensity and range were significantly stronger during the passive movement of the affected fingers compared to the active movement of the affected fingers (p < 0.05). However, there were no significant differences between active and passive movements of unaffected fingers in SMC activation intensity and range in the unaffected hemisphere (p > 0.05). In addition, the passive movement activated many other regions of the brain. The brain regions activated by passive movements of the affected fingers tended to center toward the contralateral SMC. CONCLUSION: Our findings suggest that passive movements induce cortical reorganization in patients with cerebral infarction. Therefore, passive movement is likely beneficial for motor function recovery in patients with cerebral infarction.
Assuntos
Encéfalo/fisiopatologia , Infarto Cerebral/fisiopatologia , Movimento/fisiologia , Adulto , Idoso , Mapeamento Encefálico , Feminino , Dedos , Humanos , Imageamento por Ressonância Magnética , Masculino , Pessoa de Meia-IdadeRESUMO
BACKGROUND: Medication adherence and the management of adverse drug reactions (ADRs) are crucial to the efficacy of antitumor drugs. A WeChat applet, also known as a "Mini Program," is similar to the app but has marked advantages. The development and use of a WeChat applet makes follow-up convenient for patients with cancer. OBJECTIVE: This study aimed to assess the usability and utility of a newly developed WeChat applet, "DolphinCare," among patients with cancer in Shanghai. METHODS: A qualitative methodology was used to obtain an in-depth understanding of the experiences of patients with cancer when using DolphinCare from the usability and utility aspects. The development phase consisted of 2 parts: alpha and beta testing. Alpha testing combined the theory of the Fogg Behavior Model and the usability model. Alpha testing also involved testing the design of DolphinCare using a conceptual framework, which included factors that could affect medication adherence and ADRs. Beta testing was conducted using in-depth interviews. In-depth interviews allowed us to assist the patients in using DolphinCare and understand whether they liked or disliked DolphinCare and found it useful. RESULTS: We included participants who had an eHealth Literacy Scale (eHEALS) score of ≥50%, and a total of 20 participants were interviewed consecutively. The key positive motivators described by interviewers were to be reminded to take their medications and to alleviate their ADRs. The majority of the patients were able to activate and use DolphinCare by themselves. Most patients indicated that their trigger to follow-up DolphinCare was the recommendation of their known and trusted health care professionals. All participants found that labels containing the generic names of their medication and the medication reminders were useful, including timed pop-up push notifications and text alerts. The applet presented the corresponding information collection forms of ADRs to the patient to fill out. The web-based consultation system enables patients to consult pharmacists or physicians in time when they have doubts about medications or have ADRs. The applet had usabilities and utilities that could improve medication adherence and the management of ADRs among patients with cancer. CONCLUSIONS: This study provides preliminary evidence regarding the usability and utility of this type of WeChat applet among patients with cancer, which is expected to be promoted for managing follow-up among other patients with other chronic disease.
RESUMO
Epidemiological evidence showed that serum high perfluorooctane sulfonate (PFOS) levels are associated with multiple eye related diseases, but the potential underlying molecular mechanisms remain poorly understood. Zebrafish and photoreceptor cell (661w) models were used to investigate the molecular mechanism of PFOS induced eye development defects. Our results showed a novel molecular mechanism of PFOS-induced inflammation response-mediated photoreceptor cell death associated with eye development defects. Inhibition of Caspase-8 activation significantly decreased photoreceptor cell death in PFOS exposure. Mechanistically, Toll-like receptor 4 (TLR4) mediates activation of Caspase-8 promote activation of NLR family pyrin domain-containing 3 (NLRP3) inflammasome to elicit maturation of interleukin-1 beta (IL-1ß) via Caspase-1 activation, facilitating photoreceptor cell inflammation damage in PFOS exposure. In addition, we also made a novel finding that Caspase-3 activation was increased via Caspase-8 activation and directly intensified cell death. Our results show the important role of Caspase-8 activation in PFOS induced eye development defects and highlight Caspase-8 mediated activation of the NLRP3 inflammation triggers activation of Caspase-1 and promote the maturation of IL-1ß in retinal inflammatory injury.
Assuntos
Ácidos Alcanossulfônicos , Caspase 8 , Fluorocarbonos , Inflamassomos , Larva , Proteína 3 que Contém Domínio de Pirina da Família NLR , Peixe-Zebra , Animais , Proteína 3 que Contém Domínio de Pirina da Família NLR/metabolismo , Inflamassomos/metabolismo , Caspase 8/metabolismo , Caspase 8/genética , Ácidos Alcanossulfônicos/toxicidade , Fluorocarbonos/toxicidade , Larva/efeitos dos fármacos , Interleucina-1beta/metabolismo , Olho/efeitos dos fármacos , Poluentes Químicos da Água/toxicidadeRESUMO
Numerous studies have suggested per-and polyfluoroalkyl substances (PFASs) are related to uric acid levels, but evidence related to PFAS alternatives is limited. Moreover, the effect of the combined exposure to PFASs and their alternatives on uric acid has not been reported. Hence, we conducted a cross-sectional study involving 1312 adults in Guangzhou, China. Generalized linear regression model was adopted to explore the effect of single PFAS exposure on serum uric acid levels. Further, multi-pollutant models such as Bayesian kernel machine regression, weighted quantile sum, and quantile G-computation were employed to investigate the combined association of PFASs and alternatives with serum uric acid levels. We performed molecular docking to understand the potential interaction of PFAS with Organic Anion Transporters (OATs), involved in the secretion of uric acid. Per log serum 6:2 Cl-PFESA and PFOA increases were accompanied with an increase of serum uric acid with statistical significance (for 6:2 Cl-PFESA: beta: 0.19 ng/mL, 95% CI 0.11-0.26 and for PFOA: beta: 0.43 ng/mL, 95% CI 0.34-0.52). The associations were strongest among overweight and elderly. Multi-pollutant models also revealed a positive association. These positive associations may be PFASs can competitively combine with OAT1 and OAT3, leading to the increase of serum uric acid.
Assuntos
Ácidos Alcanossulfônicos , Poluentes Ambientais , Fluorocarbonos , Adulto , Humanos , Idoso , Ácido Úrico , Estudos Transversais , Teorema de Bayes , Simulação de Acoplamento Molecular , Fluorocarbonos/análise , ChinaRESUMO
The emissions and exposure limits for airborne PM0.1 are lacking, with limited scientific data for toxicity. Therefore, we continuously monitored and calculated the number and mass concentrations of airborne PM0.1 in December 2017, January 2018 and March 2018 during the high pollution period in Guangzhou. We collected PM0.1 from the same period and analyzed their chemical components. A549, THP-1 and A549/THP-1 co-cultured cells were selected for exposure to PM0.1, and evaluated for toxicological responses. Our aims are to 1) measure and analyze the number and mass concentrations, and chemical components of PM0.1; 2) evaluate and compare PM0.1 toxicity to different airway cells models at different time points. Guangzhou had the highest mass concentration of PM0.1 in December 2017, while the number concentration was the lowest. Chemical components in PM0.1 vary significantly at different time periods, and the correlation between the chemical composition or source of PM0.1 and the mass and number concentration of PM0.1 was dissimilar. Exposure to PM0.1 disrupted cell membranes, impaired mitochondrial function, promoted the expression of inflammatory mediators, and interfered with DNA replication in the cell cycle. The damage caused by exposure to PM0.1 at different times exhibited variations across different types of cells. PM0.1 in March 2018 stimulated co-cultured cells to secrete more inflammatory mediators, and CMA was significantly related to the expression of them. Our study indicates that it is essential to monitor both the mass and number concentrations of PM0.1 throughout all seasons annually, as conventional toxicological experiments and the internal components of PM0.1 may not effectively reveal the health damages caused by elevated number levels of PM0.1.
Assuntos
Poluentes Atmosféricos , Poluição do Ar , Poluentes Atmosféricos/análise , Material Particulado/toxicidade , Material Particulado/análise , China , Mediadores da Inflamação , Tamanho da Partícula , Monitoramento AmbientalRESUMO
Contaminants may induce immune response polarization, leading to immune diseases, such as allergic diseases. Evidence concerning the effects of chlorinated paraffins (CPs), an emerging persistent organic pollutant, on immune system is scarce, particularly for epidemiological evidence. This study explores the association between CPs exposure and allergic diseases (allergic rhinitis, atopic eczema, and allergic conjunctivitis) in children and adolescents in the Pearl River Delta (PRD) in China. Herein, 131,304 children and adolescents from primary and secondary schools in the PRD were included and completed the questionnaire survey. The particulate matter (PM) samples were collected in the PRD and the PM2.5-bound CP concentrations were analyzed. In the multivarious adjustment mixed effect model (MEM), an IQR increase in ∑CPs was significantly associated with allergic diseases (rhinitis, eczema, and conjunctivitis) with the estimated odds ratios (ORs) for 1.11 (95% CI: 1.10, 1.13), 1.17 (95% CI: 1.15, 1.19), and 1.82 (95% CI: 1.76, 1.88), respectively. Interaction analysis indicated that overweight and obese individuals might have greater risk. Similar effect estimates were observed in several sensitivity analyses. This study provided epidemiological evidence on the immunotoxicity of CPs. More studies to confirm our findings and investigate mechanisms are needed.
Assuntos
Parafina , Humanos , Adolescente , Criança , Masculino , Feminino , China/epidemiologia , Parafina/toxicidade , Parafina/análise , Hipersensibilidade/epidemiologia , Exposição Ambiental/efeitos adversos , Hidrocarbonetos Clorados/toxicidade , Hidrocarbonetos Clorados/análise , Poluentes Atmosféricos/toxicidade , Poluentes Atmosféricos/análise , Material Particulado/toxicidade , Material Particulado/análise , Dermatite Atópica/epidemiologia , Dermatite Atópica/induzido quimicamente , Rinite Alérgica/epidemiologia , Rinite Alérgica/induzido quimicamenteRESUMO
Maternal exposure to environment toxicants is an important risk factor for neurobehavioral health in their offspring. In our study, we investigated the impact of maternal exposure to chlorinated polyfluoroalkyl ether sulfonic acids (Cl-PFESAs, commercial name: F-53B) on behavioral changes and the potential mechanism in the offspring larvae of zebrafish. Adult zebrafish exposed to Cl-PFESAs (0, 0.2, 2, 20 and 200 µg/L) for 21 days were subsequently mated their embryos were cultured for 5 days. Higher concentrations of Cl-PFESAs in zebrafish embryos were observed, along with, reduced swimming speed and distance travelled in the offspring larvae. Molecular docking analysis revealed that Cl-PFESAs can form hydrogen bonds with brain-derived neurotropic factor (BDNF), protein kinase C, alpha, (PKCα), Ca2+-ATPase and Na, K - ATPase. Molecular and biochemical studies evidenced Cl-PFESAs induce dopaminergic dysfunction, eye developmental defects and disrupted Ca2+ homeostasis. Together, our results showed that maternal exposure to Cl-PFESAs lead to behavioral alteration in offspring mediated by disruption in Ca2+ homeostasis, dopaminergic dysfunction and eye developmental defects.
Assuntos
Ácidos Alcanossulfônicos , Fluorocarbonos , Poluentes Químicos da Água , Animais , Feminino , Peixe-Zebra/metabolismo , Ácidos Alcanossulfônicos/metabolismo , Cálcio/metabolismo , Larva , Simulação de Acoplamento Molecular , Fluorocarbonos/metabolismo , Poluentes Químicos da Água/metabolismo , Adenosina Trifosfatases/metabolismoRESUMO
Anthropogenic heat has been reported to have significant health impacts, but research on its association with childhood adiposity is still lacking. In this study, we matched the 2008-2012 average anthropogenic heat flux, as simulated by a grid estimation model using inventory methods, with questionnaire and measurement data of 49,938 children randomly recruited from seven cities in Northeast China in 2012. After adjusting for social demographic and behavioral factors, we used generalized linear mixed-effect models to assess the association between anthropogenic heat flux and adiposity among children. We also examined the effect modification of various social demographic and behavioral confounders. We found that each 10 W/m2 increase in total anthropogenic heat flux and that from the industry source was associated with an increase of 5.82% (95% CI = 0.84%-11.05%) and 6.62% (95% CI = 0.87%-12.70%) in the odds of childhood adiposity. Similarly, the excess rate of adiposity among children were 5.26% (95% CI = -1.33%-12.29%) and 8.51% (95% CI = 2.24%-15.17%) per 1 W/m2 increase in the anthropogenic heat flux from transportation and buildings, and was 7.94% (95% CI = 2.28%-13.91%) per 0.001 W/m2 increase in the anthropogenic heat flux from human metabolism. We also found generally greater effect estimates among female children and children who were exposed to passive smoking during pregnancy, born by caesarean section, non-breastfed/mixed-fed, or lived within 20 m adjacent to the main road. The potential deleterious effect of anthropogenic heat exposure on adiposity among children may make it a new but major threat to be targeted by future mitigation strategies.
Assuntos
Adiposidade , Temperatura Alta , Criança , Humanos , Feminino , Gravidez , Cesárea , China/epidemiologia , Obesidade , Atividades HumanasRESUMO
Environmental pollutants exposure might disrupt cardiac function, but evidence about the associations of per- and polyfluoroalkyl substances (PFASs) exposure and cardiac conduction system remains sparse. To explore the associations between serum PFASs exposure and electrocardiogram (ECG) parameters changes in adults, we recruited 1229 participants (mean age: 55.1 years) from communities of Guangzhou, China. 13 serum PFASs with detection rate > 85% were analyzed finally. We selected 6 ECG parameters [heart rate (HR), PR interval, QRS duration, Bazett heart rate-corrected QT interval (QTc), QRS electric axis and RV5 + SV1 voltage] as outcomes. Generalized linear models (GLMs) and Bayesian kernel machine regression (BKMR) model were conducted to explore the associations of individual and joint PFASs exposure and ECG parameters changes, respectively. We detected significant associations of PFASs exposure with decreased HR, QRS duration, but with increased PR interval. For example, at the 95th percentile of 6:2 Cl-PFESA, HR and QRS duration were - 6.98 [95% confidence interval (CI): - 9.07, - 4.90] and - 6.54(95% CI: -9.05, -4.03) lower, but PR interval was 7.35 (95% CI: 3.52, 11.17) longer than those at the 25th percentile. Similarly, significant joint associations were observed in HR, PR interval and QRS duration when analyzed by BKMR model.
Assuntos
Poluentes Ambientais , Fluorocarbonos , Humanos , Adulto , Pessoa de Meia-Idade , Teorema de Bayes , Exposição Ambiental , Eletrocardiografia , Fluorocarbonos/toxicidadeRESUMO
OBJECTIVE: To evaluate the value of diffusion-weighted imaging (DWI) in the differentiation of axillary inflammatory hyperplastic and metastatic lymph nodes. METHODS: Forty female New Zealand white rabbits were divided randomly into 2 groups (n = 20 each). And the animal models of axillary inflammatory hyperplastic and metastatic lymph nodes were established. All successfully implanted models received conventional magnetic resonance imaging (MRI) and diffusion-weighted imaging (DWI) examinations. The features of signal intensity and shapes of lymph nodes were observed in two groups. The sizes of lymph nodes were measured on the selected axial T(2)WI. The signal intensity and appearance diffusion coefficient (ADC) value of lymph nodes and dorsal muscle at the same slice were measured on the selected T(2)WI, DWI and ADC map respectively. The relative signal intensity (rSIT(2)WI, rSIDWI) and relative ADC (rADC) value of lymph nodes to dorsal muscle were calculated and compared. The diagnostic efficacy of differentiating benign and malignant lymph nodes was analyzed with rADC value through the receiver operating characteristic curve. The correlation between rADC value and cell density was assessed with pathological findings as reference standard. RESULTS: The differences of size, rSIT(2)WI and rSIDWI were not statistically significant between two groups. The rADC value of inflammatory lymph nodes was greater than that of metastatic lymph nodes (0.91 ± 0.14 vs 0.64 ± 0.18). Significant difference existed (t = 3.879, P = 0.03). But there was a little overlap between two groups. With 0.78 as the diagnostic threshold of rADC value, the sensibility and specificity was 86.2% and 74.4% respectively. The correlation between rADC value and cell density of inflammatory hyperplastic and metastatic lymph nodes was significantly inverse (r = -0.53, P = 0.003). CONCLUSIONS: As compared with the routine MRI sequence, rADC value has a higher diagnostic efficacy in the differentiation of benign and malignant lymph nodes. Cell density may be the most important influencing factor for the differences of rADC value between two groups of lymph nodes.
Assuntos
Imagem de Difusão por Ressonância Magnética , Linfonodos/patologia , Metástase Linfática/diagnóstico , Pseudolinfoma/diagnóstico , Animais , Axila/patologia , Diagnóstico Diferencial , Feminino , Inflamação , Linfadenite/patologia , Metástase Linfática/patologia , Pseudolinfoma/patologia , CoelhosRESUMO
Environmental lead exposure is closely related to the progression of Alzheimer's disease (AD). Our previous study has shown that exposure to lead could result in the cholesterol unbalance and increase amyloid-beta (Aß) generation in the brain. However, the potential effect of lead exposure on Aß transportation is poorly reported. In this study, we sought to explore whether lead exposure in developmental ages impaired the integrity of BCSFB and BBB, two highly vascularized structures in the brain in a rat model. The Aß clearance in the liver was also assessed. Our results showed that lead treatment in developmental ages increased the number of TUNEL-positive apoptotic cells in rat choroid plexus and microvessels. Moreover, lead exposure markedly increased pro-inflammatory factors expression including TNF-α and IL-1ß in rat choroid plexus and microvessels. Interestingly, lead treatment increased the expression of AQP-1 and reduced the expression of TTR, two key proteins associated with the functions of choroid plexus and microvessels. Additionally, the expressions of ABCB1, LRP-1, and RAGE, three major receptors responsible for Aß transportation, were disturbed by developmental lead exposure. All these pathologies resulted in Aß1-40 deposition within BCSFB and BBB and malfunctions of these two vascularized structures. Finally, we found that lead treatment remarkably inhibited the gene expression of LRP-1, which is responsible for Aß endocytosis, in the liver tissue of the rat model. Collectively, our results provide the first evidence that developmental lead exposure induces Aß deposition in BCSFB and BBB and impairs Aß clearance in the liver, which would ultimately disturb Aß transportation via choroid plexus/brain microvessels and facilitate Aß deposition in the brain.
Assuntos
Barreira Hematoencefálica , Chumbo , Peptídeos beta-Amiloides/metabolismo , Animais , Encéfalo/metabolismo , Chumbo/metabolismo , Fígado/metabolismo , RatosRESUMO
Numerous epidemiological studies have investigated the lipid interference effects of legacy PFASs, however, no studies on PFAS alternatives and blood lipids have been published. In this study, we explored the association between Cl-PFESAs, a typical PFASs alternative in China, and blood lipid profiles in 1336 Guangzhou community residents using linear and non-linear regression models. The results showed a deleterious effect of Cl-PFESAs and blood lipids: adjusted estimates (ß) for TC, TG, LDL-C and HDL-C per natural log unit increase of 6:2 Cl-PFESA were 0.029 (95% CI: 0.020, 0.038), 0.075 (95% CI: 0.049, 0.101), 0.035 (95% CI: 0.021, 0.049) and -0.071 (95% CI: -0.084, -0.058), respectively. The association between Cl-PFESAs and dyslipidemia was also positively significant (P < 0.05). Furthermore, a non-linear relationship was observed in Cl-PFESAs and serum lipid levels using a restricted cubic splines (RCS) model. In summary, our research suggested a negative impact of Cl-PFESAs on blood lipid patterns and a possible non-linear association.