Rat kidney mitochondrial damage induced by acute cadmium administration / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To evaluate effect of acute cadmium administration on mitochondria from rat kidney.</p><p><b>METHODS</b>24 male Sprague-Dawley (SD) rats were randomly divided into four groups. Four groups of rats were injected with saline, 0.6, 1.2, and 1.8 mg/kg weight subcutaneously, once daily, for 5 days, respectively. Ultrastructural change of rat kidney mitochondria was observed, and respiration function, membrane potential, mitochondria swelling, and superoxide level were determined.</p><p><b>RESULTS</b>Ultrastructural changes included matrix vacuolation, swelling and condensation of mitochondria. In group of 1.8 mg/kg body weight, the oxygen consumption rate during state 3 respiration [(6.25 +/- 0.61) nmol/L O2 x min(-1) x mg(-1)] and RCR value (2.45 +/- 0.23) were significantly lower than those of control group [(9.66 +/- 1.16) nmol/L O2 x min(-1) x mg(-1)] (P < 0.05), indicating respiration inhibition. The membrane potential and superoxide level of the same group were 85.89% +/- 3.82% and 116.33% +/- 3.06% of control values (P < 0.05), respectively.</p><p><b>CONCLUSIONS</b>Acute cadmium administration can cause rat kidney mitochondrial damage in a dose-effect manner, including inhibition of respiration, dissipation of membrane potential, swelling of mitochondria matrix. Such damage might be related to the increase of mitochondrial free radical.</p>

Risk assessment of nerve conduction velocity in workers exposed to lead / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>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.</p><p><b>METHODS</b>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.</p><p><b>RESULTS</b>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.</p><p><b>CONCLUSION</b>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.</p>

Risk assessment of renal dysfunction caused by occupational lead exposure / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To assess the risk of renal dysfunction caused by occupational lead exposure through epidemiological investigation.</p><p><b>METHODS</b>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.</p><p><b>RESULTS</b>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.</p><p><b>CONCLUSION</b>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.</p>

Influencing factors of pulmonary dysfunction in coal worker's pneumoconiosis / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To investigate the possible influencing factors of pulmonary dysfunction in coal worker's pneumoconiosis (CWP).</p><p><b>METHODS</b>A total of 141 patients with CWP and 200 control miners with similar exposure histories but without apparent pulmonary disease or inflammation were interviewed with the detailed questionnaires (including histories of coal dust-exposure, smoking habits, alcohol consumption, protective mask uses, et al). Lung function examinations were performed at the same time. Predicted formula of lung function index were established by the local healthy residents characters and the pulmonary dysfunction was classified by the ratios between tested and predicted values.</p><p><b>RESULTS</b>All parameters of lung function were significantly lower in CWP cases when compared with that of control miners and the healthy controls (P < 0.05). The main types of pulmonary dysfunction were restrictive and mixed ventilation disorders in CWP patients. The factors such as the category of CWP, the mask worn, the smoking quantity and exposure to coal mine dust were included in the unconditional logistic regression model.</p><p><b>CONCLUSIONS</b>The category of CWP, the usage of mask, the smoking and long duration exposure to coal mine dust may be the main possible influencing factors of pulmonary dysfunction of CWP. Influencing factor analyses were given to inform choice of pertinence preventive measures.</p>

Insulin expression in rats exposed to cadmium / 生物医学与环境科学（英文）

<p><b>OBJECTIVES</b>To investigate the effects of cadmium exposure on insulin expression in rats.</p><p><b>METHODS</b>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.</p><p><b>RESULTS</b>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.</p><p><b>CONCLUSIONS</b>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.</p>

Application of benchmark dose (BMD) in estimating biological exposure limit (BEL) to cadmium / 生物医学与环境科学（英文）

<p><b>OBJECTIVE</b>To estimate the biological exposure limit (BEL) using benchmark dose (BMD) based on two sets of data from occupational epidemiology.</p><p><b>METHODS</b>Cadmium-exposed workers were selected from a cadmium smelting factory and a zinc product factory. Doctors, nurses or shop assistants living in the same area served as a control group. Urinary cadmium (UCd) was used as an exposure biomarker and urinary beta2-microgloburin (B2M), N-acetyl-13-D-glucosaminidase (NAG) and albumin (ALB) as effect biomarkers. All urine parameters were adjusted by urinary creatinine. Software of BMDS (Version 1.3.2, EPA.U.S.A) was used to calculate BMD.</p><p><b>RESULTS</b>The cut-off point (abnormal values) was determined based on the upper limit of 95% of effect biomarkers in control group. There was a significant dose response relationship between the effect biomarkers (urinary B2M, NAG; and ALB) and exposure biomarker (UCd). BEL value was 5 microg/g creatinine for UB2M as an effect biomarker, consistent with the recommendation of WHO. BEL could be estimated by using the method of BMD. BEL value was 3 microg/g creatinine for UNAG as an effect biomarker. The more sensitive the used biomarker is, the more occupational population will be protected.</p><p><b>CONCLUSION</b>BMD can be used in estimating the biological exposure limit (BEL). UNAG is a sensitive biomarker for estimating BEL after cadmium exposure.</p>

Effects of cadmium on zinc metabolism and its functions in rats / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To explore the effects of cadmium on zinc metabolism and its function and the protective effects of pre-supplement zinc to it.</p><p><b>METHODS</b>NS or different doses of CdCl(2) were injected to pregnant dams intraperitoneally at the 7th, 10th and 13th day of gestation respectively. At the 21st pregnant day embryos were taken out from the pregnant rats. Another rats of pre-supplement zinc or no pre-supplement zinc group were injected different doses of CdCl(2) or NS intraperitoneally after 6 days. After 24 hours the rats were killed. The contents of Cd, Zn and relative biomarkers of effect of liver, brain or serum were detected in both embryos and adult rats.</p><p><b>RESULTS</b>Compared with control group, the contents of T-AOC and Ach were significantly reduced in the Cd treatment group in the embryonic brains, the activity of AKP in the embryonic liver tissues was decreased, and The Cd content was increased significantly in embryonic liver and was negatively correlated with the Zinc content in the embryonic brain. There were no differences in the activities of SOD and AKP and the contents of Cd and MDA between pre-supplement Zn control group and no supplement Zn control group, but higher content of Zn in liver and serum in the former. Compared with no supplement Zn control group, there were higher contents of Cd in liver and serum, Zn and MDA in liver, lower activities of SOD in liver and AKP in liver and serum, and lower content of Zn in serum in the Cd treatment groups. Pre-supplement Zn significantly increase the content of Zn and the activities of SOD in liver and AKP in serum, decrease the content of MDA in liver and Cd in serum resulted by Cd treatment only. The content of Zn and the activity of AKP in serum and the activities of SOD and AKP in liver were negatively correlated with the content of Cd in corresponding tissue significantly.</p><p><b>CONCLUSION</b>Cadmium can enter embryo and enter brain by permeating the brain-blood barrier during the embryonic period. The decrease of AKP activity, some neural transmitter and capacity of anti-lipid peroxidation that are related with Zn in embryos are caused when the pregnant rats are administered with cadmium. Cd can inhibits the activities of AKP and SOD in liver, and the activity of AKP in serum respectively, and increase the content of MDA in liver dose-dependently. The effects induced by cadmium are related with zinc abnormal distribution. Pre-supplement zinc to rats can antagonize these effects in different degree.</p>

Effects of occupational lead exposure on bone mineral density and bone metabolism in workers / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To investigate the effects of occupational lead exposure on the bone mineral density and the bone metabolism in exposed workers.</p><p><b>METHODS</b>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).</p><p><b>RESULTS</b>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.</p><p><b>CONCLUSIONS</b>The occupational exposure to lead could cause the decrease of the bone mineral density, lead to the osteoporosis, and may affect the bone metabolism.</p>

Effects of occupational lead exposure on lumbar vertebral fracture in male workers / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To investigate the effects of occupational lead exposure on lumbar vertebral fracture in exposed male workers.</p><p><b>METHODS</b>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.</p><p><b>RESULTS</b>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).</p><p><b>CONCLUSION</b>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.</p>

DNA damage and oncogenic protein expression induced by cadmium / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To explore the DNA damage and the expression of oncogenic protein induced by cadmium in vitro (human cells) and in vivo in rats.</p><p><b>METHODS</b>The colony formation assay and the MTT assay were employed to determine the cytotoxicity of cadmium. The DNA damage and the cell cycle were measured by the comet assay and the flow cytometry, respectively. The western bolt and the X-Gal staining were also used to determine the change of oncogenic protein and the senescent marker.</p><p><b>RESULTS</b>The cadmium inhibited the proliferation of cells and induced DNA damage significantly not only in human cultured cells but also in vivo animal cells. The comet rate increased from 6.1% in the control group to 23.2% in 200 microM cadmium treatment group (P < 0.01). The comet rate increased in all organs of male rats with the increase of dosage, and there were significant difference between treatment the groups and the control group in kidney and ventral prostate (P < 0.05). Furthermore, the cadmium blocked the cell cycle progression. At the same time, the expression of c-myc, c-Jun and beta-Gal were increased by cadmium.</p><p><b>CONCLUSION</b>The cadmium could induce DNA damage and block the cell cycle, and further cause senescence, and death. However, the cadmium induced the DNA damage and the oncogenic protein expression may be the important factors to cause cancer.</p>

Inhibitory effect of isoflavones on prostate cancer cells and PTEN gene / 生物医学与环境科学（英文）

<p><b>OBJECTIVE</b>To explore the mechanisms by which genistein and daidzein inhibit the growth of prostate cancer cells.</p><p><b>METHODS</b>LNCaP and PC-3 cells were exposed to genistein and daidzein and cell viability was determined by MTT assay and cytotoxicity of the drugs by LDH test. Flow cytometry (FCM) was used to assess the cell cycle in LNCaP and PC-3 cells. Reverse transcription-polymerase chain reaction (RT-PCR) was applied to examine the expression of PTEN gene (a tumor suppressor gene), estrogen receptor alpha gene (ERalpha), estrogen receptor beta gene (ERbeta), androgen receptor gene (AR) and vascular endothelial growth factor gene (VEGF).</p><p><b>RESULTS</b>The viability of PC-3 and LNCaP cells decreased with increasing concentrations and exposure time of genistein and daidzein. Genistein increased G2/M phase cells in PC-3 cells while decreased S phase cells in LNCaP cells in a dose-dependent manner. Daidzein exerted no influence on the cell cycle of LNCaP and PC-3 cells, but the apoptosis percentage of LNCaP cells was elevated significantly by daidzein. Genistein induced the expression of PTEN gene in PC-3 and LNCaP cells. Daidzein induced the expression of PTEN gene in LNCaP but not in PC-3 cells. The expression of VEGF, ERalpha and ERbeta genes decreased and AR gene was not expressed after incubation with genistein and daidzein in PC-3 cells. In LNCaP cells, the expression of VEGF and AR gene decreased but there was no change in the expression of ERalpha and ERbeta gene after incubation with genistein and daidzein. Conclusion Genistein and daidzein exert a time- and dose-dependent inhibitory effect on PC-3 and LNCaP cells. The down-regulation of ER gene by daidzein influences the growth of PC-3 cells directly. The inhibition of PC-3 cells by genistein and that of LNCaP cells by genistein and daidzein may be via Akt pathway that is repressed by PTEN gene, which subsequently down-regulates the expression of AR and VEGF genes. Our results suggest that the expression of PTEN gene plays a key role and several pathways may be involved in the suppression of prostate cancer cells by genistein and daidzein.</p>

Metallothionein 1 isoform gene expression induced by cadmium in human peripheral blood lymphocytes / 生物医学与环境科学（英文）

<p><b>OBJECTIVE</b>To study the gene expression of metallothionein 1 (MT-1) isoforms in human peripheral blood lymphocytes (HPBLs).</p><p><b>METHODS</b>The expression of mRNA representing the seven active MT-1 genes was determined in HPBLs by quantitative RT-PCR before and after exposure to cadmium.</p><p><b>RESULTS</b>Basal expressions of MT-1X, and MT-1A in HPBLs were similar to expression of housekeeping gene. In contrast, the basal gene expressions of MT-1H, 1F, 1E, and 1G were a little transcripts in human HPBLs. No signal was detected for MT-1B. There was a sex difference (P < 0.05). in basal gene expression of MT-1E. The levels of gene expression of MT-1A, 1E, 1F, 1G, 1H, and 1X increased, but the level of MT-1B did not increase after exposure to cadmium.</p><p><b>CONCLUSIONS</b>Gene expressions of MT-1G, MT-1H, MT-1F, and MT-1X in HPBLs can be used as a potential biomarker of cadmium exposure.</p>

Combined effect of fluoride and arsenate on gene expression of osteoclast differentiation factor and osteoprotegerin / 生物医学与环境科学（英文）

<p><b>OBJECTIVE</b>To study the combined effect of fluoride and arsenate on the expression of SD rat osteoblastic osteoclast differentiation factor (ODF) mRNA and osteoprotegerin (OPG) mRNA.</p><p><b>METHODS</b>Osteoblasts were obtained by enzymatic isolation from newborn SD rats. A factorial experiment was performed. Osteoblasts were exposed to NaF (0.5 mmolF/L, 4 molF/L) and Na3AsH2 (12.5 micromolAs/L and 200 micromolAs/L) separately or F plus As and cultured for 48 h. The gene expression of osteoblastic ODF and OPG was observed by RT-PCR.</p><p><b>RESULTS</b>The expression of ODF mRNA increased in F0.5, F4 groups compared with control group and two groups of F0.5As200, F4As200 compared with As200 group, and decreased significantly in groups of F4Asl2.5, F0.5As200, and F4AS200. The expression of OPG mRNA decreased in groups of F4, As200, F4As12.5, F0.5AS200, and F4AS200.</p><p><b>CONCLUSION</b>The joint effect of fluoride and arsenate on the gene expression of ODF is antagonistic, while the combined effect on the gene expression of OPG is synergistic. F4, F4As12.5, and F0.5As200 promote bone resorption of rat osteoclasts, whereas F0.5As12.5 inhibits osteolytic effect of rat osteoclasts.</p>

The effects of cadmium on the levels of insulin in smelters / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To investigate the effects of cadmium on the levels of insulin and blood glucose in exposed workers.</p><p><b>METHODS</b>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.</p><p><b>RESULTS</b>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.</p><p><b>CONCLUSION</b>The exposure to cadmium can cause the decrease of serum insulin and may affect the level of blood glucose.</p>

Relationship between plasma anti-metallothionein antibody and renal dysfunction in cadmium exposed workers / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To investigate whether renal dysfunction induced by cadmium is related to plasma anti-metallothionein antibody (anti-MT Ab) in workers occupationally exposed to cadmium.</p><p><b>METHODS</b>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).</p><p><b>RESULTS</b>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).</p><p><b>CONCLUSION</b>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.</p>

Application of metallothionein gene isoforms expression as biomarkers in cadmium exposure / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To investigate the feasibility of metallothionein (MT) gene expression level in human peripheral blood lymphocytes (HPBLs) as a biomarker in cadmium exposure.</p><p><b>METHODS</b>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.</p><p><b>RESULTS</b>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.</p><p><b>CONCLUSION</b>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.</p>

Heme oxygenase-1 expression and apoptosis induced by cadmium in human embryon kidney cells / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To investigate apoptosis and expression of heme oxygenase-1 (HO-1) induced by cadmium in human embryonic kidney cells (HEK239T).</p><p><b>METHODS</b>The MTT method was used for determining the cell proliferation activity. The apoptosis was determined by the flow cytometry. The HO-l mRNA expression and protein level were detected by RT-PCR method and Western blot respectively.</p><p><b>RESULTS</b>The ratios of apoptosis in HEK239T cells were 11.90% +/- 0.28%, 9.27% +/- 1.73%, 9.79% +/- 0.67% and 8 .97% +/- 1.60% at the concentration of 5.0, 10.0, 20.0 and 40.0 micromol/L CdCl(2) respectively, higher than those in the control group (6.69% +/- 0.46%) with the significant difference (P < 0.01). The CdCl(2) of between 10 and 40 micromol/L could highly induce the expression of HO-1 of the human embryonic kidney cells. The expression would increase slowly till the flat stage with the increase of the dosage and then would decrease slightly over time.</p><p><b>CONCLUSION</b>The cadmium can induce the apoptosis of the human embryonic kidney cells and up-regulate the expression of HO-1.</p>

Application of Benchmark dose (BMD) in estimating biological exposure limit (BEL) / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>Based on two sets of data from occupational epidemiology, Benchmark dose (BMD) was applied to estimate biological exposure limit (BEL).</p><p><b>METHODS</b>Cadmium exposed workers were selected from a cadmium smelting and a zinc products factory and control group was selected from doctors or nurses and staff from shops living in the same area; Urinary cadmium (UCd) was used as exposure biomarker and urinary beta(2) microglobulin (UBM), NAG (UNAG) and albumin (UALB) were as effect biomarkers. All urine parameters were adjusted by urinary creatinine. Software of BMDS (Version 1.3.2, EPA.U.S) was used to calculate BMD.</p><p><b>RESULTS</b>Calculated abnormal prevalence was based on the upper limit of 95% of effect biomarkers in control group; There are significant dose response relationship between the prevalence of effect biomarkers (UBM, UNAG and UALB) and exposure biomarker (UCd); BEL was 5 microg/g creatinine for UBM as effect biomarker, It consists with the recommendation of WHO; BEL was 3 microg/g creatinine for UNAG as effect biomarker; BEL can be estimated by using the method of BMD; the more sensitive biomarker would used, the more occupational people would protected.</p><p><b>CONCLUSION</b>The application of BMD in estimating biological exposure limit (BEL) is proper. UNAG is suggested as most sensitive biomarker to be used to estimate BEL for cadmium exposure.</p>

Application of benchmark dose (BMD) in a bone-effect study on a general population environmentally exposed to cadmium / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To estimate the benchmark dose for osteoporosis caused by cadmium exposure in a Chinese general population with an epidemiological study.</p><p><b>METHODS</b>The inhabitants living in both cadmium polluted and non-polluted areas served as the exposure group and the control group. Urinary cadmium (UCd) and Blood cadmium (BCd) were used as exposure biomarkers while the Z score was used as effect biomarker for the osteoporosis.</p><p><b>RESULTS</b>The UCd and BCd in the habitants of the polluted areas were significantly higher than those in the habitants of the control area on average (P < 0.05) and the UCd and BCd in the habitants of the highly polluted areas were significantly higher than those in the habitants of the moderately polluted area on average (P < 0.05). The bone mineral density was significantly decreased in the groups of the highest UCd and BCd level compared with the 5 microg/g Cr group with the significant difference (P < 0.05). The morbidity of the osteoporosis would increase significantly with the increase of the cadmium exposure (P < 0.05) with the linear correlation (P < 0.05). BMDs were calculated using BMDS Version l.3.2 software and BMDLs were also determined. The BMDL of UCd for cadmium-induced osteoporosis was higher than those representing cadmium-induced renal dysfunction.</p><p><b>CONCLUSION</b>High level of cadmium exposure can induce osteoporosis, which occurs later than renal damage related to cadmium exposure. The BMD is a practical method.</p>

Epidemiological feature of metabolic syndrome in Shanghai residents aged 15 - 74 years / 中华预防医学杂志

<p><b>OBJECTIVE</b>To assess the prevalence of the metabolic syndrome in Shanghai residents.</p><p><b>METHODS</b>A cross-sectional study was conducted in Shanghai with a representative sample of 14,327 Chinese adults from 15 to 74 years of age. The sample was randomly selected using stratified cluster sampling. The criteria of International Diabetes Federation (IDF), the US National Cholesterol Education Program Adult Treatment Panel III (ATP III) guidelines and the China Diabetes Society (CDS), respectively, were applied for diagnosis.</p><p><b>RESULTS</b>Diagnosed by using the IDF criterion, the crude prevalence of metabolic syndrome was 17.51%, and the age and gender-adjusted prevalence was 12.81% (95% CI: 12.26 - 13.36). The prevalence of the metabolic syndrome was higher in females than in males (14.79% and 10.93%, respectively), and higher in urban residents than in rural ones (13.71% and 10.72%, respectively). The age-specific prevalence of the metabolic syndrome increased in both male and female residents and the prevalence of metabolic syndrome in females 45 years of age or elder was significantly increased. The prevalence of having at least 3 parameters of metabolic syndrome was 22.28%. According to the ATP III guideline, the crude and age-adjusted prevalence of metabolic syndrome was 12.03% and 8.62%, respectively. Based on the criterion of CDS, they were 13.98% and 10.41%.</p><p><b>CONCLUSION</b>There is a high prevalence of metabolic syndrome in Shanghai residents. Metabolic syndrome has become a noteworthy public health problem. It suggests that community-integrated control of metabolic syndrome should have its priority.</p>