Workers in aluminum smelting and processing, besides aluminum, are also chronically exposed to other complex metal mixtures in their working settings, yet integrated evidence linking internal dose, blood neurodegeneration biomarkers, and mild cognitive impairment (MCI) remains limited for occupational surveillance. We measured plasma concentrations of 10 metals (Al, Zn, Li, Cr, Mn, Fe, Co, Cu, Se, Pb) and plasma neurodegeneration-related biomarkers (Aβ42/Aβ40, GFAP, NfL, Total-tau, P-tau181, P-tau396) in 382 aluminum workers in Shanxi, China, and evaluated associations with MCI. Multivariable logistic regression with restricted cubic splines and Bayesian kernel machine regression were applied to characterize exposure-response relationships and mixture effects, while structural equation modeling explored biomarker pathways. Higher Al and lower Zn were consistently associated with greater odds of MCI, and GFAP, NfL, and P-tau396 were positively associated with MCI. Pathway analyses suggested partial mediation of Al- and Zn-related associations through NfL and P-tau396. Integrating metals with biomarkers improved discrimination compared with single indicators (best AUC = 0.924). Model-averaged benchmark dose analysis (BMR = 10% extra risk) yielded an aluminum BMDL of ∼31 μg/L, within the observed exposure range, providing a candidate biomonitoring reference point to inform derivation of biological exposure limits.

This study explored the association between plasma levels of multiple metals and cognitive impairment (CI) in 455 aluminum electrolysis workers from a northern Chinese plant, divided into CI (256) and control (199) groups by MoCA scores. Using inductively coupled plasma mass spectrometry, 11 metals were measured, with analyses via conditional logistic regression,generalized linear models (GLM), Bayesian kernel machine regression (BKMR), and age stratification (40 years). Plasma aluminum (Al), lead (Pb), lithium (Li), manganese, cobalt, and copper were significantly higher in the CI group (all P < 0.05), while zinc showed no difference. Single-element analysis found Al, Pb, and Li negatively correlated with MoCA total and subscores (e.g., visuospatial function; P < 0.05), and zinc positively correlated with attention (β = 1.10, P < 0.05). BKMR confirmed metal mixtures above the 25th percentile reduced MoCA scores (β = -0.875, 95 % CI: -1.379 to -0.371), with Al, Pb, and Li as key contributors (PIP > 0.6). Subgroup analysis showed Al primarily affected those <40, while Pb had greater impact in those >40. Findings indicate elevated Al, Pb, and Li associate with higher CI risk, metal mixtures synergistically exacerbate impairment, and age modifies these effects, aiding occupational cognitive impairment prevention.

Aluminum causes learning and memory impairments, and is an environmental and occupational toxicant. This in vivo and in vitro study assessed the implications of Lnc_000151 on aluminum-induced neurotoxicity through competitive binding to miR-96-5p. Fifty-six male SpragueDawley rats were randomly divided into eight groups: untreated, sham-operated, saline + sham-operated, Al(mal)₃ + sham-operated, saline + AAV-NC, Al(mal)₃ + AAV-NC, saline + AAV-Lnc_000151 shRNA, and Al(mal)₃ + AAV-Lnc_000151 shRNA. PC12 cells were separated into groups of 0, 100, 200, and 400 µM Al (mal)₃, and transfection groups including Lnc_000151 NC/siRNA, miR-96-5p NC/inhibitor, and IRS1 NC/siRNA. The learning and memory functions of rats were assessed via Morris water maze. Hippocampal CA1 neuronal count and synaptic structure were detected with hematoxylin-eosin staining and transmission electron microscopy. Cell apoptosis was measured using flow cytometry. Relative expression of Lnc_000151, miR-96-5p, and the IRS1/AKT/GSK3β pathway was determined using RT-PCR and Western blotting. The dual-luciferase assay confirmed targeted binding of Lnc_000151 to miR-96-5p and miR-96-5p to IRS1. In vivo and in vitro experiments demonstrated that under aluminum exposure, inhibition of Lnc_000151 expression exacerbated learning and memory impairments, neuronal loss, synaptic damage, increased Tau and p-Tau (Ser396) expression, and cell apoptosis. In vitro experiments further verified that under aluminum exposure and Lnc_000151 inhibition, suppressing miR-96-5p expression reduced Tau and p-Tau (Ser396) expression and cell apoptosis, while activating the IRS1/AKT/GSK3β pathway. However, further inhibition of IRS1 expression abrogated these ameliorative effects. In conclusion, this study demonstrates that Lnc_000151 can competitively bind to miR-96-5p in a competing endogenous RNA (ceRNA)-dependent manner, thereby regulating IRS1 expression, modulating the AKT/GSK3β pathway, and affecting aluminum-induced neurotoxicity.

This study aims to analyze the connection between mixed metal exposure and abnormal blood glucose (defined as fasting plasma glucose ≥6.1 mmol/L, according to the World Health Organization diagnostic criteria) among aluminum plant workers. A total of 384 male workers from a large aluminum plant in Shanxi Province were surveyed between July and August 2024. Fasting glucose and eight plasma metals were measured. Logistic regression, Restricted cubic spline (RCS) analyses, least absolute shrinkage and selection operator (LASSO) regression, Weighted quantile sum (WQS) regression, and Bayesian kernel machine regression (BKMR) were used to examine single-metal and mixture effects. Following adjustment for potential confounders, the highest quartile (Q4) of plasma aluminum, selenium, and copper was associated with higher odds of abnormal blood glucose, with adjusted ORs of 2.93 (95

BACKGROUND:Occupational aluminum exposure correlates with cognitive decline; however, the correlational mediating roles of specific inflammatory cytokines across distinct cognitive domains remain unclear. METHODS:This cross-sectional study enrolled 516 male workers aged 21-59 years from a Shanxi aluminum plant. Cognitive function was assessed via MoCA, AVLT and TMT; four latent cognitive domains (memory, executive, expressive, visuospatial function) were extracted by exploratory factor analysis. Plasma aluminum was detected using ICP-MS, and serum inflammatory cytokines (IL-1β, IL-18, IL-4, IL-10) were measured by ELISA. Multivariable linear regression, correlational mediation models and restricted cubic spline (RCS) analysis were used to explore variable associations, statistical mediation patterns and cohort-specific exploratory aluminum reference thresholds. RESULTS:Plasma aluminum was stratified into four quartiles (<25.13, 25.13-48.47, 48.47-81.39, ≥81.39 µg/L). Significant differences in global cognition and all inflammatory cytokines were detected across quartile groups (all P < 0.05). Higher plasma aluminum and inflammatory cytokine levels were correlated with lower executive and expressive function scores (Ptrend < 0.001). Inflammatory mediators presented a joint correlational mediating pattern for the association between aluminum exposure and global cognition. IL-1β/IL-18 acted as correlational intermediaries for the association between aluminum exposure and executive dysfunction, while IL-4/IL-10 played similar correlational roles in expressive dysfunction. RCS yielded cohort-specific exploratory thresholds: 59.93 µg/L (global cognition), 58.10 µg/L (executive function), and 20.15 µg/L (expressive function). CONCLUSIONS:Occupational aluminum exposure is correlated with impaired executive and expressive function, with overall observational evidence supporting that inflammatory mediators link these variables via a statistical mediating pathway. Plasma aluminum and circulating inflammatory cytokines can serve as auxiliary biomarkers for early cognitive decline risk screening among aluminum-exposed workers.

Background Cognitive impairment (CI) is a condition in which an individual experiences noticeable impairment in thinking abilities. Long-term exposure to aluminum (Al) can cause CI. This study aimed to determine the relationship between CI and MRI-related changes in postroom workers exposed to Al.Methods Thirty patients with CI and 25 healthy controls were recruited. Plasma aluminum levels were measured using inductively coupled plasma-mass spectrometry. Cognitive function was assessed using the Montreal Cognitive Assessment (MoCA) and an auditory-verbal learning test (AVLT). All participants underwent magnetic resonance imaging scans. 3D T1-weighted anatomical images and resting-state functional magnetic resonance imaging data were acquired, and voxel-based morphometry and ROI-based FC were used for analysis. A mediation analysis was also conducted.Results Plasma aluminum levels were significantly higher in the CI group than in the normal control group. The gray matter (GM) volume in the left caudate and bilateral hippocampus was lower in the CI group and was positively correlated with cognitive scale scores. There was no significant difference in functional connectivity (FC) between the left caudate and the whole brain between the two groups. Significant alterations in hippocampal FC were observed in certain brain areas, mainly in the left cerebellar vermis, left middle frontal gyrus (BA9), and right superior frontal gyrus relative to the supplementary motor area (BA6). The FC coefficients were also associated with cognitive scale scores. Furthermore, plasma Al concentration was negatively correlated with the Montreal Cognitive Assessment score, bilateral hippocampal GM volume, and FC coefficient between the left hippocampus and left cerebellar vermis. Mediation analysis showed GM alteration of left caudate and bilateral hippocampus and FC alteration of left hippocampus to left cerebellar vermis could explained 19.80-32.07% of the effect of MoCA scores change related to Al exposure, besides the GM alteration of right hippocampus acted as indirect mediator (68.75%) of the association between Al and AVLT delayed recall scores.Conclusion Our data indicates that alterations in the structure and function of special brain domain, especially the hippocampus, are associated with Al-induced CI. These brain regions can partly explain the effect of Al on cognitive impairment.

INTRODUCTION:The relationship between aluminium exposure and cognitive impairment remains to be fully elucidated. Furthermore, studies examining potential mediating mechanisms are limited. OBJECTIVES:The study investigated the relationship between plasma aluminium (P-Al) levels and cognitive impairment (was defined as a Montreal Cognitive Assessment (MoCA) score < 26 (i.e., mild cognitive impairment, MCI). The parallel mediating effects of systolic blood pressure (SBP) and fasting blood glucose (FBG) in the association between plasma aluminum (P-Al) and cognitive function were analyzed. METHODS:In this cross-sectional study of 229 aluminum workers (2024 survey), we conducted a three-step analysis:Descriptive statistics: Demographic and clinical variables were summarized as mean ± SD or median (IQR) for continuous data, and frequencies (%) for categorical data.Group comparisons: ANOVA with Bonferroni correction (normal-distributed variables) and Kruskal-Wallis H test were used to compare differences across P-Al quartiles (Q1 - Q4). Categorical variables were analyzed by χ² or Fisher's exact tests.Mediation analysis: A dual-pathway mediation model (SBP and FBG as parallel mediators) was tested using bootstrap method. Effects were reported as standardized β coefficients with 95 % CIs. RESULTS:Workers in the high P-Al group had significantly lower MoCA scores (P < 0.05) and higher incidence of cognitive dysfunction (P < 0.05). P-Al levels were negatively correlated with MoCA scores (r = -0.716, P < 0.05) and indirectly affected cognitive function through the parallel mediating pathways of SBP (7.41 % of indirect effect) and FBG (18.52 % of indirect effect), with the direct effect accounting for 74.07 % of the total effect. CONCLUSION:Aluminum exposure is significantly associated with cognitive impairment, which may have dual effects on metabolic disorders (elevated FBG) and vascular damage (elevated blood pressure) pathways.In order to reduce the risk of occupational cognitive dysfunction, it is necessary to implement enhanced P-Al monitoring and metabolic index interventions for aluminium workers.

Occupational aluminum (Al) exposure is associated with cognitive decline, but the underlying molecular mechanisms remain unclear. This study investigates the role of Kalirin in Al-induced neurotoxicity. A cross-sectional study was conducted in 2019 with 172 workers from a Shanxi aluminum plant. Participants were categorized into high and low Al exposure groups based on plasma aluminum levels, and cognitive function was assessed using the MoCA test. Phosphoproteomic analysis revealed a significant 90 % reduction in Kalirin expression in the high-exposure group compared to the low-exposure group (P < 0.05). Multiple regression analysis demonstrated that Al exposure negatively correlated with Kalirin, GAP43, MAP2 expression, and cognitive function, while Kalirin was positively correlated with these factors (q < 0.05). Bayesian network modeling indicated that decreased Kalirin expression, along with reduced GAP43 and MAP2 levels, increased the risk of cognitive impairment. In vitro, HT22 neurons exposed to aluminum maltolate showed reduced neuronal activity, impaired dendritic development, and disruption of the Kalirin-Rac1 pathway. Overexpression of Kalirin via lentiviral transfection reversed these effects, restoring neuronal integrity (P < 0.05). These findings suggest that Al-induced neurotoxicity involves disruption of the Kalirin pathway, highlighting Kalirin as a potential therapeutic target for mitigating Al-related cognitive dysfunction.

This study aimed to elucidate the associations among occupational aluminum exposure, plasma phosphorylated tau (P-tau), and cognitive function, with particular attention to the modulatory effects of key factors involved in tau protein synthesis and degradation. A total of 208 aluminum plant workers were enrolled, with assessments conducted for plasma aluminum concentrations, cognitive performance, levels of phosphorylated tau (P-tau181 and P-tau231), and biomarkers related to tau synthesis and degradation pathways. Elevated plasma aluminum levels were inversely associated with scores on cognitive assessments, including the MMSE, DSP, DSR, DS, FOM, and CDT, while showing positive associations with STRA and STRF scores. Higher plasma aluminum concentrations were also significantly associated with increased levels of P-tau181 and P-tau231. P-tau181 and P-tau 231 concentrations are negatively correlated with MMSE, DSP, DSR, DS, and FOM scores, and positively correlated with STRA, STRF, and CDT scores. Mediation analysis revealed that P-tau181 and P-tau231 were statistically consistent with mediating 16.6 % and 35.9 % of the association between aluminum exposure and MMSE scores, respectively, with P-tau231 demonstrating a stronger mediating effect. Moderated mediation analysis further indicated that factors regulating tau synthesis had a more pronounced influence on this mediating role than those involved in degradation[ΔR2(PP2A, CDK5)= 0.016 > ΔR2(CHIP, Ub)= 0; ΔR2(PP2A, CDK5)= 0.027 > ΔR2(CHIP, Ub)= 0], with PP2A-mediated regulation exerting a greater effect than CDK5[ΔR2(PP2A)= 0.021 > ΔR2(CDK5)= 0.006; ΔR2(PP2A)= 0.016 > ΔR2(CDK5)= 0.008]. These results are statistically consistent with the hypothesis that P-tau231 and PP2A are critical targets for early intervention and biomonitoring in the context of aluminum-related cognitive impairment, offering novel directions for occupational health risk management and protection.

Objective:To investigate the partial mediating role of the inflammatory marker hemoglobin-to-red cell distribution width ratio (HRR) in the association between occupational aluminum exposure and cognitive function impairment, and its significance. Methods:In this study, 401 workers from a Shanxi aluminum plant were selected by Cluster Sampling. Fasting elbow venous blood was collected for measuring routine blood counts, plasma aluminum concentration (P-Al) was measured using inductively coupled plasma mass spectrometry (ICP-MS), Montreal Cognitive Assessment (MoCA) was used to assess the cognitive function. Multiple linear regression was used to analyze the relationship between P-Al and cognitive function and HRR, and a restricted cubic spline model was used to fit the dose-response relationship, and mediated effects analysis was performed. Results:The median plasma aluminum concentration ( P 25 , P 75 ) of the workers was 50.74 (23.45, 85.52) μg/L, the mean HRR was 11.87, the median MoCA total score ( P 25 , P 75 ) was 24.00 (22.00, 26.00). A dose-response relationship showed that the MoCA score decreased with increasing P-Al. After adjusting for demographic and lifestyle covariates, multiple linear regression showed that P-Al was negatively correlated with the HRR and MoCA score. For each unit increase in P-Al, the HRR decreased by an average of 0.17, and the total MoCA score decreased by an average of 0.9. HRR mediated 9.89% of the effect between P-Al and MoCA score. Conclusion:Occupational aluminum exposure negatively affects workers' cognitive function and HRR levels. HRR can partially explain the effects of occupational aluminum exposure on workers' cognitive function.

Although aluminum is ubiquitously present on Earth, it is not necessary for life. Aluminum is a metal element that can induce neurotoxicity. The neurotoxicity of aluminum is mainly caused by the aggregation of abnormally phosphorylated tau protein to form neurofibrillary tangles (NFTs). The phosphorylation of tau is regulated by both kinases and phosphatases. ERK is involved in PHF-type tau hyperphosphorylation. Recent studies have revealed that the interaction between microRNAs (miRNAs) and the ERK/MAPK cascade is related to maintaining the normal function of the nervous system. miR-195 is involved in the early development of AD with a potential impact on cognition. Therefore, we speculate that miRNA-195 may regulate ERK activity, thereby causing hyperphosphorylation of tau protein and neurotoxicity. The purpose of this study was to explore the role of miRNA-195-5p in regulating ERK in the process of aluminum maltol-induced tau hyperphosphorylation. The results showed that aluminum exposure decreased the expression level of miRNA-195-5p and increased the expression of P-ERK, abnormal phosphorylated tau. After inhibiting the activity of ERK, the expression of phosphorylation tau protein decreased. There is an interaction effect between inhibiting the activity of ERK and aluminum exposure on the expression of phosphorylated tau proteins. After the overexpression of miRNA-195-5p, the activity of ERK was inhibited. There is an interaction effect between miRNA-195-5p and aluminum exposure on the expression of phosphorylated tau. In conclusion, miRNA-195-5p regulates ERK involvement in the abnormal phosphorylation of tau protein by Al (mal)3in PC12 cells.

Aluminum, a ubiquitous environmental neurotoxin, has been implicated in the pathogenesis of neurodegenerative disorders, including Alzheimer’s disease (AD). While Aβ deposition is a hallmark of AD progression, the molecular mechanisms underlying aluminum-induced Aβ aggregation remain incompletely understood. This study examines the role of the ciRs-7–miR-7–UBE2A axis in aluminum-induced Aβ deposition. Healthy male SD rats and PC12 cells were stratified into groups based on aluminum maltolate exposure levels to establish an in vivo and in vitro neurotoxicity model. Hippocampal aluminum content, along with the expression levels of ciRs-7, miR-7, UBE2A, and Aβ1-42, were systematically analyzed. The results demonstrated a dose-dependent decrease in ciRs-7 and UBE2A expression with escalating aluminum exposure, accompanied by concurrent upregulation of miR-7 and Aβ1-42 accumulation. Conversely, ciRs-7 overexpression reversed these pathological trends. Mechanistically, aluminum exposure downregulates ciRs-7 in the hippocampus, thereby derepressing miR-7 activity, which suppresses UBE2A expression and ultimately promotes Aβ deposition. These results identify a novel circRNA-dependent mechanism in aluminum neurotoxicity, suggesting therapeutic targets for AD intervention.

BACKGROUND:Trace element and metal exposure is closely related to the occurrence of chronic diseases, particularly affecting blood pressure and blood glucose. Current studies suggest that heavy metal exposure is a risk factor for hypertension and diabetes. Aluminum can enter the human body through daily life and occupational exposure from food, environment, drugs, and other sources, affecting the cardiovascular, endocrine, and other systems. Therefore, it is significant to observe the effect of aluminum on blood pressure and blood glucose in workers with high concentration. OBJECTIVE:In this study, electrolytic workers naturally exposed to high concentrations of aluminum were selected. The aim of the 5-year cohort study was to investigate the effects of continuous occupational aluminum exposure on blood pressure and blood glucose in workers and to assess the risk of potential cardiovascular and metabolic diseases due to heavy metal exposure. METHODS:In 2014, 183 participants from an electrolysis workshop at an aluminum plant in Shanxi were enrolled. Inductively coupled plasma mass spectrometry (ICP-MS) was performed to determine the plasma aluminum (P-Al) concentration of the workers and measured their blood pressure and glucose levels. At the 2019 follow-up, all parameters were measured again in the same workers. The relationship of the P-Al concentration with blood pressure and glucose levels was assessed using generalized linear regression, and risks of developing hypertension and hyperglycemia (diabetes or pre-diabetes) due to Al exposure were assessed using binary logistic regression. Dose-response relationships between average annual rates of change in P-Al and average annual rates of change in blood pressure and blood glucose were analyzed using RCS. The relative risk (RR) and attributable risk (AR) were also calculated. RESULTS:Generalized linear regression showed that the average annual rate of change in P-Al concentration was positively correlated with the annual rates of change in SBP, DBP, and blood glucose levels, with each e-fold increase in P-Al concentration increasing the annual rates of change in SBP and DBP by 3.55 % (P < 0.01) and 3.43 % (P = 0.03), respectively. Binary logistic regression showed that as the average annual rate of change in P-Al concentration (categorical variable) increased, the risk of developing hypertension increased (Ptrend < 0.05). The RCS results showed that the relationship between the average annual rate of change in P-Al and the average annual rate of change in SBP was a showed a dose-response relationship (P for overall association<0.05). RR and AR increased with increasing P-Al concentration in both hypertensive and diabetic patients. CONCLUSION:Persistent occupational aluminum exposure is associated with elevated blood pressure levels in workers and increases the risk of developing hypertensive disorders.

OBJECT:This objective of this study was to investigate how aluminum affects the PKA-PGC1α-BACE1 pathway in PC12 cells and its role in neurotoxicity. METHOD:According to the exposure dose of aluminum maltol, PC12 cells were selected for research and divided into five experimental groups and six intervention groups. After 24 h of 8-Bromo-cAMP intervention, they were treated with Al-(mal)3 for 24 h. After the experiment, cell morphology was observed, and the cell survival rate was assessed using the Cell Counting Kit-8 (CCK-8) assay. Western blot and ELISA techniques were used to detect the expression of relevant proteins, enzyme activity, and Aβ levels. RESULT:Under the microscope, the number of cells in the aluminum maltol group decreased, the morphology changed, and the number of intercellular connections decreased. However, after treatment with the 8-Bromo-cAMP agonist, a significant increase in the number of cells was observed, and significant morphological changes occurred, with a gradual increase in intercellular connections. CCK-8 assays showed that cell viability gradually decreased with increasing aluminum exposure doses. Western blot showed that PKA and PGC1α expressions decreased with higher aluminum doses, while BACE1 increased; agonist treatment upregulated PGC1α and downregulated BACE1, with minimal effect on PKA; and ELISA results indicated that aluminum reduced PKA enzyme activity but increased BACE1 activity and Aβ levels. CONCLUSION:Exposure to aluminum inhibits the PKA-PGC1α-BACE1 signaling pathway, while PKA agonists can alleviate neurotoxicity by restoring this pathway.

Aluminum (Al) has emerged as a pervasive environmental and industrial risk factor for cognitive impairment and neurodegenerative diseases, such as Alzheimer’s disease and Parkinson’s disease. Nowadays, N6-methyladenosine (m6A) modification mechanism contributing to aluminum toxicity is gradually gaining attention. m6A modification determines the fate of RNA through m6A “readers”. Novel findings indicate that YTH N6-methyladenosine RNA binding protein 1 (YTHDF1, a kind of “readers”) participates in various pathological processes induced by some toxic chemicals. Here, we investigated the function of YTHDF1 in neuronal apoptosis induced by aluminum and explored the molecular mechanisms. We first observed the YTHDF1 expression both in vivo and in vitro neuronal apoptosis model induced by aluminum, as well as the reversal effect of YTHDF1 overexpression by lentivirus transfection in vitro. Further, we explored Bcl-2 as a target gene of YTHDF1 and probed their m6A modification manner and molecular mechanism using RIP assay, Me-RIP assay, and Actinomycin D (ActD) assay. Finally, we examined the regulatory role of YTHDF1/m6A/Bcl-2 axis in aluminum neurotoxicity in vitro and in vivo. Functionally, Al(mal)3 treatment decreased YTHDF1 expression, which negatively regulates apoptosis via m6A modification manner. Mechanistically, Bcl-2 acted as the target of YTHDF1, and YTHDF1 regulated Bcl-2 by enhancing its mRNA stability. Collectively, Al(mal)3 treatment inhibited the YTHDF1/m6A/Bcl-2 axis, thereby promoting neuronal apoptosis and subsequent cognitive impairment. This study provides a novel protective strategy against aluminum toxicity.

OBJECTIVE:To investigate the interaction between plasma polymetallic exposure and lifestyle factors on cognitive function abnormalities in occupational aluminum workers. The aim is to develop a new occupational health management model that integrates lifestyle behaviors with occupational activities to comprehensively protect the health of these workers. METHOD:476 Participants were recruited from an aluminum factory in Shanxi, China. Cognitive functioning was assessed using the Montreal Cognitive Assessment Scale (MoCA). Plasma polymetallic levels were measured using ICP-MS. Logistic regression analyzed the relationship between nine plasma metals, lifestyle factors, and cognitive abnormalities. A 3D model validated the interaction between metals and analyzed the combined effects of plasma metals and lifestyle on MoCA scores. The Chi-squared Automatic Interaction Detector (CHAID) decision tree was used to identify factors influencing cognitive dysfunction. RESULTS:High blood aluminum concentration (>47.85 μg/L), high blood lithium concentration(>3.15 μg/L), as well as sleep time(≤7 h and > 8 h), smoking, alcohol consumption, and length of mobile phone use(≥2 h) were risk factors for abnormal cognitive functioning. In addition aluminum and lithium have a multiplicative interaction on cognitive function(OR=1.86,95 %CI:1.14,3.050). There was an interaction between high plasma levels of aluminum and lithium and smoking on cognitive function in workers, and an interaction between high plasma levels of aluminum and lithium and sleep duration ≤7 or >8 h on cognitive function in workers. CONCLUSION:The levels of blood metal elements aluminum and lithium, as well as sleep time, smoking, drinking, and length of mobile phone use, are risk factors for cognitive dysfunction in occupational aluminum workers. There are the synergetic effect to increase the risk of cognitive dysfunction between blood aluminum concentration ≥50.59μg/L and blood lithium concentration ≥3.44μg/L, sleep duration ≤7h& >8 h, smoking, drinking, mobile phone use ≥2 h.

Objective To assess the diagnostic utility of lncRNA 51A in detecting cognitive decline among aluminum-exposed workers occupationally. Methods 921 male workers from an aluminum manufacturing facility underwent cognitive assessments, measurement of plasma aluminum levels and quantification of lncRNA 51A levels. Receiver Operating Characteristic (ROC) curves were constructed to assess the diagnostic potential of lncRNA 51A. Bayesian network model was utilized to predict the likelihood of cognitive decline among the study population. Results Significant differences in lncRNA 51A levels, plasma aluminum concentration and MMSE scores were observed between cognitive normal and decline groups. The lncRNA 51A expression was negatively correlated with MMSE scores. The area under the curve (AUC) was 0.894, with 89.3% sensitivity and 73.9% specificity. The Bayesian network model indicated varying probabilities of cognitive decline based on lncRNA 51A expression levels. Conclusion Plasma lncRNA 51A shows potential as an excellent biomarker for cognitive decline diagnosis in aluminum-exposed workers.

Background: The correlation between metals and hypertension, such as sodium, zinc, potassium, and magnesium, has been confirmed, while the relationship between aluminum and hypertension is not very clear. This study aimed to evaluate the correlation between plasma aluminum and hypertension in electrolytic aluminum workers by the Bayesian networks (BN).Methods: In 2019, 476 male workers in an aluminum factory were investigated. The plasma aluminum concentration of workers was measured by inductively coupled plasma mass spectrometry. The influencing factors on the prevalence of hypertension were analyzed by the BN.Results: The prevalence of hypertension was 23.9% in 476 male workers. The risk of hypertension from plasma aluminum in the Q2, Q3, and Q4 groups was 5.20 (1.90-14.25), 6.92 (2.51-19.08), and 7.33 (2.69-20.01), respectively, compared with that in the Q1 group. The risk of hypertension from the duration of exposure to aluminum of >10 years was 2.23 (1.09-4.57), compared without aluminum exposure. Area under the curve was 0.80 of plasma aluminum and the duration of exposure to aluminum was based on covariates, indicating that aluminum exposure had important predictive value in the prevalence of hypertension in the occupational population. The results of the study using the BN model showed that if the plasma aluminum of all participants was higher than Q4 (≥47.86 μg/L) and the participants were drinking, smoking, diabetes, central obesity, dyslipidemia, and aged >50 years, the proportion of hypertension was 71.2%.Conclusions: The prevalence of hypertension increased significantly with the increase of plasma aluminum level.

[背景]铝、氟具有神经毒性,单独铝暴露与作业工人的总体认知功能密切相关,关于铝、氟交互作用对认知功能的影响目前尚不清楚.[目的]探讨血铝和尿氟的交互作用对铝厂作业工人总体认知功能的影响.[方法]采用整群抽样方法,选取山西省某市铝业集团公司电解车间230名作业工人为调查对象,采用电感耦合等离子体质谱法(ICP-MS)测定血浆铝含量,采用离子选择电极法测定尿氟.将研究对象血铝浓度根据中位数(M)分为低血铝组和高血铝组,尿氟浓度根据临床有关标准限值(0.272～2.160 mg·L-1)以2.160 mg·L-1为界分为低尿氟组和高尿氟组.采用《蒙特利尔认知评估量表北京版》(MoCA-BJ)评估工人总体认知功能.采用logistic回归模型分析血铝、尿氟与轻度认知功能障碍(MCI)之间的关系,包括相乘交互作用分析和关联性分析;采用R语言拟合血铝、尿氟对MCI的相加交互作用模型并计算交互作用指数(S)、交互作用超额相对危险度(RERI)和交互作用归因比(API)等交互作用指标.[结果]230名作业工人中,血铝浓度中位数(P25,P75)为40.11(25.16,58.89)μg·L-1,尿氟异常者104例,异常率45.2％.血铝和尿氟的交互作用对铝厂作业工人总体认知功能的影响存在相乘交互作用(OR=7.783,95％CI:1.377～43.991),不存在相加交互作用(RERI=0.030,95％CI:-0.498～0.559;API=0.018,95％CI:-0.279～0.316;S=1.049,95％CI:0.519～2.118).多因素 logistic回归分析结果显示,在调整不同影响因素后,既有高血铝又有高尿氟人群患MCI的风险是低血铝低尿氟人群的12.105(95％CI:2.802～52.287)倍.[结论]职业性高浓度血铝和高浓度尿氟是认知功能障碍的危险因素,两者同时存在会增加作业工人MCI的发生风险,存在相乘交互作用.

Aluminum (Al) is a neurotoxic substance associated with cognitive dysfunction and neurodegenerative diseases, such as Alzheimer's disease, but the mechanisms for aluminum neurotoxicity remain to be identified. In this work, we try to investigate a novel potential biomarker of cognitive dysfunction following aluminum exposure and the mechanism involved. Recently, miR-134-3p was reported as a novel regulator of cognitive function. To address this, we investigate the expression level of miR-134-3p in plasma from 280 aluminum factory workers and analyzed the correlation between miRNA-134-3p, blood Al concentration, and Montreal Cognitive Assessment Scale (MoCA scale) score. The results implied that occupational aluminum exposure elevated miR-134-3p expression in the plasma of workers accompanied by cognitive impairment. Our experiment studies using both animal models and PC12 cells validated the upregulation of miR-134-3p caused by aluminum. In addition, we identified that palmitoylation enzyme zDHHC3 was the target of miR-134-3p, and the decreasing AMPAR receptor (AMPAR) trafficking was related to the learning and memory impairment induced by aluminum. More importantly, using transfection and interference approaches in PC12 cells, inhibition of miR-134-3p resulted in a recovery of zDHHC3-AMPARs axis to a certain extent in response to aluminum. In summary, miR-134-3p was found to be involved in aluminum neurotoxicity by targeting zDHHC3-AMPARs axis and could serve as a potential biomarker or helpful target.