Urinary cadmium and peripheral blood telomere length predict the risk of renal function impairment: a study of 547 community residents of Shanxi, China.

Few reports have investigated the predictive value of urinary cadmium (UCd) and telomere length on renal function impairment. Therefore, we constructed nomogram models, using a cross-sectional survey to analyze the potential function of UCd and telomere length in renal function impairment risk. We randomly selected two community populations in Shanxi, China, and general information of the subjects was collected through face-to-face questionnaire surveys. Venous blood of subjects was collected to detect absolute telomere length (ATL) by real-time quantitative chain reaction (RT-PCR). Collecting urinary samples detected UCd and urinary N-acetyl-ß-d-glucosaminidase (UNAG). Estimated glomerular filtration rate (eGFR) was obtained based on serum creatinine (SCr). Nomogram models on risk prediction analysis of renal function impairment was constructed. After adjusting for other confounding factors, UCd (ß = 0.853, 95% confidence interval (CI): 0.739 ~ 0.986) and ATL (ß = 1.803, 95%CI: 1.017 ~ 1.154) were independent risk influencing factors for increased UNAG levels, and the risk factors for eGFR reduction were UCd (ß = 1.011, 95%CI: 1.187 ~ 1.471), age (ß = 1.630, 95%CI: 1.303 ~ 2.038), and sex (ß = 0.181, 95%CI: 0.105 ~ 0.310). Using UCd, ATL, sex, and age to construct the nomogram, and the C-statistics 0.584 (95%CI: 0.536 ~ 0.632) and 0.816 (95%CI: 0.781 ~ 0.851) were obtained by internal verification of the calibration curve, C-statistics revealed nomogram model validation was good and using decision curve analysis (DCA) confirmed a good predictive value of the nomogram models. In a nomogram model, ATL, UCd, sex, and age were detected as independent risk factors for renal function impairment, with UCd being the strongest predictor.

Association of sleep quality with job burnout among Chinese coal mine staff: a propensity score weighting analysis.

This study examines the association of sleep quality with job burnout among Chinese coal mine staff. 3832 subjects were selected from a coal mine group located in Shanxi Province in China. Job burnout was evaluated by the Maslach Burnout Inventory-General Survey and sleep quality was acquired with a self-reported questionnaire. We used the inverse probability of treatment weighting with propensity score to mimic the randomization and to minimize bias in estimations. Sensitivity analysis was conducted to test the robustness of our findings. We identified that good sleep quality was significantly associated with lower risk of job burnout (OR: 0.70; 95%CI, 0.60 to 0.82, p = 6.02e-06), with 0.21 decrease in the score of exhaustion (95%CI,-0.29 to -0.12, p = 5.00e-06), and with 0.13 decrease in the score of cynicism (95%CI,-0.21 to -0.04, p = 3.73e-03). Sensitivity analysis demonstrated that the results were robust to the choice of estimation models, as well as unmeasured confounding. Stratification analysis demonstrated that the associations of sleep quality with job burnout were largely heterogeneous for male and female workers. This study implicated that good sleep quality benefits the workers in relief of job burnout. Further research may be warranted in support of a definite causal relationship and intervention strategy.

Plasma Homocysteine Levels Predict the Risk of Acute Cerebral Infarction in Patients with Carotid Artery Lesions.

This study examined the association between elevated plasma homocysteine (Hcy) levels and the risk of acute cerebral infarction in patients with carotid artery lesions. A total of 78 patients were divided into two groups, the high Hcy group (n = 38; Hcy levels >15 umol/L) and the low Hcy group (n = 40; Hcy levels ≤15 umol/L). High-resolution B-mode ultrasounds were performed to assess intima media thickness (IMT), infarcts, plaques, and stenosis in the extracranial carotid artery of these patients. All patients underwent 3 T MR scanners to evaluate cerebral artery stenosis in the intracranial cerebral artery. The plasma Hcy levels did not show any statistically significant differences when comparisons were based on gender, age, blood pressure, diabetes, hyperlipidemia, and systolic and diastolic pressures. Importantly, the incidence of carotid plaque and severe stenosis of intracranial and extracranial artery were significantly higher in the high Hcy group compared to the low Hcy group. Pearson's test indicated that plasma Hcy levels positively correlated with IMT, total number of plaques and unstable plaques. Overall, the elevated plasma Hcy levels correlated with increased frequency of carotid plaque formation, extra- and intracranial arterial stenosis, and the degree of stenosis. In conclusion, we find a significant correlation between elevated plasma Hcy levels and the increased incidence of acute cerebral infarction in patients with carotid artery lesions.

[Risk assessment of nerve conduction velocity in workers exposed to lead].

OBJECTIVE: To explore the dose-effect relationship between lead exposure and nerve conduction velocity, and to assess risk characteristics of nerve conduction velocity induced by lead exposure. METHODS: The external dose, internal dose (blood lead, urine lead) and the conduction velocity of peripheral nerve were examined. The benchmark dose of a population exposed to occupational lead was estimated to develop risk assessment of nerve conduction velocity in worker exposed to lead by use of BMDS (version 1.3.3). The BMDL in terms of blood lead and urine lead was calculated. RESULTS: There was correlation between blood lead and urine lead. The sense nerve conduction velocity was decreased significantly in the group of lead exposure workers (P < 0.05). The BMDLs-05 for median nerve conduct velocity, ulnar nerve conduction velocity, and superficial peroneal nerve conduction velocity in terms of blood lead were 456.99, 332.36 and 468.38 microg/L respectively; the BMDLs-05 in terms of urine lead were 14.1, 9.2 and 13.6 microg/gCr respectively. CONCLUSION: The internal dose is the better index to reflect the level of lead exposure. Blood lead is identified as a specific and sensitive biomarker for sense nerve conduction velocity reduction. Ulnar nerve conduction velocity can be used as highly sensitive biomarkers to screen the high risk population of lead exposure.

[Risk assessment of renal dysfunction caused by occupational lead exposure].

OBJECTIVE: To assess the risk of renal dysfunction caused by occupational lead exposure through epidemiological investigation. METHODS: The workers in a battery factory were selected as the subjects for the exposure and effect assessment. The occupational environmental monitoring data was collected and used to calculate the total external dose of lead. The relationship between external dose and internal dose of lead was analyzed. The external dose, blood lead (BPb) and urinary lead (UPb) were used as exposure biomarkers while the urinary N-acetyl-D-glucosaminidase (UNAG), and urinary albumin (UALB) were used as the effect biomarkers for the renal dysfunction caused by lead. Software of BMDS (BMDS 11311) was used to calculate BMD. RESULTS: The external and internal does of lead was positively correlated (BPb: r = 0.466, P < 0.01; UPb: r = 0.383, P < 0.01). The levels of BPb, UPb in exposure group (654.03 microg/L, 143.45 microg/g Cr) were significantly higher than those in the control group (57.12 microg/L, 7.20 microg/g Cr), so were UALB, UNAG; in addition, all of them presented significant dose-response relationship. The BPb BMD of UALB, UNAG were 607.76, 362.56 microg/L respectively and the UPb BMD of UALB, UNAG were 117.79, 78.79 microg/gCr respectively. CONCLUSION: Occupational lead exposure can cause renal dysfunction, which presents dose-response relationship; the risk assessment of renal dysfunction caused by occupational lead exposure is performed by BMD calculation of BPb and UPb.

Insulin expression in rats exposed to cadmium.

OBJECTIVES: To investigate the effects of cadmium exposure on insulin expression in rats. METHODS: Eighteen adult SD rats were administered cadmium subcutaneously (0.5, 1.0, and 2.0 mg/kg x bw). The effects on endocrine of pancreas were assessed. The levels of cadmium and zinc in pancreas, blood and urine glucose, serum insulin and urine NAG (N-acyetyl-beta-glucosaminidase) were determined. The gene expressions of metallothionein (MT) and insulin were also measured, and the oral glucose tolerance tests (OGTT) were carried out. RESULTS: The contents of cadmium in pancreas in cadmium-treated rats were higher than that in the control group, which was associated with slight increase of zinc in pancreas. Cadmium-exposed rats (1.0 and 2.0 mg/kg x bw) demonstrated a marked glucose intolerance. But the levels of serum insulin did not change significantly after cadmium administration, and the UNAG had no change in Cd-treated group. The gene expression of insulin decreased in 1.0 and 2.0 mg/kg x bw cadmium-exposed groups, compared with the control group. The expression of MT-I was higher in the groups exposed to 1.0 and 2.0 mg/kg x bw cadmium while the expression of MT-II was higher in the group exposed to 2.0 mg/kg x bw cadmium. CONCLUSIONS: Cadmium may be accumulated in the pancreas, resulting in the change of the expression of insulin, MT-I and MT-II genes. Cadmium can influence the biosynthesis of insulin, but does not induce the release of insulin. The dysfunction of pancreas occurs earlier than that of kidney after administration of cadmium.

[Effects of occupational lead exposure on bone mineral density and bone metabolism in workers].

OBJECTIVE: To investigate the effects of occupational lead exposure on the bone mineral density and the bone metabolism in exposed workers. METHODS: Two hundred and ninety-eight lead-exposed workers in a storage battery plant in Shanghai were selected as the exposed subjects while eighty-one healthy officers in the plant who were not occupationally exposed to lead were treated as the control. The blood lead (BPb) and the urinary lead (UPb) were used as the exposure biomarkers while the Z score, the urinary hydroxyproline (HYP) the serum alkaline phosphatase (ALP) the serum alkaline phosphatase bone isoenzyme BALP and the serum osteocalcin BGP were used as the effect biomarkers for the bone effect caused by the lead. Bone mineral density (BMD) was measured by the single-photon absorptiometry (SPA-4). RESULTS: The BPb, UPb, HYP, ALP, BALP in the occupational lead exposure group were higher than those in the control group with significantly statistical difference in male (P < 0.01). The levels of BGP in the exposure group was higher than that in the control group without significantly statistical difference (P > 0.05). The BMD in the exposure group was lower than that in the control group without significantly statistical difference (P > 0.05). The BMD was significantly decreased in the groups of the UPb 10 approximately microg/g Cr level compared with the 0 approximately microg/g Cr group with the significant difference (P < 0.01). In males, the BMD was significantly decreased in the group of the BPb 300 approximately microg/L level compared with the 0 approximately microg/L group with the significant difference (P < 0.01). The levels of HYP, ALP, BALP, BGP in the UPb 20 approximately microg/g Cr group were significantly higher than those in the UPb 0 approximately microg/g Cr group (P < 0.05). The levels of HYP, ALP, BALP, BGP in the BPb 300 approximately microg/L group were significantly higher than those in the BPb 0 approximately microg/L group (P < 0.05). The prevalence of both osteoporosis and the abnormal bone metabolisms indexes would increase significantly with the increase of the lead exposure (P < 0.01) with the linear correlation (P < 0.01). But the prevalence of higher BGP had no significant correlation with UPb (P > 0.05). BMDs were calculated using BMDS Version 1.3.2 software and BMDLs were also determined. The BMDLs of BPb and UPb for lead-induced osteoporosis were higher than those representing the change of bone metabolism induced by lead. CONCLUSIONS: The occupational exposure to lead could cause the decrease of the bone mineral density, lead to the osteoporosis, and may affect the bone metabolism.

Estimation of benchmark dose for pancreatic damage in cadmium-exposed smelters.

The aim of this study was to estimate the benchmark dose (BMD) for pancreas dysfunction caused by cadmium (Cd) exposure in smelters. Smelter workers who had been exposed to Cd for more than 1 year and matching nonoccupationally exposed subjects were asked to participate in this study. Urinary cadmium (UCd) was used as a biomarker for exposure, serum insulin and amylase were used as biomarkers for pancreatic effects. In this study, serum insulin and amylase were lower in the smelter workers than in the nonoccupationally exposed subjects. A significant dose-response relationship with UCd was displayed. BMDs in terms of urinary Cd corrected for creatinine were calculated by use of BMDS (version 1.3.2). The benchmark dose lower limit of a one-sided 95% confidence interval (BMDL) for 10% excess risk was also determined. It was found that the BMDL10 for serum insulin and serum amylase was 3.7 and 5.3 microg/g Cr, respectively. Compared to the BMDL for renal damage caused by Cd exposure, identified by the effect biomarkers urinary beta2-microglobulin, urinary N-acetyl-beta-glucosaminidase, and urinary albumin (UALB), it was shown that BMDL10 for serum insulin is the lowest among all values and UALB gave the highest value (5.8 microg/g Cr). This study indicates that Cd exposure can result in pancreatic dysfunction and the effect appears at lower urinary Cd level than renal dysfunction. The endocrine function of the pancreas was affected at lower urinary levels of Cd, compared to the exocrine function, which was seen at higher urinary levels of Cd than those giving rise to renal tubular dysfunction.

[Effects of occupational lead exposure on lumbar vertebral fracture in male workers.].

OBJECTIVE: To investigate the effects of occupational lead exposure on lumbar vertebral fracture in exposed male workers. METHODS: One hundred and fifty-two lead-exposed male workers in a storage battery plant in Shanghai were selected as the study population. The blood lead (BPb) and the urinary lead (UPb) were measured by graphite-furnace atomic absorption spectrometry (GF-AAS). Bone mineral density (BMD) was measured by the monophoton absorptiometry(SPA-4) and Z score was determined. Anteroposterior and lateral lumbar spinal X-ray films were taken to determine lumbar vertebral fracture. RESULTS: For the occupationally lead-exposed workers, geometric mean of BPb was 0.85 (0.33 approximately 1.90) micromol/L, geometric mean of UPb was 4.84 (0.46 approximately 21.31) microg/g Cr, and the prevalence of lumbar vertebral fracture was 19.7%. The prevalence of lumbar vertebral fracture would increase with the increase of age and work year, but with no significantly statistical difference (P > 0.05). The bone mineral density (BMD) would decrease with the increase of BPb and UPb (P < 0.05). The prevalence of lumbar vertebral fracture would increase significantly with the increase of the lead exposure (P < 0.05) with the linear correlation (P < 0.05). The prevalence of lumbar vertebral fracture would increase significantly with the decrease of the bone mass (P < 0.01) with the linear correlation (P < 0.01). CONCLUSION: The occupational exposure to lead could cause the decrease of the bone mineral density and the increase of the prevalence of lumbar vertebral fracture. The development of lumbar vertebral fracture is associated with the decrease of bone mass.

[The effects of cadmium on the levels of insulin in smelters].

OBJECTIVE: To investigate the effects of cadmium on the levels of insulin and blood glucose in exposed workers. METHODS: Ninety-eight cadmium-exposed workers in a smeltery in the mid-south district of our country were selected as the exposed subjects while the healthy doctors in the workers hospital who were not exposed to the cadmium were treated as the control. The subjects were grouped according to the exposure time, the blood cadmium and the urine cadmium. The variety of the level of serum insulin was investigated for the workers in different groups of the exposure time, the blood cadmium and the urine cadmium. The variety of the levels of the blood zinc and urine zinc were also determined. The relationships among the blood cadmium, the blood zinc and the serum insulin were analyzed. RESULTS: The level of blood glucose in the group of the exposure time of more than 20 years [(4.9 +/- 0.6) mmol/L] was significantly higher than that in the control group [(4.6 +/- 0.60) mmol/L] with significantly statistical difference (P < 0.01). The level of serum insulin in the group of the exposure time of more than 10 years [(8.58 +/- 4.91) microIU/ml] was significantly lower than that in the control group [(11.57 +/- 5.42) microIU] with the significantly statistical difference (P < 0.05) and the level of serum insulin would be decreased significantly with the increase of the blood cadmium and urinary cadmium. The level of the urine zinc was increased significantly in the workers of the exposure time of more than 20 years. The correlation analysis indicated that the negative correlation was found between the level of serum insulin and the level of blood cadmium, as well as between the level of the serum insulin and the level of the urinary cadmium; the positive correlation was found between the level of blood glucose and the level of insulin, as well as between the level of blood glucose and the level of C peptide in serum. CONCLUSION: The exposure to cadmium can cause the decrease of serum insulin and may affect the level of blood glucose.

[Relationship between plasma anti-metallothionein antibody and renal dysfunction in cadmium exposed workers].

OBJECTIVE: To investigate whether renal dysfunction induced by cadmium is related to plasma anti-metallothionein antibody (anti-MT Ab) in workers occupationally exposed to cadmium. METHODS: The male workers in a smeltery were selected as the subjects for the exposure and effect assessment. The urine cadmium (UCd), the blood cadmium (BCd) and the occupational cadmium intake (TTCd) served as the exposure indexes while the urine beta(2) microglobulin (Ubeta(2)-MG), the N-acetyl-beta-D-glucosaminidase (UNAG) and the urine albumin concentration (UALB) served as the effect markers for the renal dysfunction caused by the cadmium. The titer of the plasma anti-metallothionein antibody was determined with the enzyme linked immunosorbent assay (ELISA). RESULTS: The UCd (3.16 microg/g Cr), BCd (9.28 microg/L), Ubeta(2)-MG (81.17 microg/g Cr) and UALB (7.03 mg/g Cr) in the occupational cadmium exposure group were significantly higher than those in the control group and the Ubeta(2)-MG, UNAG and UALB as well as the occurrence rate of abnormality would be increased with the increase of the level of the occupational cadmium exposure. There was no significant difference in the titer of anti-MT Ab between the exposure group and the control group (P > 0.05). The titer of the anti-MT Ab would not be increased with the increase of the dosage of the exposure and had no significant correlation with BCd, UCd and TTCd (P > 0.05). The positive correlation were found between anti-MT Ab and UNAG as well as between anti-MT Ab and Ubeta(2)-MG in the exposure group with the correlation coefficient of 0.302 and 0.218 respectively. The workers with high level anti-MT Ab are more susceptible to cadmium nephrotoxicity than those with low anti-MT Ab with the odds ratio (OR) value of 4.200 and the 95% CI between 1.213 and 14.541 (P < 0.05). CONCLUSION: There is a dose-effect relationship between cadmium exposure and renal dysfunction in workers occupationally exposed to cadmium, but no correlation is found between cadmium exposure and plasma anti-MT Ab. The workers occupationally exposed to the cadmium with higher level of anti-MT Ab are easier to suffer from renal dysfunction caused by cadmium. Plasma anti-MT Ab could be used as a biomarker of susceptibility in the workers exposed to cadmium.

[Application of metallothionein gene isoforms expression as biomarkers in cadmium exposure].

OBJECTIVE: To investigate the feasibility of metallothionein (MT) gene expression level in human peripheral blood lymphocytes (HPBLs) as a biomarker in cadmium exposure. METHODS: The MT gene expression level in HPBLs of workers exposed to cadmium was examined using RT-PCR technique, and the exposure assessment and effect assessment were conducted in exposed workers. RESULTS: The basal MT-1A, IE, IF, IX and MT-2A expression level in workers exposed to cadmium were significantly higher than those in the control group (P < 0.05). The basal MT-1A, IE, IF, IX and MT-2A expression level would be significantly increased with the increase of the blood cadmium (BCd) level (P < 0.05). There was a trend of increase for the mRNA expression of the basal MT-1A, 1E, IF, IX, MT-2A, especially for the mRNA expression of MT-1A and MT-2A (P < 0.05) with the increase of the level of the urine cadmium (UCd). There was a good dose-response relationship between basal MT-1A expression and UCd. The basal MT-1A, IE, IF, IX and MT-2A expression level were significantly correlated with BCd (P < 0.05) while the basal MT-1A, IF and MT-2A expression level were significantly correlated with UCd (P < 0.05). There were dose-effect relationships of BCd to the basal MT-1E, MT-1F, MT-1X and MT-2X expression level respectively and there were also dose-effect relationships of UCd, beta(2)-MG and the urine metallothionein to the basal MT-1A expression. CONCLUSION: The expression of the MT gene isoforms in HPBLs can serve as the biomarker for the cadmium exposure and MT-1A can also serve as the effective biomarkers for the cadmium-induced renal toxicity.

[Effects of cadmium on levels of insulin in rats].

OBJECTIVE: To explore the effect of cadmium on insulin in rats. METHODS: 96 of SD rats were administered with cadmium at different doses (0, 50, 100, 200 mg/L) by drinking water for 30 days, 60 days, and 90 days. The levels of insulin, the contents of cadmium in the blood, urine, and tissues (liver, kidney, and pancreas) were determined. RESULTS: The level of insulin were decreased in the groups of 100 and 200 mg/L at the 30-day and in the group of 100 mg/L at the 60-day. Cadmium in blood and tissues (liver, kidney, and pancreas) were higher in exposed groups than those in control group. But the contents of cadmium in pancreas are lower than that in kidney and liver. CONCLUSION: It is suggested that cadmium could be accumulated in pancreas. Then it maybe related to the change of the levels of insulin in serum.

[The toxic effects of cadmium on pancreas.].

OBJECTIVE: In order to explore the toxic effects of cadmium on functions of endocrine and exocrine of pancreas. METHODS: 96 SD rats were administered with cadmium at different doses (0, 50, 100, 200 mg/L) by drinking water for 30 days, 60 days and 90 days. The contents of cadmium and zinc in the blood and pancreas, also the glucose level in blood and urine, the levels of insulin and the activity of amylase were determined. The gene expression of metallothionein (MT), insulin and pancreatic amylase were also measured. RESULTS: The results showed that the contents of cadmium in the serum and pancreas were higher than that of the control groups (P < 0.05). The contents of zinc in serum were decreased in the groups of 100 and 200 mg/L cadmium at the 90-day. As well as increased zinc in pancreas. The gene expression of insulin was not different compared with those of the control group except the middle-dose group at the 60-day. And the expression of amylase were higher in the groups of 100 and 200 mg/L cadmium at the 60-day and the 90-day. The expression of MT-1 and -2 were higher in the pancreas after cadmium administration. CONCLUSION: It is suggested that cadmium could be accumulated in the pancreas and caused the change of the zinc levels. Then it resulted in the change of the expression of gene and protein, and influence of the functions of both endocrine and exocrine in pancreas.