Study on determination of 2-thioxothiazolidine-4-carboxylic Acid in urine by high performance liquid chromatography / 中华劳动卫生职业病杂志

Objective: To establish a high performance liquid chromatography method for the determination of 2-thioxothiazolidine-4-carboxylic acid (TTCA) in urine. Methods: After acidification with hydrochloric acid, TTCA in urine was first extracted by ethyl acetate with excessive sodium chloride, then gradient separated by a symmetry C18 column and then detected by a diode array detector. The quantification was based on a working curve of external standard method. Results: The linear relationship of TTCA in urine was good in the range of 0.03-10.00 mg/L, and the correlation coefficient was 0.9999. The detection limit and minimum quantitative concentration of TTCA in urine were 0.008 mg/L and 0.027 mg/L. The intra-assay precision of the method was 0.9%-1.4%, the inter-assay precision was 1.3%-3.5%, and the average recovery was 85.0%-92.7% while the concentrations of TTCA in urine was 0.8, 2.0 and 8.0 mg/L, respectively (n=6) . Conclusion: The gradient elution high performance liquid chromatography method has simple operation and high sensitivity, and it is suitable for the determination of TTCA on a low level in urine for occupational workers exposure to carbon disulfide.

Urinary Trans, Trans-Muconic Acid is Not a Reliable Biomarker for Low-level Environmental and Occupational Benzene Exposures

BACKGROUND: Benzene is a known occupational and environmental pollutant. Its urinary metabolite trans, trans-muconic acid (tt-MA) has been introduced by some environmental and occupational health regulatory associations as a biological index for the assessment of benzene exposure; however, recently, doubts have been raised about the specificity of tt-MA for low-level benzene exposures. In the present study, we investigated the association between urinary levels of tt-MA and inhalational exposure to benzene in different exposure groups. METHODS: Benzene exposure was assessed by personal air sampling. Collected benzene on charcoal tube was extracted by carbon disulfide and determined by a gas chromatograph (gas chromatography with a flame ionization detector). Urinary tt-MA was extracted by a strong anion-exchange column and determined with high-performance liquid chromatography–UV. RESULTS: Urinary levels of tt-MA in intensive benzene exposure groups (chemical workers and police officers) were significantly higher than other groups (urban and rural residents), but its levels in the last two groups with significant different exposure levels (mean = 0.081 ppm and 0.019 ppm, respectively) showed no significant difference (mean = 388 μg/g creatinine and 282 μg/g, respectively; p < 0.05). Before work shift, urine samples of workers and police officers showed a high amount of tt-MA and its levels in rural residents’ samples were not zero. CONCLUSION: Our results suggest that tt-MA may not be a reliable biomarker for monitoring low-level (below 0.5 ppm) benzene exposures.

Carbon disulfide exposure estimate and prevalence of chronic diseases after carbon disulfide poisoning-related occupational diseases

BACKGROUND: In Korea, Carbon disulfide (CS2) toxicity was an important social problem from the late 1980s to the early 1990s but there have been few large-scale studies examining the prevalence of diseases after CS2 exposure discontinuance. So we investigated past working exposure to CS2 characteristics from surviving ex-workers of a rayon manufacturing plant including cumulative CS2 exposure index. Furthermore, we studied the prevalence of their chronic diseases recently after many years. METHODS: We interviewed 633 ex-workers identified as CS2 poisoning-related occupational diseases to determine demographic and occupational characteristics and reviewed their medical records. The work environment measurement data from 1992 was used as a reference. Based on the interviews and foreign measurement documents, weights were assigned to the reference concentrations followed by calculation of individual exposure index, the sum of the portion of each time period multiplied by the concentrations of CS2 during that period. RESULTS: The cumulative exposure index was 128.2 ppm on average. Workers from the spinning, electrical equipment repair, and motor repair departments were exposed to high concentrations of ≥10 ppm. Workers from the maintenance of the ejector, manufacturing of CS2, post-process, refining, maintenance and manufacturing of viscose departments were exposed to low concentrations below 10 ppm. The prevalence for hypertension, coronary artery disease, cerebrovascular disease, diabetes, arrhythmia, psychoneurotic disorder, disorders of the nervous system and sensory organ were 69.2%, 13.9%, 24.8%, 24.5%, 1.3%, 65.7%, 72.4% respectively. CONCLUSIONS: We estimated the individual cumulative CS2 exposure based on interviews and foreign measurement documents, and work environment measurement data. Comparing the work environment measurement data from 1992, these values were similar to them. After identified as CS2 poisoning, there are subjects over 70 years of average age with disorders of the nervous system and sensory organs, hypertension, psychoneurotic disorder, cerebrovascular disease, diabetes, coronary artery disease, and arrhythmia. Because among ex-workers of the rayon manufacturing plant, only 633 survivors recognized as CS2 poisoning were studied, the others not identified as CS2 poisoning should also be investigated in the future.

Recognition and Using Status of Carbon Disulfide (CS₂) as Fumigant for Controlling Chestnut Weevil, Curculio sikkimensis among Chestnut Farmers / 農村醫學 地域保健

OBJECTIVES: We surveyed the awareness and current status of using fumigant carbon disulfide for exterminate Curculio sikkimensis among chestnut farmers in Chungnam Province to suggest directions for health education and public relations. METHODS: We designed questionnaires to evaluate recognition of fumigant carbon disulfide. We conducted a questionnaire survey to assess recognition and recognition level of fumigant carbon disulfide by the study variables. RESULTS: The recognition status for fumigant carbon disulfide was 74.5%, but the recognition level was low (know well 27.5%). The path of recognition was 45.1% and 15.7% for neighbor and rural technology center, respectively. The recognition status for warning label of fumigant carbon disulfide was 52.9%. Recognition for warning label of fumigant carbon disulfide was tended to increase with high educational attainment, bigger owning land area. Recognition on the content of warning label were 29.4%, 27.5%, 21.6%, and 21.6% for inflammability, toxicity, hazard, and explosiveness, respectively. Using personal protection equipment was tended to increase with the high status of awareness on fumigant carbon disulfide. CONCLUSIONS: Health education programs for using fumigant carbon disulfide are needed for chestnut farmers. In addition, publicity information activities about prevention and protection of carbon disulfide poisoning are needed for high risk farmers.

Effect of carbon disulfide exposure on fatty acid metabolism in ApoE knockout and C57BL/6J mice / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To study the influences of carbon disulfide (CS2) exposure on fatty acid metabolism in apolipoprotein E (ApoE) knockout mice and C57BL/6J mice.</p><p><b>METHODS</b>Twenty-four male ApoE knockout mice were randomly and equally divided into four groups: a CS2-exposed normal diet group, a CS2-unexposed normal diet group, a CS2-exposed high-fat diet group, and a CS2-unexposed high-fat diet group. Twenty-four C57BL/6J male mice were divided into four groups in the same way. The CS2-exposed groups were exposed to CS2 (1 g/m(3)) by static inhalation for 5 hours a day, 5 days a week. After two weeks, the whole blood of mice was collected. Methyl ester derivatization of fatty acids was performed using an acid-catalyzed method. Fatty acid contents before and after exposure were compared by gas chromatography-mass spectroscopy.</p><p><b>RESULTS</b>There were significant differences in fatty acid contents of mice between the four groups. For the C57BL/6J mice, the arachidic acid contents in the CS2-exposed high-fat diet group were significantly lower than those in the CS2-unexposed high-fat diet group (P = 0.045 0). For the ApoE knockout mice, the arachidonic acid contents in the CS2-exposed normal diet group were significantly lower than those in the CS2-unexposed control diet group (P = 0.045 2). For the ApoE knockout mice, the γ-linolenic acid contents in the CS2-exposed high-fat diet group were significantly higher than those in the unexposed high-fat diet group (P = 0.044 7).</p><p><b>CONCLUSION</b>Exposure to CS2 can induce fatty acid metabolism disorder in mice, indicating that CS2 may increase the risk of atherosclerosis and other cardiovascular diseases.</p>

Rapid determination of 28 pesticides and tetramine in whole blood by online gel permeation chromatography coupled with gas chromatography-mass spectrometry / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To study the influences of carbon disulfide (CS2) exposureon fatty acid metabolism in apolipoprotein E (ApoE) knockout mice and C57BL/6J mice.</p><p><b>METHODS</b>Twenty-four male ApoE knockout mice were randomly and equally divided into four groups: a CS2-exposed normal diet group, a CS2-unexposed normal diet group, a CS2-exposed high-fat diet group, and a CS2-unexposed high-fat diet group. Twenty-four C57BL/6J male mice were divided into four groups in the same way. The CS2-exposed groups were exposed to CS2 (1 g/m³) by static inhalation for 5 hours a day, 5 days a week. After two weeks, the whole blood of mice was collected. Methyl ester derivatization of fatty acids was performed using an acid-catalyzed method. Fatty acid contents before and after exposure were compared by gas chromatography-mass spectroscopy.</p><p><b>RESULTS</b>There were significant differences in fatty acid contents of mice between the four groups. For the C57BL/6J mice, the arachidic acid contents in the CS2-exposed high-fat diet group were significantly lower than those in the CS2-unexposed high-fat diet group (P = 0.0450). For the ApoE knockout mice, the arachidonic acid contents in the CS2-exposed normal diet group were significantly lower than those in the CS2-unexposed control diet group (P = 0.0452). For the ApoE knockout mice, the γ-linolenic acid contents in the CS2-exposed high-fat diet group were significantly higher than those in the unexposed high-fat diet group (P = 0.0447).</p><p><b>CONCLUSION</b>Exposure to CS2 can induce fatty acid metabolism disorder in mice, indicating that CS2 may increase the risk of atherosclerosis and other cardiovascular diseases.</p>

Determination of n-pentanol in workplace air by solvent desorption gas chromatography / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To develop a solvent desorption gas chromatographic method for determination of n-pentanol in the workplace air.</p><p><b>METHODS</b>n-Pentanol in the workplace air was collected with activated carbon tubes, desorbed with 2% 2-propanol in carbon disulfide, separated with a nitroterephthalic acid-modified FFAP capillary column, and detected with flame ionization detector.</p><p><b>RESULTS</b>The limit of detection was 0.2 mg/L; the lower limit of quantification was 0.6 mg/L; the linear range was 0.6-4072.0 mg/L. The minimum detectable mass concentration was 0.2 mg/m3 for 1.5 L of air sample. This method was highly repeatable. The relative standard deviations were 2.3%-5.4%. The average desorption efficiencies were 86.9%-94.2%. The absorption efficiencies were 100%. The breakthrough volume was above 8.0 mg in 100-mg activated carbon. The samples in activated carbon tubes could be stored for at least 14 days at room temperature.</p><p><b>CONCLUSION</b>The method is feasible for determination of n-pentanol in the workplace air.</p>

Detection rate analysis on neurological sign of workers exposed to different concentrations of carbon disulfide / 中华预防医学杂志

<p><b>OBJECTIVE</b>To study the effects of exposed to different concentrations of carbon disulfide on neurological signs of workers.</p><p><b>METHODS</b>Collection the information of concentration of carbon disulfide in the workplace or workers individuals exposed of a chemical fiber industry from 2004 to 2011, a total of 3 537 workers exposed to carbon disulfide were detected muscle strength and muscle tone, knee reflex, Achilles tendon reflex, trembling limbs, sensory function, and three chatter. Chi-square test was used for statistical analysis on abnormal neurological signs of workers.</p><p><b>RESULTS</b>Eight hours time-weighted average concentration range of workers exposed to carbon disulfide in this chemical fiber industry was 0.2-41.0 mg/m(3), geometric mean was 2.38 mg/m(3). Concentration of carbon disulfide exposure of 1 771 workers was from 0.2 to 2.5 mg/m3( ≤ 2.5 mg/m(3)), 642 workers was 2.6-4.8 mg/m(3) (< 5.0 mg/m(3)), other 1 051 workers was from 5.1 to 41.0 mg/m(3) ( > 5.0 mg/m(3)) in all subjects. The different detection rates of knee reflex were 3.0% (31/1 045), 3.7% (21/574), 4.8% (16/331), 3.3% (10/305), 5.9% (11/187), 6.7% (68/1 022), the different detection rates of Achilles tendon reflex were 2.2% (23/1 045), 3.7% (21/574), 2.7% (9/331), 2.3% (7/305), 2.1% (4/187), 5.6% (57/1 022), the different detection rates of sensory dysfunction were 0.4% (4/1 045), 0.5% (3/574), 0.6% (2/331), 0.0% (0/305), 2.1% (4/187), 1.7% (17/1 022) in different cumulative amount of contact groups ( ≤ 10.0, 10.1-20.0, 20.1-30.0, 30.1-40.0, 40.1-50.0, >50.0 mg/m(3) per year), and the differences were statistically significant (χ(2) = 19.53, 21.27 and 15.89, all P values were <0.01) . Stratified according to age and gender, in addition to the ≤ 25 years group the difference of detection rate analysis on Achilles tendon reflex was statistically significant in the different concentration group (the ratio of on Achilles tendon reflex in the different groups of concentration of carbon disulfide exposure of 2.5, 2.6-5.0, ≥ 5.0 mg/m(3) were 0.4% (2/511), 1.0% (1/98), 2.1% (7/327), χ(2) = 5.59, P = 0.045) , the difference of detection rate analysis on neurological sign was not statistically significant in the different concentration group on the rest of the age and gender groups (P > 0.05).</p><p><b>CONCLUSION</b>Within the concentration range of the object of study contact actual, different concentrations of carbon disulfide in addition to individual neurological signs of individual ages influential, it has no significant effect on the various signs of nervous system of workers of most age and gender groups, expect the age below the 25 years old group.</p>

Changes in expression of motor protein for axonal transport in nerve tissues of carbon disulfide-intoxicated rats / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To study the changes in microtubule motor protein expression in the spinal cord and sciatic nerve of rats exposed to carbon disulfide, and to investigate the possible molecular mechanism of changes in axonal transport in carbon disulfide-induced peripheral neuropathy.</p><p><b>METHODS</b>Healthy adult male Wistar rats were randomly divided into one control group and three experimental groups (10 rats per group). The rats in experimental groups were intoxicated by gavage of carbon disulfide at a dose of 200, 400, or 600 mg/kg 6 times a week for 6 consecutive weeks, while the rats in control group were given the same volume of corn oil by gavage. Animals were sacrificed after exposure, with nerve tissue separated. The levels of dynein, dynactin, and kinesin in the spinal cord and sciatic nerve were determined by Western blot.</p><p><b>RESULTS</b>The content of dynein, dynactin, and kinesin in the sciatic nerve decreased significantly under exposure to carbon disulfide. The levels of dynein in the sciatic nerve were reduced by 23.47% and 33.34% at exposure doses of 400 and 600 mg/kg, respectively. The levels of dynactin in the sciatic nerve of the three experimental groups were reduced by 19.91%, 24.23%, and 41.30%, respectively. The level of kinesin was reduced by 25.98%under exposure to 600 mg/kg carbon disulfide. All the differences were statistically significant (P < 0.01). As compared with the control group, the 600 mg/kg group experienced a 28.24% decrease in level of dynactin in the spinal cord (P < 0.01), but no significant change was observed in the level of dynein or kinesin.</p><p><b>CONCLUSION</b>Carbon disulfide has an impact on microtubule motor protein expression in nerve tissues, which might be involved in the development of carbon disulfide-induced peripheral neuropathy.</p>

Determination of methyl propyl ketone in air of workplace by capillary gas chromatography / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To establish a gas chromatography method for determination of methyl propyl ketone in the air of workplace.</p><p><b>METHODS</b>Methyl propyl ketone in the air of workplace was collected with activated carbon tubes and desorbed with carbon disulfide before sample loading. The target toxicant was separated with the capillary column and detected with a hydrogen flame ionization detector, identified by retention time, and quantified by peak area.</p><p><b>RESULTS</b>The linear range of methyl propyl ketone in the air of workplace was 202.5∼4 860.0 µg/ml, with a correlation coefficient of 0.999 98. The limit of detection was 1.5 µg/ml. The lower limit of quantification was 5.0 µg/ml. The minimum detectable concentration was 1.0 mg/m(3) under 1.5 L sampling volume and 1.0 ml desorption solution volume. The relative standard deviation of different methyl propyl ketone concentrations was 1.42%∼1.65%, and the recovery rate was 94.9%∼ 97.9%.</p><p><b>CONCLUSION</b>This method has high sensitivity, precision, and accuracy, and it is applicable for determination of methyl propyl ketone in the air of workplace.</p>

Effects of carbon disulfide inhalation on lipid levels of ApoE gene knockout mice and C57BL/6J mice / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To investigate the effects of carbon disulfide (CS(2)) inhalation on the lipid levels of ApoE knockout gene mice and C57BL/6J mice.</p><p><b>METHODS</b>Fifty-one male ApoE gene knockout mice were randomly divided into four groups: CS(2)-exposed normal diet group, CS(2)-unexposed normal diet group, CS(2)-exposed high-fat diet group, and CS(2)-unexposed high-fat diet group. Fifty male C57BL/6J mice were divided into four groups in the same way. The exposed groups received 1000 mg/m3 CS(2) by static inhalation (5h/d, 5d/w) for four weeks. The weight of each mouse was determined and recorded once a week. On the 14th day of exposure, six mice in each group were randomly selected to measure serum total cholesterol (TC) levels. On the 28th day of exposure, the serum levels of TC and low-density lipoprotein (LDL) in the remaining mice were measured.</p><p><b>RESULTS</b>The mean weight gain of exposed groups was less than that of the unexposed groups. On the 14th and 28th days of experiment, the TC levels of the CS2-exposed high-fat diet group were significantly higher than those of the CS(2)-unexposed high-fat diet group among ApoE knockout gene mice (P < 0.01 for both). On the 14th day of experiment, the TC levels of the CS(2)-unexposed high-fat diet group were significantly higher than those of the CS(2)-unexposed normal-diet group among C57BL/6J mice group (P < 0.05). On the 28th day of experiment, the LDL levels of the CS(2)-exposed high-fat diet group were significantly higher than those of the CS(2)-unexposed high-fat diet group among ApoE knockout gene mice (P = 0.003).</p><p><b>CONCLUSION</b>CS(2) exposure, high-fat diet, and ApoE gene knockout can elevate blood lipids in mice, thus increasing the risk of atherosclerosis.</p>

Effects of carbon disulfide exposure during peri-implantation on estrogen receptor-α expression in uterus and serum level of estrogen in pregnant mice / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To evaluate the effects of carbon disulfide (CS(2)) exposure during peri-implantation on the estrogen receptor-α (ER-α) expression in the uterus and serum level of estradiol (E(2)) in pregnant mice, and to explore the mechanism of embryotoxicity of CS(2).</p><p><b>METHODS</b>Healthy female mice were exposed to a single dose of CS(2) (631.4 mg/kg) or olive oil (solvent control) on gestational day (GD)3, GD4, GD5, or GD6. At different time points after exposure, the serum E(2) levels of the pregnant mice were measured by enzyme-linked immunosorbent assay, and the expression levels of ER-α in the uterus were measured by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and Western blot.</p><p><b>RESULTS</b>Compared with the control group, the GD3, GD4, GD5, and GD6 exposure groups showed significantly decreased serum E(2) levels on day 7 of gestation (P < 0.05); the GD3 and GD5 exposure groups showed significantly decreased serum E(2) levels on day 6 of gestation (P < 0.05). The expression level of ER-α in the GD 4 exposure group was 23.6% lower than that in the control group on day 5 of gestation, and the expression level of ER-α in the GD 5 exposure group was 72.9% lower than that in the control group on day 6 of gestation (P < 0.05); the GD 3 and GD 6 exposure groups showed lower expression levels of ER-α than the control group at any time point, but no significant difference was found (P > 0.05).</p><p><b>CONCLUSION</b>CS(2) exposure during peri-implantation can reduce the ER-α expression in the uterus and the serum level of E(2) in pregnant mice, which may be one of the mechanisms of embryotoxicity of CS(2).</p>

DNA damage of splenic lymphocytes in pregnant mice exposed to carbon disulfide in implantation phase / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To investigate the DNA damage of splenic lymphocytes in pregnant mice exposed to carbon disulfide (CS2) in the implantation phase and to explore the mechanism of abnormal implantation induced by CS2 from the perspective of immune injury.</p><p><b>METHODS</b>Mice were exposed to CS2 at different doses or at different time points in the implantation phase to establish model 1 and model 2. For model 1, mice were assigned to four groups to receive a single intraperitoneal injection of low-dose CS2 (0.1 LD50, 157.8 mg/kg), middle-dose CS2 (0.2 LD50, 315.7 mg/kg), and high-dose CS2 (0.4 LD50, 631.4 mg/kg) as well as an equal volume of olive oil (control) on gestational day (GD) 4. For model 2, mice were assigned to four groups to receive a single intraperitoneal injection of CS2 (0.4 LD50, 631.4 mg/kg) or an equal volume of olive oil (control) on GD3, GD4, GD5, and GD6. At the end, single cell suspension of splenic lymphocytes was prepared. Cell viability was measured by trypan blue staining, and the DNA damage of splenic lymphocytes was evaluated by alkaline single cell gel electrophoresis assay.</p><p><b>RESULTS</b>The middle-dose and high-dose exposure groups showed significantly more DNA damage of splenic lymphocytes than the control group (P < 0.01); there was significant regression relationship between indicators of DNA damage and exposure doses (P < 0.01). The GD3, GD4, GD5, and GD 6 exposure groups showed significantly more DNA damage of splenic lymphocytes than the control group (P < 0.01), and the GD 4 exposure group had the most DNA damage.</p><p><b>CONCLUSION</b>Exposure to CS2 in the implantation phase can induce DNA damage of splenic lymphocytes in pregnant mice, and the DNA damage was aggravated with the increase in CS2 concentration. GD4 may be the sensitive time point for DNA damage of splenic lymphocytes induced by CS2 in pregnant mice.</p>

Effect of carbon disulfide on mitochondrial respiratory chain in spermatogenic cells in male rats / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To investigate the effect of carbon disulfide (CS(2)) on the mitochondrial respiratory chain in testicular spermatogenic cells in male rats and to explore the possible mechanism of reproductive system damage caused by CS(2) in male rats.</p><p><b>METHODS</b>Twenty-four male Sprague-Dawley rats (clean grade) were randomly divided into four groups: three CS(2) exposure groups (CS(2) concentrations: 50, 250, and 1250 mg/m(3)) and a control group. The rats in CS(2) exposure groups were exposed to CS(2) by static inhalation for 10 weeks (2 h/d, 5 d/w), while the rats in control group were exposed to air. Then, all rats were sacrificed by decapitation; testicular tissues were collected, and mitochondrial protein in spermatogenic cells were extracted; the levels of mitochondrial respiratory chain enzyme complex I∼V were measured by enzyme-linked immunosorbent assay.</p><p><b>RESULTS</b>Compared with the control group, all CS(2) exposure groups had significantly increased levels of mitochondrial respiratory chain enzyme complex I∼V in spermatogenic cells (P < 0.05). There were no significant differences in the levels of respiratory chain enzyme complex I∼IV between the CS(2) exposure groups (P < 0.05), but the level of respiratory chain enzyme complex V rose significantly as the concentration of CS(2) increased (P<0.05).</p><p><b>CONCLUSION</b>Various levels of CS(2) exposure may increase the levels of mitochondrial respiratory chain enzyme complex in testicular spermatogenic cells among male rats, thus affecting the normal oxidative phosphorylation in mitochondria.</p>

Effect of carbon disulfide on mitochondrial apoptosis-related proteins in cytoplasm of testicular tissue among male rats / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To investigate the role of mitochondrial pathway in the apoptosis of spermatogenic cells induced by inhalation of carbon disulfide in male rats.</p><p><b>METHODS</b>Twenty-four male Sprague-Dawley rats (clean grade) were divided into four groups according to their body weights: three CS(2) exposure groups (CS(2) concentrations: 50, 250, and 1250 mg/m(3)) and a control group. The rats in CS(2) exposure groups were exposed to CS(2) by static inhalation for 10 weeks (2 h/d, 5 d/w), while the rats in control group were exposed to air. Then, all rats were sacrificed by decapitation; testicular tissues were collected, and cytoplasmic proteins were extracted; the levels of apoptosis-inducing factor (AIF), cytochrome c (cyto c), Bcl-2, Bax, procaspase-9, and procaspase-3 were measured by Western blot, and the activities of caspase-9 and caspase-3 were measured using a test kit.</p><p><b>RESULTS</b>Compared with the control group, all CS(2) exposure groups had significantly increased levels of cyto c in the cytoplasm of testicular tissue (P<0.05); in the 250 mg/m(3) CS(2) exposure group, the Bax/Bcl-2 ratio and activities of caspase-9 and caspase-3 increased significantly (P<0.05), and the content of procaspase-9 and procaspase-3 decreased significantly (P<0.05); in the 1250 mg/m(3) CS(2) exposure group, the relative expression levels of Bax and AIF in cytoplasm increased significantly (P<0.05), and the expression level of Bcl-2 decreased significantly (P<0.05).</p><p><b>CONCLUSION</b>Mitochondrial pathway plays an important role in the CS(2)-induced apoptosis of spermatogenic cells in testicular tissue among male rats.</p>

Effect of carbon disulfide exposure during peri-implantation period on levels of calcitonin and progesterone in uterus of mice / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To evaluate the effect of carbon disulfide (CS2) exposure during the peri-implantation period on the levels of calcitonin (CT) and progesterone (P4) in the uterus of pregnant mice and to investigate the mechanism of embryo loss induced by CS2 exposure during the peri-implantation period.</p><p><b>METHODS</b>A total of 168 healthy pregnant Kunming mice were randomly assigned to receive an intraperitoneal injection of CS2 (631.4 mg/kg) or olive oil (control) on gestational day (GD) 3, GD4, GD5, or GD6. The experiment was completed at different end points (GD4, GD5, GD6, GD7, and GD9). The levels of CT and P4 in the uterus were measured by enzyme-linked immunosorbent assay at each end point.</p><p><b>RESULTS</b>The numbers of implanted embryos in GD3, GD4, GD5, and GD6 exposure groups significantly decreased by 42.85%, 63.74%, 60.45%, and 47.26%, respectively,compared with those in control group (P < 0.01). The GD3, GD4, GD5, and GD6 exposure groups had significantly decreased CT levels at each end point (P < 0.05), and the GD3, GD4, and GD5 exposure groups had significantly decreased P4 levels (P < 0.05). In the GD3, GD4, GD5, and GD6 exposure groups, the number of implanted embryos was positively related with the levels of CT and P4 expressed in the uterus (r = 0.670, P < 0.01; r = 0.632, P < 0.01); the expression level of CT was positively related with that of P4 in the uterus of pregnant mice (r = 0.325, P < 0.01).</p><p><b>CONCLUSION</b>Exposure to CS2 during the peri-implantation period can reduce the expression levels of CT and P4 in the uterus of pregnant mice, which might be one of the molecular mechanisms of embryo loss induced by CS2 exposure.</p>

Occupational Neurotoxic Diseases in Taiwan

Occupational neurotoxic diseases have become increasingly common in Taiwan due to industrialization. Over the past 40 years, Taiwan has transformed from an agricultural society to an industrial society. The most common neurotoxic diseases also changed from organophosphate poisoning to heavy metal intoxication, and then to organic solvent and semiconductor agent poisoning. The nervous system is particularly vulnerable to toxic agents because of its high metabolic rate. Neurological manifestations may be transient or permanent, and may range from cognitive dysfunction, cerebellar ataxia, Parkinsonism, sensorimotor neuropathy and autonomic dysfunction to neuromuscular junction disorders. This study attempts to provide a review of the major outbreaks of occupational neurotoxins from 1968 to 2012. A total of 16 occupational neurotoxins, including organophosphates, toxic gases, heavy metals, organic solvents, and other toxic chemicals, were reviewed. Peer-reviewed articles related to the electrophysiology, neuroimaging, treatment and long-term follow up of these neurotoxic diseases were also obtained. The heavy metals involved consisted of lead, manganese, organic tin, mercury, arsenic, and thallium. The organic solvents included n-hexane, toluene, mixed solvents and carbon disulfide. Toxic gases such as carbon monoxide, and hydrogen sulfide were also included, along with toxic chemicals including polychlorinated biphenyls, tetramethylammonium hydroxide, organophosphates, and dimethylamine borane. In addition we attempted to correlate these events to the timeline of industrial development in Taiwan. By researching this topic, the hope is that it may help other developing countries to improve industrial hygiene and promote occupational safety and health care during the process of industrialization.

Occupational Neurotoxic Diseases in Taiwan

Occupational neurotoxic diseases have become increasingly common in Taiwan due to industrialization. Over the past 40 years, Taiwan has transformed from an agricultural society to an industrial society. The most common neurotoxic diseases also changed from organophosphate poisoning to heavy metal intoxication, and then to organic solvent and semiconductor agent poisoning. The nervous system is particularly vulnerable to toxic agents because of its high metabolic rate. Neurological manifestations may be transient or permanent, and may range from cognitive dysfunction, cerebellar ataxia, Parkinsonism, sensorimotor neuropathy and autonomic dysfunction to neuromuscular junction disorders. This study attempts to provide a review of the major outbreaks of occupational neurotoxins from 1968 to 2012. A total of 16 occupational neurotoxins, including organophosphates, toxic gases, heavy metals, organic solvents, and other toxic chemicals, were reviewed. Peer-reviewed articles related to the electrophysiology, neuroimaging, treatment and long-term follow up of these neurotoxic diseases were also obtained. The heavy metals involved consisted of lead, manganese, organic tin, mercury, arsenic, and thallium. The organic solvents included n-hexane, toluene, mixed solvents and carbon disulfide. Toxic gases such as carbon monoxide, and hydrogen sulfide were also included, along with toxic chemicals including polychlorinated biphenyls, tetramethylammonium hydroxide, organophosphates, and dimethylamine borane. In addition we attempted to correlate these events to the timeline of industrial development in Taiwan. By researching this topic, the hope is that it may help other developing countries to improve industrial hygiene and promote occupational safety and health care during the process of industrialization.

Outbreak of Sudden Cardiac Deaths in a Tire Manufacturing Facility: Can It Be Caused by Nanoparticles?

OBJECTIVES: The purpose of this study was to review clinical characteristics and working environments of sudden cardiac death (SCD) cases associated with a tire manufacturer in Korea, and review possible occupational risk factors for cardiovascular disease including nanoparticles (ultrafine particles, UFPs). METHODS: We reviewed (i) the clinical course of SCD cases and (ii) occupational and non-occupational risk factors including chemicals, the physical work environment, and job characteristics. RESULTS: Possible occupational factors were chemicals, UFPs of rubber fume, a hot environment, shift work, overworking, and noise exposure. The mean diameter of rubber fume (63-73 nm) was (larger than diesel exhaust [12 nm] and outdoor dust [50 nm]). The concentration of carbon disulfide, carbon monoxide and styrene were lower than the limit of detection. Five SCD cases were exposed to shift work and overworking. Most of the cases had several non-occupational factors such as hypertension, overweight and smoking. CONCLUSION: The diameter of rubber fume was larger than outdoor and the diesel exhaust, the most well known particulate having a causal relationship with cardiovascular disease. The possibility of a causal relation between UFPs of rubber fume and SCD was not supported in this study. However, it is necessary to continue studying the relationship between large sized UFPs and SCD.

Work Environments and Exposure to Hazardous Substances in Korean Tire Manufacturing

OBJECTIVES: The purpose of this study is to evaluate the tire manufacturing work environments extensively and to identify workers' exposure to hazardous substances in various work processes. METHODS: Personal air sampling was conducted to measure polycyclic aromatic hydrocarbons, carbon disulfide, 1,3-butadiene, styrene, methyl isobutyl ketone, methylcyclohexane, formaldehyde, sulfur dioxide, and rubber fume in tire manufacturing plants using the National Institute for Occupational Safety Health Manual of Analytical Methods. Noise, carbon monoxide, and heat stress exposure were evaluated using direct reading instruments. Past concentrations of rubber fume were assessed using regression analysis of total particulate data from 2003 to 2007, after identifying the correlation between the concentration of total particulate and rubber fume. RESULTS: Workers were exposed to rubber fume that exceeded 0.6 mg/m3, the maximum exposure limit of the UK, in curing and production management processes. Forty-seven percent of workers were exposed to noise levels exceeding 85 dBA. Workers in the production management process were exposed to 28.1degrees C (wet bulb globe temperature value, WBGT value) even when the outdoor atmosphere was 2.7degrees C (WBGT value). Exposures to other substances were below the limit of detection or under a tenth of the threshold limit values given by the American Conference of Governmental Industrial Hygienists. CONCLUSION: To better classify exposure groups and to improve work environments, examining closely at rubber fume components and temperature as risk indicators in tire manufacturing is recommended.