Prostate cancer is the second most common cancer in men worldwide. There are many occupational factors that have been suggested to cause prostate cancer. Our aim was to evaluate the evidence for causality by a literature review of occupational factors. We searched literature in Medline and SCOPUS from 1966 to June 30, 2015 to identify occupational risk factors for prostate cancer. The following risk factors were selected: farmers/agricultural workers, pesticides – whole group, and separately organophosphate and organochlorine pesticides, carbamates and triazines, cadmium, chromium, cutting fluids, acrylonitrile, rubber manufacturing, whole body vibration, shift work, flight personnel, ionizing radiation, and occupational physical activity. For each factor a literature search was performed and presented as meta-analysis of relative risk and heterogeneity (Q and I² index). A total of 168 original studies met the inclusion criteria with 90,688 prostate cancer cases. Significantly increased risks were observed for the following occupational exposures: pesticides (metaRR = 1.15, 95% confidence interval [CI] = 1.01–1.32; I² = 84%), and specifically group of organochlorine pesticides (meta relative risk [metaRR] = 1.08, 95% CI = 1.03–1.14; I² = 0%), chromium (metaRR = 1.19, 95% CI = 1.07–1.34; I² = 31%), shift work (metaRR = 1.25, 95% CI = 1.05–1.49; I² = 78%) and pilots (metaRR = 1.41, 95% CI = 1.02–1.94; I² = 63%) and occupational physical activity in cohort studies (metaRR = 0.87, 95% CI = 0.81–0.94; I² = 0%). The literature review supports a causal association for a few of the previously suggested factors.
Acrylonitrile ; Cadmium ; Carbamates ; Chromium ; Cohort Studies ; Epidemiologic Studies ; Humans ; Male ; Motor Activity ; Occupational Exposure ; Pesticides ; Population Characteristics ; Prostate ; Prostatic Neoplasms ; Radiation, Ionizing ; Risk Factors ; Rubber ; Triazines ; Vibration

OBJECTIVETo explore the effects of acrylonitrile on T lymphocyte subsets, expression of toll-like receptor 4 and related cytokines in rats.

METHODSSixty-four Sprague-Dawley rats were randomly divided into 4 female groups and 4 male groups, and there were 8 rats in each group. Rats in each group were respectively given a single dose of 0, 5, 10 and 20 mg/kg acrylonitrile by gavage, once a day, 5 days a week, for 13 weeks. Blood and spleen T lymphocyte subsets was detected by flow cytometry, the mRNA expression of TLR4, IL-1β and TNF-α was analyzed by real-time quantitative PCR, the protein expression of TLR4 was evaluated by Western blot.

RESULTSCompared with control group, the percentages of blood CD3, CD4 T cells in 20 mg/kg female group and CD4/CD8 ratio in 5, 10 and 20 mg/kg female groups was significantly decreased, CD8 T cells in 20 mg/kg group was significantly increased (P < 0.05 or P < 0.01), blood CD3 T cells in 5 mg/kg male group, CD4 T cells and CD4/CD8 ratio in 20 mg/kg male groups were lower than that of control group, CD8 T cells in 20 mg/kg make group was significantly in oreased (P < 0.05 or P < 0.01). Spleen CD4, CD8 T lymphocyte percentages and CD4/CD8 ratio in 20 mg/kg female group decreased significantly, CD8 T cells in 20 mg/kg male group was significantly increased (P < 0.05 or P < 0.01), spleen CD3, CD4, CD8 T cells in 20 mg/kg male group and CD4/CD8 ratio in 10, 20 mg/kg male groups was also significantly decreased, CD3 T cells in 20 mg/kg and CD8 T cells in 10, 20 mg/kg male groups were significantly increased (P < 0.05 or P < 0.01) (TLR4 mRNA was lower expressed in 5, 10 and 20 mg/kg male groups and 10 mg/kg female group (P < 0.05 or P < 0.01), and TLR4 protein in 5 mg/kg female group and 20 mg/kg male group was significantly lower than control group (P < 0.05). The expression level of IL-1β mRNA was significantly decreased in 5, 10 and 20 mg/kg female group and 5, 10 mg/kg male group (P < 0.05 or P < 0.01), TNF-α mRNA was lower expressed in 10, 20 mg/kg female groups and 5, 10 mg/kg male groups (P < 0.01).

CONCLUSIONAcrylonitrile may lead to the changes of CD3, CD4, CD8 T lymphocyte percentages and CD4/CD8 ratio in rat blood and spleen, and also significantly effected the expression level of TLR4 mRNA and protein together with the secretion of IL-1β, TNF-α. This may cause effects on the cellular immune function.

Acrylonitrile ; toxicity ; Animals ; Female ; Interleukin-1beta ; metabolism ; Male ; Rats ; Rats, Sprague-Dawley ; T-Lymphocyte Subsets ; drug effects ; immunology ; Toll-Like Receptor 4 ; metabolism ; Tumor Necrosis Factor-alpha ; metabolism

OBJECTIVETo establish a method for rapid determination of airborne acrylonitrile using a portable gas chromatograph.

METHODSA single standard sample of acrylonitrile was prepared in a laboratory and sampled by the built-in constant flow pump of the portable gas chromatograph. The sample was then preconcentrated by the preconcentrator, thermally desorbed, separated by capillary columns, and detected by a micro argon ionization detector to determine the retention time. Retention time was then used to perform qualitative analysis. Under the set condition of gas chromatography, the external standard method was used to create a standard curve for quantitative analysis of acrylonitrile.

RESULTSThe linear range of acrylonitrile on the portable gas chromatograph was 0.25 to 3.00 mg/m(3). The regression equation was y = 10(-5) x-0.0275, r = 0.9977. The limit of detection was 0.005 mg/m(3), and the lower limit of quantification was 0.25 mg/m(3). The relative standard deviation was lower than 7.09%, and the degree of accuracy was 91.09-105.54%.

CONCLUSIONPortable gas chromatography is a simple, repeatable, and accurate method for rapid determination of airborne acrylonitrile.

Acrylonitrile ; analysis ; Air Pollutants, Occupational ; analysis ; Chromatography, Gas ; instrumentation ; Workplace

Acrylonitrile ; poisoning ; Adult ; Female ; Humans ; Male ; Middle Aged ; Occupational Diseases ; therapy

OBJECTIVETo study the effect of acrylonitrile (ACN) to cell growth, apoptosis, proliferation and related gene expression of rat normal glial cells (DI TNC1) and tumor glial cells (C6).

METHODSThe concentration of ACN on DI TNC1 and C6 were 25, 50 and 75 microg/ml. For cell growth, proliferation and apoptosis assay, the treated time was 24 hours, for microarray assay, the treated time was 4 and 24 hours.

RESULTSAfter treatment of DI TNC1 cell with 25,50 and 75 microg/ml ACN, the DNA synthesis index were decreased 93.1%, 81.3% and 74.9% as compared to control respectively, the apoptosis index was increased 118%, 122% and 143% as compared to controls respectively. The DNA synthesis and apoptosis indexes of C6 cell showed no change after treatment with ACN. The cell cycle and apoptosis pathway related genes, such as cyclin and p53, also showed changes after treatment with ACN.

CONCLUSIONACN inhibited the cell proliferation of DI TNC1, induced the apoptosis of DI TNC1 and had no effect on cell proliferation and apoptosis of C6 cells, and the related regulation gene expression changes further confirmed the results.

Acrylonitrile ; toxicity ; Air Pollutants ; toxicity ; Animals ; Apoptosis ; drug effects ; Cell Proliferation ; drug effects ; Cells, Cultured ; Gene Expression ; Neuroglia ; cytology ; drug effects ; Rats ; Tumor Cells, Cultured

Acrylonitrile ; toxicity ; Carcinogens ; toxicity ; Humans ; Mutagens ; toxicity ; Occupational Exposure

Acrylonitrile ; toxicity ; Animals ; Male ; Mice ; Mice, Inbred Strains ; Testis ; drug effects ; pathology

OBJECTIVETo investigate the application of micronucleus test of buccal mucosal cells in monitoring the genetic effect of acrylonitrile in the population exposed to the acrylonitrile.

METHODSForty-one healthy male workers in a chemical factory in Shanghai were selected as the low concentration acrylonitrile exposed group while forty-seven healthy male workers in an acrylonitrile factory in Shanghai were selected as the intermediate concentration acrylonitrile exposed group. At the same time, thirty-one male workers who had no toxicant exposure and lived in the same community were selected as the control group. The micronucleus test in buccal mucosal cells and lymphocytes were used respectively for assessing the genetic damage status of these men.

RESULTSThe rate of micronucleus in buccal mucosal cells in both acrylonitrile groups (the low concentration group: 3.68% +/- 2.72%; the intermediate concentration group: 4.00% +/- 2.38%) was significantly higher than that in the control group (2.03% +/- 2.20%) (P < 0.05). The rate of micronucleus in the intermediate concentration group (4.23% +/- 3.34%) was significantly higher than that in the control group (2.48% +/- 1.46%) (P < 0.05). There was the correlation between the micronucleus test of buccal mucosal cells and the micronucleus test of the lymphocytes in the peripheral blood in the acrylonitrile exposed population (r = 0.299-0.359, P < 0.05).

CONCLUSIONThe micronucleus test of buccal mucosal cells replacing the micronucleus test of the lymphocytes in the peripheral blood can be used as one of the screening indexes in the surveillance of the genetic damage in the acrylonitrile exposed population.

Acrylonitrile ; toxicity ; Adult ; Carcinogens ; toxicity ; Dose-Response Relationship, Drug ; Humans ; Lymphocytes ; drug effects ; Male ; Micronuclei, Chromosome-Defective ; chemically induced ; Micronucleus Tests ; Mouth Mucosa ; cytology ; Occupational Exposure

Acrylonitrile ; poisoning ; Acute Disease ; Adult ; Humans ; Male ; Parkinsonian Disorders ; chemically induced

OBJECTIVETo explore the mechanism of male reproductive toxicity induced by acrylonitrile (ACN).

METHODSMale Sprague-Dawley rats were daily administrated ACN by intraperitoneal injection 5 times a week for 13 weeks at the dose of 0, 7.5, 15.0 and 30.0 mg/kg body weight, respectively. The rats were sacrificed and testes were removed at the end of 4, 8, 13 or 15 weeks, respectively. The activities of glutathione peroxidase (GSH-Px), superoxide dismutase (SOD) and glutathione S-transferase (GST) and the levels of glutathione (GSH) and malonaldehyde (MDA) were detected in testes.

RESULTSFollowing ACN treatment of 4 weeks, the levels of GSH in ACN 15.0 mg/kg and 30.0 mg/kg group were (7.44 +/- 0.77) mg/g pro and (6.95 +/- 0.77) mg/g pro respectively, and the activity of GSH-Px was (70.89 +/- 4.01) U/mg pro in 30.0 mg/kg group, all of which were significantly higher than the control group (P < 0.05, P < 0.01). After 8 weeks, the levels of GSH decreased to (2.50 +/- 0.94) mg/g pro in ACN 30.0 mg/kg group (P < 0.01); the activities of SOD increased to (102.08 +/- 16.08) NU/mg pro and (113.30 +/- 17.20) NU/mg pro in ACN 15.0 mg/kg and 30.0 mg/kg group (P < 0.01). After 13 weeks, the levels of GSH declined in ACN 15.0 mg/kg and 30.0 mg/kg group, and the activities of GST decreased in ACN 30.0 mg/kg group, and of GSH-Px decreased in both doses group. However, the level of MDA [(0.68 +/- 0.16) nmol/mg pro] were significantly higher in 30.0 mg/kg group than that in control group [(0.38 +/- 0.12) nmol/mg pro] (P < 0.01). 2 weeks after stopping ACN treatment, the level of GSH restored to normal but the levels of MDA or the activity of GSH-Px in 30.0 mg/kg group were still higher or lower respectively than those of control (P < 0.05).

CONCLUSIONACN may impair the balance of antioxidant system, thus induce lipid peroxidation damage to rat testes.

Acrylonitrile ; toxicity ; Animals ; Dose-Response Relationship, Drug ; Glutathione ; metabolism ; Glutathione Peroxidase ; metabolism ; Glutathione Transferase ; metabolism ; Lipid Peroxidation ; drug effects ; Male ; Malondialdehyde ; metabolism ; Rats ; Rats, Sprague-Dawley ; Superoxide Dismutase ; metabolism ; Testis ; drug effects ; metabolism