This study applied integrated multi-omics to explore the role of plasma elements, blood clinical indicators, and metabolome in cervical cancer (CC). Based on data from 436 subjects, untargeted/targeted metabolomics and ICP-MS analyses revealed significant plasma metabolome reprogramming in CC. This was characterized by upregulated levels of estrone glucuronide and cortisol, and downregulation of androstenedione. A random forest model constructed with four metabolites (androstenedione, calcitriol, paraxanthine, theobromine) achieved an AUC of 0.884, superior to conventional markers (CEA, CA125). Among nine metals linked to CC risk, Cd, Cr, Pb, Ba, and Li increased risk, while Mn, Cu, and Sn were protective; mixed metal exposure elevated risk dose-dependently. CC patients also showed abnormal blood parameters, including reduced RBC and lymphocyte counts, and higher TG, GLU, CEA, and CA125. Multi-omics network analysis indicated co-clustering of Li, Cr, and Co with estrone glucuronide, 5-HIAA, GLU, PCT, and CA125; Pb and Ba with L-valine; Mn with paraxanthine, androstenedione, A/G, and GLOB; cortisol, caffeine, and theobromine with RBC and LYM#. These integrated network highlights complex interactions among metals, clinical indicators, and metabolites, providing new insights for non-invasive diagnosis and environmental health interventions in CC.

Background Studies have indicated that exposure to household pesticides is prevalent among the population. Nevertheless, the relationship and contributing factors linking urinary metabolites of household pesticides to circulating levels of sex steroid hormones in human serum remain insufficiently explored. Objective To examine the correlation between household pesticides metabolites and serum sex steroid hormones levels. Methods This study utilized data from 3884 participants obtained through the National Health and Nutrition Examination Survey (NHANES) conducted between 2013 and 2016. NHANES measured urinary metabolites of household pesticides and serum levels of sex steroid hormones. The study utilized weighted multiple linear regression modeling combined with restricted cubic spline (RCS) analysis to investigate relationships and dose-response patterns between residential pesticide metabolites and serum sex steroid hormones across both genders. Additionally, the research examined potential modifying effects of obesity status on pesticide metabolite-sex hormone associations through interaction analysis. Results Following adjustment for potential confounders, concentrations of 3,5,6-trichloro-2-pyridinol (TCPY), para-nitrophenol (PNP), and 3-phenoxybenzoic acid (3-PBA) demonstrated negative correlations with total serum testosterone (TT), estradiol concentrations(E2), and free androgen index (FAI) across all three statistical models (Ps < 0.05), while positive relationships emerged with sex hormone-binding globulin (SHBG). We found the similar results among male participants. However, the negative correlation was not found between TCPY, PNP, 3-PBA and SHBG among female participants RCS modeling revealed complex nonlinear interactions between DCBA and serum sex steroid hormone levels. Analysis stratified by body mass index showed that TCPY, PNP and 3-PBA exhibited similar negative correlations with TT, E2 and FAI in the non-obese participants. Conclusions The study reveals that the metabolites from household pesticides exhibited negative correlations with serum sex steroid hormone levels across both genders. Associations were more consistent for non-obese populations.

This study investigates the association between exposure to the PFOS alternative F-53B (6:2 Cl-PFESA) and cervical cancer risk in Chinese women, and elucidates its dual mechanisms of cervical toxicity and malignant progression. A case-control study (181 patients, 164 controls) measured plasma concentrations of 8 PFAS by UPLC-MS/MS, and logistic regression, WQS, and BKMR models were used to assess PFAS-cervical cancer associations. Human cervical epithelial cells (HcerEpic, HeLa, SiHa) were exposed to acute (425 μM) or long-term low-dose (1 μM) F-53B, followed by transcriptomics, ferroptosis phenotyping, functional assays, and protein/gene expression analyses. In vivo validation was performed using C57BL/6 mice (subacute exposure, metabolomics) and BALB/c nude mice (xenograft model). Epidemiological analysis identified F-53B as the predominant driver of cervical cancer risk within PFAS mixture exposure. Acute high-dose F-53B induced ferroptosis in cervical epithelial cells. At a concentration relevant to occupational exposure (1 μM), F-53B promoted malignant phenotypes by driving cell cycle progression, inhibiting apoptosis, enhancing migration/invasion, and inducing EMT. In vivo, F-53B caused cervical ferroptosis and systemic lipid metabolic reprogramming in C57BL/6 mice, and promoted xenograft growth and lymphatic metastasis in nude mice. This first multi-level evidence identifies F-53B, a widely used PFOS substitute, as an environmental risk factor for cervical cancer. It exerts acute toxicity via ferroptosis and drives malignant progression over the long term through multiple oncogenic phenotypes, underscoring the need for stringent risk assessment of emerging PFAS alternatives.

The increasing global use of organophosphate esters (OPEs) has raised concerns about their environmental and health impacts, with evidence suggesting adverse effects on reproductive system health. As a widely used OPE, triphenyl phosphate (TPHP) has drawn attention for its endocrine-disrupting properties; however, its effects on cervical epithelial cells and association with cervical diseases remain unclear. In this study, analysis of 12 urinary OPE metabolites (mOPEs) in 116 cervical cancer (CC) cases and 116 controls revealed that multiple exposure biomarkers, particularly those related to TPHP exposure, were significantly positively associated with CC risk, suggesting a potential link between OPE exposure and disease development. In toxicological experiments, acute exposure to TPHP (50 μM, 24 h) induced significant cytotoxicity in human cervical epithelial cells (HcerEpic), characterized by reduced cell viability, cell cycle disruption, apoptosis, and oxidative stress. Conversely, chronic low-dose exposure (100 nM, 30 weeks) conferred a survival advantage to HcerEpic cells and enhanced their epithelial-mesenchymal transition (EMT) capacity, with enhanced tumor formation ability observed in a nude mouse xenograft model. Transcriptomic analysis revealed that ferroptosis was a significantly enriched pathway in both exposure models. Furthermore, experimental validation confirmed that acute TPHP exposure induced ferroptosis in HcerEpic cells, whereas chronically exposed cells exhibited ferroptosis resistance. Collectively, our findings highlight the critical role of ferroptosis dysregulation in TPHP-induced acute and chronic toxicities in HcerEpic cells, suggesting that TPHP may be a potential risk factor for CC and underscoring the need for further attention to the health risks associated with OPE exposure.

Inflammation-related disorders constitute a major global health challenge, with annual incidence exceeding tens of millions of cases and economic losses surpassing hundreds of billions USD. These burdens significantly impact both healthcare systems and socioeconomic development. Current clinical therapies are limited by suboptimal efficacy, which poses health risks to patients and underscores the demand for innovative therapeutic strategies. Emerging evidence demonstrates that extracellular vesicles (EVs) exhibit significant therapeutic advantages over conventional pharmacological interventions in managing inflammatory disorders. Native EVs possess inherent advantages including superior biocompatibility, structural integrity, and unique biological barrier penetration capacities, positioning them as promising therapeutic agents for inflammatory conditions. Engineered EVs can be functionalized with targeted delivery systems to transport bioactive components, such as miRNAs and proteins, enabling precise modulation of inflammatory signaling pathways. This approach enhances therapeutic efficacy, shortens treatment duration, reduces morbidity rates, and decreases healthcare costs. This review examines the therapeutic potential of EVs in inflammatory diseases and summarizes recent advances in their application to specific inflammatory disorders. We discuss the clinical translation challenges of EVs and highlight their prospects for inflammatory disease therapeutics.

The transition from HPV infection to cervical cancer (CC) remains unclear, especially concerning small extracellular vesicles (sEVs). We analyzed plasma-sEVs from HPV-negative individuals (HPVN-sEVs), HPV-positive individuals (HPVP-sEVs), and HPV-positive CC patients (HPVC-sEVs) via proteomics (n = 5/5/9) and transcriptomics (n = 3/3/4). Multiomics revealed HPVP-sEVs harbor antiviral and pro-inflammatory signals early in infection, whereas HPVC-sEVs shift toward immunosuppression to sustain persistent infection. Specifically, IFITM2─an antiviral gene─was markedly enriched in HPVP-sEVs versus HPVN-sEVs (P < 0.001) and HPVC-sEVs (P = 0.014). Both HPVP-sEVs (P = 0.004) and HPVC-sEVs (P < 0.001) suppressed M2 macrophages, with HPVC-sEVs further reducing IL-6 (HPVN-sEVs, P = 0.005; HPVP-sEVs, P = 0.015). Notably, IFITM2 mRNA and protein levels in plasma-sEVs distinguished HPVP from HPVC patients, showing superior diagnostic accuracy (AUC = 0.833 and 0.822, respectively) over CA-125. These findings underscore sEVs' dynamic role in HPV-driven carcinogenesis and their potential as noninvasive biomarkers for CC diagnosis.

Dibutyl phthalate (DBP), a widespread phthalate with reproductive toxicity and potential carcinogenicity, its cervical effects remain unclear. This study explored DBP's cervical toxicity and mechanisms via epidemiological analysis, network toxicology, and in vivo/in vitro models. Urinary 6 phthalate metabolites in 104 cervical cancer (CC) patients and 104 controls (detected by UPLC-MS/MS) showed elevated levels of MBP, MEHP, MEOHP, MEHHP, MECPP, and ΣDEHP in CC patients; MBP had the strongest CC risk association (adjusted OR = 2.54, P < 0.001). Network toxicology identified 9 core targets of DBP (e.g., CASP3, MAPK8/14, ESR1) and key pathways involved (TNF, MAPK, apoptosis, oxidative stress, etc.). Short-term DBP exposure (mice: 10-50 mg/kg/day; HcerEpic cells: 100-400 μM) induced cervical injury/oxidative stress, suppressed NRF2, and activated MAPK/NF-κB; N-acetylcysteine (NAC) supplementation mitigated damages. Long-term exposure to environmentally relevant DBP concentrations (10-7 M) promoted HcerEpic cell malignant transformation (e.g., enhanced proliferation, migration, invasion, epithelial-mesenchymal transition) via activation of the TGF-β/Smad2/3 and MAPK pathways, with in vivo tumorigenicity validated in nude mice. In conclusion, our findings not only elucidate the molecular mechanisms underlying DBP-induced cervical injury and malignant transformation, but also provide theoretical evidence for evaluating the health risks of phthalates (PAEs) and guiding prevention strategies for environmental pollutant-related female reproductive malignancies.

4 -NP (4-nonylphenol), a prevalent environmental endocrine disruptor with estrogenic properties, is commonly detected in drinking water and food sources. It poses a significant risk of endocrine disruption, thereby influencing the onset and progression of diverse diseases, including tumorigenesis. However, its specific impact on cervical cancer remains to be fully elucidated. Our study focused on the biological effects of sustained exposure to low -dose 4 -NP on human normal cervical epithelial cells (HcerEpic). After a continuous 30 -week exposure to 4 -NP, the treated cells exhibited a significant malignant transformation, whereas the solvent control group showed limited malignant phenotypes. Subsequent analyses of the metabolomic profiles of the transformed cells unveiled marked irregularities in glutathione metabolism and unsaturated fatty acid metabolism. Analyses of transcriptomic profiles revealed significant activation of the MAPK signaling pathway and suppression of ferroptosis processes in these cells. Furthermore, the expression of MT2A was significantly upregulated following 4 NP exposure. Knockdown of MT2A restored the aberrant activation of the MAPK signaling pathway, elevated antioxidant capacity, ferroptosis inhibition, and ultimately the development of malignant phenotypes that induced by 4 -NP in the transformed cells. Mechanistically, MT2A increased cellular antioxidant capabilities and facilitated the removal of toxic iron ions by enhancing the phosphorylation of ERK1/2 and JNK MAPK pathways. The administration of activators and inhibitors of the MAPK pathway confirmed that the MAPK pathway mediated the 4 -NP -induced suppression of ferroptosis and, ultimately, the malignant transformation of cervical epithelial cells. Overall, our findings elucidated a dynamic molecular transformation induced by prolonged exposure to 4 -NP, and delineated comprehensive biological perspectives underlying 4 -NP -induced cervical carcinogenesis. This offers novel theoretical underpinnings for the assessment of the carcinogenic risks associated with 4 -NP.

Abstract Background LncRNAs play essential roles in multiple tumors. However, research on genome-wide lncRNA alterations and their functions in cervical cancer (CC) is limited. This study aims to explore key lncRNAs in CC progression and uncover the molecular mechanisms involved in the development of CC. Methods In this study, we analyzed 30 tissues from CC, cervical intraepithelial neoplasia (CIN), and normal (NOR) using transcriptome sequencing and weighted gene co-expression network analysis to establish gene modules related to the NOR-CIN-CC transition. Machine learning diagnostic models were employed to investigate the role of lncRNAs in this transition. Molecular biological experiments were conducted to elucidate the potential mechanisms of CARMN in CC, with a particular focus on its transcriptional and post-transcriptional regulation of abnormal expression in CC. Results CARMN was identified as a hub gene in two modules significantly associated with the NOR-CIN-CC transition. Analysis using ten machine learning models confirmed its critical role in this progression. The results of RNA-seq, qPCR and RNAScope performed in another cohort of 83 cervical tissues all showed that CARMN was significantly downregulated in CC. CARMN significantly enhanced the interaction between Keap1 and Nrf2, leading to increased ROS levels. The elevated ROS levels suppressed the Akt/mTOR signaling pathway, leading to autophagy arrest via autophagic flux blockade. Additionally, CARMN interacted with TFAP2α to repress MAPK13 transcription, further inhibiting the MAPK cascade. A promoter SNP (rs12517403) was found to increase CC risk (OR = 1.34, 95% CI = 1.11–1.61) and reduce CARMN expression by decreasing SP1 binding. Furthermore, the RNA binding proteins that could modulate CARMN RNA stability were also determined using RNA-pulldown assay. The results demonstrated that YBX1, a component of the coding region instability determinant (CRD)-mediated mRNA stabilization complex, promoted CARMN RNA stability. DHX9, another component of complex, acted as a scaffold to bridge YBX1 and CARMN. Conclusions CARMN exerts an anti-cancer effect in CC progression by inhibiting the Akt-mTOR and MAPK signaling pathways. rs12517403 and the YBX1/DHX9 complex are key mechanisms influencing its transcription and stability in CC cells. CARMN represents a promising biomarker for CC diagnosis and therapeutic target.

SUMOylation, an important post-translational protein modification, plays a critical role in cancer development and immune processes. This study aimed to construct diagnostic and prognostic models for cervical cancer (CC) using SUMOylation-related genes (SRGs) and explore their implications for novel clinical therapies. We analyzed the expression profiles of SRGs in CC patients and identified 15 SRGs associated with CC occurrence. After the subsequent qPCR verification of 20 cases of cancer and adjacent tissues, 13 of the 15 SRGs were differentially expressed in cancer tissues. Additionally, we identified molecular markers associated with the prognosis and recurrence of CC patients, based on SRGs. Next, a SUMOScore, based on SRG expression patterns, was generated to stratify patients into different subgroups. The SUMOScore showed significant associations with the tumor microenvironment, immune function features, immune checkpoint expression, and immune evasion score in CC patients, highlighting the strong connection between SUMOylation factors and immune processes. In terms of immune therapy, our analysis identified specific chemotherapy drugs with higher sensitivity in the subgroups characterized by high and low SUMOScore, indicating potential treatment options. Furthermore, we conducted drug sensitivity analysis to evaluate the response of different patient subgroups to conventional chemotherapy drugs. Our findings revealed enrichment of immune-related pathways in the low-risk subgroup identified by the prognostic model. In conclusion, this study presents diagnostic and prognostic models based on SRGs, accompanied by a comprehensive index derived from SRGs expression patterns. These findings offer valuable insights for CC diagnosis, prognosis, treatment, and immune-related analysis.

Cervical cancer (CC) remains one of the most common malignancies among women worldwide, posing a serious threat to women's health. N6-methyladenosine (m6A) modification, as the most abundant type of RNA methylation modification, and has been found to play a crucial role in various cancers. Current research suggests a close association between RNA m6A modification and the occurrence and progression of CC, encompassing disruptions in m6A levels and its regulatory machinery. This review summarizes the current status of m6A modification research in CC, explores the mechanisms underlying m6A levels and regulators (methyltransferases, demethylases, reader proteins) in CC and examines the application of small-molecule inhibitors of m6A regulators in disease treatment. The findings provide new insights into the future treatment of CC.

PurposeThe abnormal regulation of lncRNA CARMN has been proved to be a tumor suppressor gene of cervical cancer (CC). However, its role in CC is still elusive. The regulation of CARMN post-transcriptional level by m(6)A modification and miRNA has not been studied. This study aims to analyze the molecular mechanism of m(6)A modification and miRNA on the abnormal expression of CARMN in CC cells, so as to provide a new theoretical basis for the diagnosis and treatment of CC.MethodsMeRIP-seq was used to identify the differential m(6)A-modified genes between tumor and normal cervical tissues. RT-qPCR assay was used to detect gene expression levels in tissues or cells. The m(6)A modification sites of CARMN was predicted by bioinformatics, and the modification of m(6)A and its regulatory effect on CARMN were analyzed by MeRIP-qPCR, Actinomycin D assay and RIP assay. RIP-microarray combined with bioinformatics methods to screen miRNAs that may target CARMN. The regulation mechanism between miRNA and CARMN was verified by RT-qPCR, nucleo-plasmic separation assay, mRNA stability assay, dual-luciferase reporter assay, and in vivo experiments.ResultsMeRIP-seq found that CARMN is a significant different gene in the abundance of m(6)A in CC, and the modification level of m(6)A in CC tissues was higher than that in normal cervical tissues. Further, this study verified that m(6)A reader YTHDF2 could recognize m(6)A-modified CARMN and promote its degradation in CC cells. miR-21-5p was proved to be the downstream target gene of CARMN, and miR-21-5p could negatively regulate the expression of CARMN. Further experiments showed that miR-21-5p could directly bind to CARMN and lead to the degradation of CARMN. The in vivo experimental results indicated that the level of miR-21-5p in the overexpressed CARMN group was significantly lower than that in the control group.Conclusionm(6)A modification and miR-21-5p play important roles in promoting the occurrence and development of tumors by regulating CARMN, provide new potential targets for the treatment of CC.

PURPOSE:To explore the function and molecular mechanism of LINC00426 in Cervical Cancer (CC), and to explore the clinical treatment strategy of LINC00426 for CC.METHODS:Bioinformatics analysis was used to explore the expression of LINC00426 and patient prognosis of CC. Cell function experiments were conducted to explore the potential effect of LINC00426 on CC malignant phenotypes. The difference in m6A modification level between the high and low expression groups of LINC00426 was analyzed by detecting the total m6A level. The luciferase reporter assay was used to confirm the binding of miR-200a-3p to LINC00426. The RIP assay was used to confirm the binding of LINC00426 to ZEB1. Cell viability assay was performed to detect the effect of LINC00426 on cellular drug resistance.RESULTS:LINC00426 is up-regulated in CC, which can enhance the proliferation, migration and invasion of CC cells. METTL3 promotes the expression of LINC00426 by m6A methylation modification. In addition, the LINC00426/miR-200a-3p/ZEB1 axis affects the proliferation, migration, and invasion of CC by regulating the expression of EMT markers. Through the detection of cell viability, we observed that overexpression LINC00426 in cells resulted in resistance to cisplatin and bleomycin, and more sensitive to imatinib.CONCLUSION:LINC00426 is a cancer-promoting lncRNA related to m6A modification. The process of EMT in CC is regulated by the LINC00426/miR-200a/3p/ZEB1 axis. LINC00426 can affect the sensitivity of CC cells to chemotherapy drugs, and is expected to become a therapeutic target for CC.

随着电离辐射在医学等领域的广泛应用,长期职业接触低剂量电离辐射对人体的远期健康影响受到越来越多的关注.通过分析国内外对低剂量电离辐射的研究成果,总结了低剂量电离辐射对人体甲状腺、免疫系统、眼晶状体、肝脏、血液系统、生殖系统等方面的影响,各研究结论虽存在差异,但低剂量电离辐射对于人体健康的影响不容忽视.应创建完善的健康监护机制,不断改进工作环境,降低放射工作人员受照剂量;放射工作人员应切实做好职业防护,严格遵守操作规程,提升自我防护意识.

Background: Pesticide poisoning is an important issue in rural China, and is also a major public health problem that affects the health of farmers. The purpose of this paper is to explore the epidemiology of pesticide poisoning in Jiangsu Province, and to put forward the relevant suggestions on the logical and discerning utilization of the pesticides. Methods: According to the data of the pesticide poisoning report card established by the health hazard detection information system, the cases of pesticide poisoning in Jiangsu Province from 2006 to 2018 were exported to Excel, and the database of pesticide poisoning was established. Furthermore, the imported data was screened and collected. A descriptive statistical analysis had been employed on this data utilizing SPSS 20.0. Results: Between the years 2006 and 2018, 38,513 pesticide poisoning cases were registered in Jiangsu Province, with a downward trend. Meanwhile, 77.83% of poisoning cases involved insecticide poisoning, followed by herbicide and rodenticide. The greater part of the diverse sorts of studied insecticide poisoning cases involved people aged between 30 and 59 years (57.51%). Poisoning cases caused by rodenticide accounted for a large proportion of people aged between 0 and 14 years (23.72%) in non-occupational pesticide poisoning. Regarding seasons, it was distinguished that more insecticide cases were reported in autumn (46.95% of the total number of cases). Pesticide poisoning was reported in 13 cities of Jiangsu Province, and among these, insecticide poisoning was reported mainly from the northern Jiangsu area, which was the same as rodenticide and herbicide. Conclusions: Although there is a decreased risk for pesticide poisoning among farmworkers in Jiangsu Province, the number of farmworkers with pesticide poisoning is still high. Further management of the pesticide utilization is necessary, especially insecticide. More attention ought to be paid to the protection of vulnerable groups, including children and the elderly.

This study was conducted to estimate the current prevalence of hypertension, cardiovascular condition and hearing difficulty of workers exposure to occupational noise, and to analyze any associations between these abnormal signs and occupational noise exposure. The subjects included 5205 noise-exposed workers. Workers with high noise exposure were more likely to have a higher threshold value than low exposure ones (P < 0.05). Subjects in the high exposure group had a significantly higher risk of hypertension and hearing loss than the ones in low exposure group. Between the ages of 30 and 45, high-level occupational noise exposure led to a significantly raising risk of both hypertension (Adjusted OR = 1.59, 95% CI, 1.19–2.11) and hearing loss (Adjusted OR = 1.28, 95% CI, 1.03–1.60) when comparing to low-level noise exposure. In male workers, the prevalence of hearing difficulty in high exposure group was approximately 1.2 times worse than in low group (P = 0.006). In addition, exposure to high noise level demonstrated a significant association with hypertension and hearing loss when the duration time to occupational noise was longer than 10 years. Hypertension and hearing difficulty is more prevalent in the noise-exposed group (higher than 85 dB[A]). Steps to reduce workplace noise levels and to improve workplace-based health are thus urgently needed.

目的 了解南京市职业接触噪声对作业工人听力损伤、心血管系统损伤的特点,更好地预防噪声对机体的损害.方法 收集2017年南京市噪声作业工人健康检查资料,包括一般情况、血尿常规、肝肾功能、心电图、内外科常规、胸部X线片、纯音听力检查等.结果 本共收集研究对象共37 667人,高频听阈损失异常者2 697人(7.16％),33 896名(89.99％)接噪工人分布于制造业中;大型企业和小型企业接触噪声工作人员较多,分别为13 567人(36.02％)和12 679人(33.66％);私有经济类型的企业中接噪人数较多,12 787人(33.95％).男性听阈损失检出率(x2 =115.11,P＜0.01);高血压检出率(x2=225.10,P＜0.01);血常规异常检出率(x2=223.55,P＜0.01);尿常规异常检出率(x2=1 888.20,P＜0.01)肝功能异常检出率(x2=668.95,P＜0.01);心电图异常检出率(x2=74.98,P＜0.01)高于女性,差异有统计学意义.高频听阈损失检出率(x2=934.18,P＜0.01)、高血压检出率(x2=2 019.10,P＜0.01)随年龄的增大而增高.高频听阈损失检出率(x2=102.95,P＜0.01)及高血压检出率(x2 =828.05,P＜0.01)随接噪工龄增长而增加.交通运输业和建筑业中工人各体检指标异常检出率均较高.结论 噪声对作业工人健康影响较大,除了特异性听力损失方面,还有包括非特异性心血管、代谢等多方面影响,因此有必要对噪声作业企业及劳动者采取有效防范措施.

[目的]了解南京市铅作业工人的血铅水平,保护工人健康.[方法]收集南京市全市职业健康检查机构2016年1月1日至12月31日参加在岗期间职业健康检查的1 097名铅作业工人的职业史以及血铅检查结果,并按照企业规模、经济类型、所在地区和行业进行分类比较.[结果]研究对象年龄17.0～60.0(32.8±9.3)岁,工龄0.6～40.0(10.3±9.0)年.作业工人的血铅水平M(P25,P75)为33.0(18.0,50.0)μg/L,血铅超标检出率1.82％.未见慢性铅中毒患者.血铅＞100 μg/L占9.0％.血铅水平与年龄、工龄呈弱的正相关关系(r年龄=0.25,r 工龄=0.12,P＜0.05).男性铅作业工人的血铅水平高于女性,差异有统计学意义(P＜0.01).专用设备制造业、化学原料和化学品制造业血铅水平均高于其余8个行业,六合区的铅作业工人血铅水平高于其余4个区,以上差异均有统计学意义(P＜0.05).微型、小型、中型、大型企业工人血铅水平依次下降,私营、外商投资、国有企业工人血铅水平也依次下降,以上两两差异均有统计学意义(P＜0.05).[结论]南京市铅作业工人血铅水平高于普通人群.要特别重视化学原料和化学品制造业、专用设备制造业、微型和小型企业以及私营企业铅作业工人的铅危害防控.

Objectives This study investigated the hearing loss characteristics among occupational noise exposure workers with hypertension and the link between hypertension and hearing loss when exposed to occupational noise. Methods A total of 267,766 occupational noise-exposed workers were enrolled, including 29,868 workers with hypertension and 240,165 without hypertension. Hypertension was diagnosed according to WHO criteria. Hypertension was classified into four grades based on blood pressure. Assessment of hearing was performed through measurement of an unadulterated tone threshold at different frequencies, which ranged between 250 and 8,000 Hz. Results A substantial link was observed to exist between hypertension and the increment in the hearing limit. The increase in the hearing threshold was substantially higher among those having grade 2 hypertension. Conclusion The current investigation suggested patients with hypertension exhibit a substantial rise in hearing loss in comparison with patients without hypertension. The rise in hearing loss was significant in patients with grade 2 hypertension. Efficient and practicable measures are required to decrease the hearing loss in workers with hypertension and work-related noise exposure.

采用电感耦合等离子体质谱分析法(ICP-MS)测定血浆中钒(v)、铬(Cr)、锰(Mn)、铁(Fe)、钻(Co)、镍(Ni)、铜(Cu)、锌(Zn)、砷(As)、硒(Se)、铷(Rb)等34种元素.探索简便、实用、高效的检测血液样品的前处理技术.采用直接稀释法对待测样本进行前处理,稀释液(0.5％ HNO3+0.005％ Triton X-100)稀释倍数为20倍.对ICP-MS测定血浆微量元素进行方法学验证,算出该检测方法的线性范围、检出限、加标回收率、日间精密度与日内精密度等.各元素的相关系数均优于0.999,元素的低、中、高加标回收率为70.0％ ～ 115.0％,各元素的日内精密度优于10％,日间精密度均优于20％.提示,采用ICP-MS法测定血浆中多种元素含量,此法实用高效,精密度、准确度、线性范围和最低检测限都达到了满意结果,可在科研及检验工作中加以应用.