OBJECTIVETo estimate the level of blood lead and some haematological parameters in the workers occupationally exposed to lead so as to know the effect of lead exposure on hematopoietic system in exposed workers.

METHODSThe graphite furnace atomic absorption spectrocopy was used to determine blood lead (BPb). The haematological parameters were determined by Sysmex KX-21 automated haematology analyzer.

RESULTSHemoglobin (Hb) in the lead-absorption group[male: (129.3 +/- 12.3) g/L, female: (112.2 +/- 9.4) g/L], and hematocrit (HCT) in the lead-absorption group[male: (0.338 +/- 0.030) L/L, female: (0.302 +/- 0.028) L/L] were significantly lower than those in normal people group and lead-exposed group (P < 0.05, P < 0.01). The relationships between BPb and Hb, HCT were weakly negative correlation. Red cell distribution width (RDW) in the lead-absorption group(male: 16.68% +/- 0.80%, female: 16.98% +/- 0.98%) were significantly higher than those in normal people group and lead exposed group, and RDW in lead exposed group (male: 14.77% +/- 0.83%, female: 14.92% +/- 1.13%) were higher than that in normal people group. BPb was weakly positively correlated with RDW.

CONCLUSIONHb, HCT and RDW were three indices which may reflect the occurrences and degrees of anaemia in lead exposed workers.

Anemia ; chemically induced ; Erythrocytes ; drug effects ; Female ; Hematocrit ; Hemoglobins ; analysis ; Humans ; Lead ; blood ; toxicity ; Male ; Occupational Exposure ; adverse effects

OBJECTIVETo compare PM2.5 pollation level between the city of coal-fuel pollution (Taiyuan) and the city of pollution mixed with coal fuels and vehicle exhausts (Beijing), to analyze the concentration of B[a]p and Pb in the pollutants, and to study the DNA damage by PM2.5.

METHODSAir fine particles (PM2.5) were collected in Beijing and Taiyuan by means of the filter membrane method, the concentration of B[a]p and Pb were analyzed by high performance liquid chromatography and atomic absorption spectroscopy respectveily, and the damage of DNA by PM2.5 was detected by single cell gel-electrophoresis (SCGE) using the human lung epithelial cells (A549) as target cells.

RESULTSThe concentration of PM2.5 in the winter of Beijing was 0.028-0.436 mg/m(3), and that in Taiyuan was 0.132-0.681 mg/m(3). The concentration of B[a]p was 0.104 and 0.156 microg/mg on PM2.5 of Beijing and Taiyuan, respectively, whereas the concentration of Pb was 1.094 and 1.137 microg/mg on PM2.5 of Beijing and Taiyuan, respectively. Exposure to PM2.5 at the concentrations of 5, 50, and 200 microg/mL for 12 h and 24 h caused DNA damage of the human alveolar epithelium, and the ratios of the tailing and length of the tail were all significantly different from those of the negative control group (P < 0.05), and indicated a dose-response relationship.

CONCLUSIONPM2.5 has certain genetic toxicity.

Air Pollutants ; analysis ; toxicity ; Animals ; Benzo(a)pyrene ; analysis ; toxicity ; China ; DNA Damage ; drug effects ; Dose-Response Relationship, Drug ; Drug-Related Side Effects and Adverse Reactions ; Environmental Monitoring ; methods ; Humans ; Lead ; analysis ; metabolism ; toxicity ; Particle Size ; Pulmonary Alveoli ; drug effects ; metabolism ; Seasons

OBJECTIVETo investigate the influence of lead exposure in rats during the developmental stage on the expression of leptin in plasma, cerebrospinal fluid, and hippocampus, as well as investigating whether leptin is associated with the mechanism of cognitive impairment induced by lead exposure.

METHODSThe rat model of cognitive impairment after chronic lead exposure was established by adding lead acetate into drinking water. According to the concentration of lead acetate in drinking water, the rats were divided into control (0 ppm), low-lead (50 ppm), medium-lead (200 ppm), and high-lead groups (1 000 ppm), with 16 rats in each group. Atomic absorption spectrometry was used to measure the content of lead in the plasma, cerebrospinal fluid and hippocampus. ELISA was used to measure the level of leptin in the plasma and cerebrospinal fluid. Immunohistochemistry was used to observe the distribution of leptin protein in the hippocampus. Western blot was used for relative quantification of leptin proteins in the hippocampus.

RESULTSCompared with the control group, the lead exposure groups showed significant increases in the content of lead in blood, cerebrospinal fluid, and hippocampus (P<0.01), as well as significant reductions in the levels of leptin in plasma and cerebrospinal fluid (P<0.05). The results of immunohistochemical staining showed that leptin was mainly distributed in the cytoplasm of pyramidal neurons in the hippocampal CA region. The results of Western blot showed that compared with the control group, the three lead exposure groups showed a slight increase in the protein expression of leptin in the hippocampus (P>0.05).

CONCLUSIONSLead exposure can reduce the levels of leptin in plasma and cerebrospinal fluid in rats, which may be associated with the mechanism of cognitive impairment induced by lead exposure.

Animals ; Apoptosis ; drug effects ; Cognition ; drug effects ; Female ; Hippocampus ; chemistry ; drug effects ; pathology ; Lead ; blood ; toxicity ; Leptin ; analysis ; blood ; cerebrospinal fluid ; Male ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo observe and explore the antagonism of rhizoma gastrodiae (RGT) to the impairment of learning and memory ability induced by lead in rats.

METHODS36 Wistar rats were randomly divided into 3 groups, 12 rats in every group, (1) control group: treated with distilled water; (2) lead group: treated with lead acetate (0.1 g.kg-1.d-1); (3) lead-RGT group: lead acetate (0.1 g.kg-1.d-1) + RGT(4.0 g.kg-1.d-1). The ability of learning and memory of the rats was measured monthly by swimming test; 3 months later, the rats were decapitated and nitric oxide(NO) and total antioxidative capacity(TAOC) in hippocampus were measured immediately and the examination for pathology was also made.

RESULTS(1) In swimming test, the number of seeking for anchorage in lead group(1, 2, 3 month: 10.10 +/- 1.10, 7.80 +/- 1.32, 5.40 +/- 0.97 respectively) were significantly decreased, compared with the control(P < 0.01); the number of seeking for anchorage in RGT-lead group(1, 2, 3 month: 11.90 +/- 0.95, 10.90 +/- 0.95, 9.70 +/- 0.96 respectively) were significantly increased, compared with lead group(P < 0.01). (2) NO (0.733 +/- 0.015) mumol/g pro and TAOC (0.945 +/- 0.017) U/mg pro in hippocampus of lead group were significantly decreased compared with the control(P < 0.01) whereas NO(0.769 +/- 0.021) mumol/g pro and TAOC(0.986 +/- 0.010) U/mg pro in hippocampus of RGT-lead group were significantly increased compared with lead group(P < 0.01). (3) Pathological examination showed that in lead group, marked atrophy in hippocampus, cellular denaturation and necrosis, dissolution and disappearance in axon were found. In lead-RGT group, the atrophy of hippocampus was not obvious, the cell morphology was nearly normal, no obvious abnormal changes were seen.

CONCLUSIONRGT is antagonistic to the impairment of hippocampus and of learning and memory ability induced by lead.

Animals ; Drugs, Chinese Herbal ; pharmacology ; Hippocampus ; drug effects ; metabolism ; pathology ; Lead ; toxicity ; Learning ; drug effects ; Memory ; drug effects ; Nitric Oxide ; analysis ; Rats ; Rats, Wistar ; Swimming

OBJECTIVETo evaluate the effect of different doses of lead acetate (1/20, 1/40 and 1/60 of LD50) on body weight gain, blood picture, plasma protein profile and the function of liver, kidney and thyroid gland.

METHODSMale albino rats were divided into four groups, the first group represented the health control animals, while the second, third and fourth groups were ingested orally with sub lethal doses of lead acetate (1/20, 1/40 and 1/60) of the oral LD50, respectively. One dose was ingested every two days during the experimental period (14 weeks) including the adaptation time. Blood was collected and used for all analysis.

RESULTSThe results showed that, the ingestion of Pb(2+) induced significant stimulation in glutamic-pyruvic transaminase (ALT) and glutamic-oxalacetic transaminease (AST) activity. Also, total soluble protein and albumin contents of plasma were significantly decreased, while the content of globulin was changed by the Pb(2+) treatments. The cholinesterase activity was inhibited, but the activities of alkaline and acid phosphates and lactate dehydrogenase were stimulated, while plasma glucose level was elevated as a result of lead acetate intoxication. In case of blood picture, Pb(2+) ingestion reduced the contents of hemoglobin and RBCs count of intoxicated rat's blood and the plasma levels of T3, T4 and blood WBCs count were decreased.

CONCLUSIONSIt can be concluded that lead acetate has harmful effect on experimental male albino rats. Therefore, the present work advises people to prevent exposure to the lead compound to avoid injurious hazard risk.

Animals ; Blood Cells ; Blood Chemical Analysis ; Kidney Function Tests ; Lead Poisoning ; pathology ; physiopathology ; Liver Function Tests ; Male ; Organometallic Compounds ; toxicity ; Rats, Sprague-Dawley ; Thyroid Function Tests

Our objective was to evaluate the relationship between intrauterine exposure to cadmium and the presence of atopic dermatitis in infants 6 months of age, adjusted for covariates including exposure to other heavy metals. The present research is a component of the Mothers' and Children's Environmental Health (MOCEH) study, a multi-center birth cohort project conducted in Korea. Study subjects were restricted to pregnant women in whom cadmium and lead levels were measured at delivery and whose infants were assessed for the presence of atopic disease at 6 months of age. The odds ratio (OR) for the presence of atopic dermatitis in 6-month-old infants whose cord blood had elevated cadmium levels, after adjustment for other covariates, was 2.350 (95% CI, 1.126-4.906). The OR for the presence of atopic dermatitis in infants whose cord blood had elevated lead levels was not significant. In the present study, the cord blood cadmium level was significantly associated with the presence of atopic dermatitis in 6-month-old infants; this was not true of the cord blood lead level. To the best of our knowledge, this is the first prospective study to show a relationship between prenatal exposure to cadmium and atopic dermatitis in infancy.
Adult ; Cadmium/analysis ; Cadmium Poisoning/*complications ; Cohort Studies ; Dermatitis, Atopic/diagnosis/*etiology ; Female ; Fetal Blood/chemistry ; Gestational Age ; Humans ; Infant ; Lead/analysis/toxicity ; Male ; Odds Ratio ; Pregnancy ; Prenatal Exposure Delayed Effects

OBJECTIVETo observe the effects of lead on levels of phosphorylated extracellular signal regulated kinase (p-ERK) in the cytoplasm of primary cultures of rat astroglial cells and the possible protective effect of basic fibroblast growth factor (bFGF) on lead-induced effects.

METHODSThe primary astroglia cells from 1~6 d old Wistar rats were cultured. The cells pretreated with the MEK1 (mitogen-activated protein kinase kinase 1) inhibitor PD98059 and bFGF, respectively, were exposed to Pb acetate of different concentrations for different times. Western blotting and reverse transcription polymerase chain reaction (RT-PCR) methods were used to detect the protein and mRNA expressions of ERK.

RESULTSmRNA expression for ERK peaked 15 min after initiation of lead exposure (P<0.05) and protein expression of p-ERK peaked at 30 min (P<0.05). ERK mRNA levels and p-ERK protein levels returned to baseline after 60 and 120 min of lead exposure, respectively (P>0.05). The increase in p-ERK levels in lead-treated cells could be inhibited by PD098059. Activation of ERK in the cells by lead was prevented by pretreatment with bFGF. Total ERK protein levels did not change under the same experimental conditions (P>0.05).

CONCLUSIONLow-level lead exposure resulted in transient activation of ERK through the MEK pathway, which then returned to basal levels in the continued presence of lead. Exogenous bFGF protected ERK signaling components in astroglia from lead poisoning.

Animals ; Astrocytes ; cytology ; drug effects ; physiology ; Cells, Cultured ; Extracellular Signal-Regulated MAP Kinases ; genetics ; metabolism ; Fibroblast Growth Factor 2 ; pharmacology ; Glial Fibrillary Acidic Protein ; analysis ; Lead ; toxicity ; Long-Term Potentiation ; Neuroprotective Agents ; pharmacology ; Phosphorylation ; RNA, Messenger ; analysis ; Rats ; Rats, Wistar

OBJECTIVETo observe the effect of long-term external use of Goupi Gao on renal function and lead accumulation in rats.

METHODRats were externally administered with Goupi Gao at different doses (7, 3.5 and 1.75 g x kg(-1)) for 90 d. At 45 days and 90 days after administration, the renal indicator, levels of blood urea nitrogen (BU) and creatinine (Cr) in serum, beta2-microglobulin (beta2-MG) and N-acetyl-beta-D-glucosaminidase (NAG) in urine were determined. Lead content in kidneys was detected by atomic absorption spectrometry.

RESULTA 90-day administration with Goupi Gao significantly enhanced the renal indicator, levels of NAG in urine and lead content in renal, when compared with the normal rats. However, the levels of BUN and beta2-MG as well as renal pathology in Goupi Gao treated rats were not obviously changed.

CONCLUSIONConsecutive administration of Goupi Gao for 90 days can increase the renal indicator and levels of NAG in urine, enhance the accumulation of lead in renal, but with no effect on excretory function of kidneys and organic changes.

Acetylglucosaminidase ; urine ; Animals ; Blood Urea Nitrogen ; Creatinine ; blood ; Drugs, Chinese Herbal ; administration & dosage ; toxicity ; Female ; Kidney ; drug effects ; metabolism ; pathology ; Lead ; analysis ; metabolism ; Male ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Spectrophotometry, Atomic ; beta 2-Microglobulin ; urine

OBJECTIVETo study the effects of extremely low frequency electromagnetic field(ELF EMF) and its combination with lead on the antioxidant system in mouse brain and liver tissues.

METHODMice were exposed to a 50 Hz sinusoidal 0.2 mT or 6.0 mT EMF for 2 weeks. At the same time, some groups were exposed to lead(50 mg/kg). After the exposure, the antioxidant system and cell membrane fluidity in brain and liver were measured.

RESULTSMalondiadehyde(MDA) content in brain and liver increased from the control levels of (1.33 +/- 0.12) and (3.95 +/- 0.21) nmol/mg pro to (1.35 +/- 0.09) and (6.15 +/- 0.28) nmol/mg pro respectively following 0.2 mT exposure, and to (3.98 +/- 0.10) and (6.50 +/- 0.79) nmol/mg pro respectively following 6.0 mT exposure. Total antioxidant capability(T-AOC) in brain and liver decreased from the control levels of (4.39 +/- 0.48) and (2.45 +/- 0.21) U/mg pro to (3.99 +/- 0.39) and (1.92 +/- 0.32) U/mg pro respectively following 0.2 mT, and to (3.12 +/- 0.37) and (1.57 +/- 0.14) U/mg pro respectively following 6.0 mT. GSH content decreased only in liver tissue from the control level of (194.60 +/- 20.93) mg/g pro to (189.24 +/- 5.61) mg/g pro(0.2 mT) and (153.04 +/- 1.18) mg/g pro(6.0 mT). Cellular membrane fluidity decreased from the control levels of (1.396 +/- 0.040) and (2.899 +/- 0.552) to (1.224 +/- 0.190) and (1.894 +/- 0.0761) (0.2 mT), (1.159 +/- 0.179) and (1.516 +/- 0.204)(6.0 mT) respectively. Compared with single EMF exposure(6.0 mT), EMF combined with lead exposure induced remarkable increase in MDA, GSH content and T-AOC and decrease in cell membrane fluidity both in the brain and liver, and increase in SOD activity only in liver.

CONCLUSIONELF EMF might alter the metabolism of free radicals, decrease anti-oxidant capability and enhance lipid peroxidation. The combination of EMF with lead showed synergic effects on lipid peroxidation.

Animals ; Antioxidants ; metabolism ; Brain ; drug effects ; metabolism ; radiation effects ; Electromagnetic Fields ; adverse effects ; Glutathione ; analysis ; Lead ; toxicity ; Lipid Peroxidation ; drug effects ; radiation effects ; Liver ; drug effects ; metabolism ; radiation effects ; Membrane Fluidity ; drug effects ; radiation effects ; Mice ; Superoxide Dismutase ; metabolism

OBJECTIVETo explore the effects of embryonic lead exposure on motor function and balance ability in offspring rats and the possible mechanisms.

METHODSAn animal model of embryonic lead exposure was prepared with the use of pregnant Sprague-Dawley rats freely drinking 0.1% (low-dose group, LG) or 0.2% (high-dose group, HG) lead acetate solution. A normal control group (NG) was also set. The male offspring rats of these pregnant rats were included in the study, consisting of 12 rats in the NG group, 10 rats in the LG group, and 9 rats in the HG group. The offspring rats' motor function and balance ability were evaluated using body turning test and coat hanger test. Eight rats were randomly selected from each group, and immunohistochemistry and Timm's staining were employed to measure the expression of c-Fos and mossy fiber sprouting (MFS) in the hippocampus.

RESULTSThe HG group had a significantly longer body turning time than the NG and LG groups (P<0.05), and the LG group had a significantly longer body turning time than the NG group (P<0.05). The HG group had a significantly lower score of balance ability than the NG and LG groups (P<0.05), and the LG group had a significantly lower score of balance ability than the NG group (P<0.05). The area percentage of c-Fos-positive neurons in the hippocampal CA1 region was significantly higher in the HG group than in the other two groups (P<0.05), and it was significantly higher in the LG group than in the NG group (P<0.05). The semi-quantitative scores of MFS in the hippocampal CA3 region and dentate gyrus were significantly higher in the HG group than in the other two groups (P<0.05), and they were significantly higher in the LG group than in the NG group (P<0.05).

CONCLUSIONSEmbryonic lead exposure could impair the offspring rats' motor function and balance ability. These changes may be related to increased c-Fos expression in the hippocampal CA3 region and abnormal MFS in the hippocampal CA3 region and dentate gyrus.

Animals ; Female ; Fetus ; drug effects ; Hippocampus ; chemistry ; drug effects ; Lead ; toxicity ; Male ; Mossy Fibers, Hippocampal ; drug effects ; Motor Activity ; drug effects ; Postural Balance ; drug effects ; Pregnancy ; Proto-Oncogene Proteins c-fos ; analysis ; Rats ; Rats, Sprague-Dawley