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AU MUTO-H, TAKIZAWA-Y. TI DIOXINS IN CIGARETTE SMOKE. SO ARCH-ENVIRON-HEALTH 44 (3). 1989. 171-174. IN DEP PUBLIC-HEALTH, AKITA UNIV SCH MED, HONDO 1-1-1, AKITA 010, JPN. AB Dioxins in cigarettes, smoke, and ash were determined using gas chromatography/mass spectrometry. The total concentration of polychlorinated dibenzo-p-dioxins (PCDDs) in cigarette smoke was approximately 5.0 .mu.g/m3 at the maximum level, whereas various congeners from tetra-octa-chlorodibenzo-p-dioxin (-CDD) were detected. Particularly, the total concentrations of hepta-CDD congeners was the highest among these congeners. Mass fragmentograms of various PCDD congeners were similar to those in flue gas samples collected from a municipal waste incinerator. The PCDD congeners that were not present in the cigarettes were found in the smoke samples. The 2,3,7,8-TCDD toxic equivalent value.sbd.an index for effects on humans.sbd.for total PCDDs in smoke was 1.81 ng/m3 using the toxic factor of the United States Environmental Protection Agency. Daily intake of PCDDs by smoking 20 cigarettes was estimated to be approximately 4.3 pg .cntdot. kg body weight/day. This value was close to that of the ADIs: 1-5 pg .cntdot. kg body weight/day reported in several countries. A heretofore unrecognized health risk was represented by the presence of PCDDs in cigarette smoke.


AU Ott-M-G, Zober-A. TI Morbidity study of extruder personnel with potential exposure to brominated dioxins and furans. II results of clinical laboratory studies. SO Occupational-and-Environmental-Medicine 53 (12). 1996. 844-846. ISSN 1351-0711. IN Occupational Med Health Protection Dep, BASF Aktiengesellschaft, D-67056 Ludwigschaften, Germany. AB Objectives-To test whether dioxins affect liver and thyroid function, lipid metabolism and glucose or immunological variables, in workers exposed to brominated dioxins and furans. Methods-34 male production employee (29 were extruder operators) and eight technical support personnel were studied, all of whom were potentially expose to polybrominated dibenzo-p-dioxins (PBDDs) and furans (PBDFs) during production of resins containing polybrominated diphenyl ethers (PBDEs). Controls were from a similar resin producing plant that did not use PBDEs. Blood samples were analysed for tetra, penta, and hexabrominated congeners, but 2,3,7,8-TBDD was the only exposure measure used in the regression analyses. Seven liver function indicators, five measures of blood lipids and glucose, four haematology and blood coagulation measures, and three measures of thyroid function were examined. Results-None of the variables was statistically related to concentration of 2,3,7,8-TBDD in the regression analyses. Cigarette smoking was related to several outcomes at the 0.05 level: aspartate aminotransferase, alanine aminotransferase, glutamate dehydrogenase (GLDH), erythrocyte sedimentation rate, and white blood cell count. Body mass index was also related to alanine aminotransferase, gamma- glutamyltranspeptidase, cholinesterase, GLDH, cholesterol, triglycerides, high density lipoprotein, low density lipoprotein, and glucose concentrations. No definitive associations between liver, blood lipid, thyroid, or immunological variables and exposure to brominated dioxins or blood lipid concentration of 2,3,7,8-TBDD were found. Conclusions-The study population was small and hence the findings must be interpreted with caution. Nevertheless, these results provide a base for interpreting the results of clinical studies in similarly exposed populations.


AU Malkin-R. TI Occupational and environmental lead and PCB exposure at a scrap metal dealer. SO Environmental-Research 70 (1). 1995. 20-23. ISSN 0013-9351. IN Div Surveillance, Hazard Evaluations Field Studies, Natl Inst Occupational Safety Health, 4676 Columbia Parkway, Mail Stop R-10, Cincinnati, OH 45226-1998, USA. AB Blood lead levels (BPb) and serum polychlorinated biphenyl levels (PCB) were obtained from 17 employees at two adjacent scrap metal dealers. One facility was located outdoors, directly on top of soil known to be contaminated with lead and PCBs, and the other was located indoors with a concrete floor. BPbs ranged from 4.0 to 39.8 mu-g/dl (mean 19.9 mu-g/dl, geometric mean 17.5 mu-g/dl) and PCB levels ranged from lt 1 to 65.3 ppb (mean 7.5 ppb). There was no significant difference in either BPb or serum PCB between the two sites. BPb was significantly correlated with the number of cigarettes smoked at work, and both BPb and serum PCB were significantly related to eating lunch outside the lunchroom, suggesting hand-to-mouth contact as a source of exposure. The lack of difference in BPb between employees of the two scrap metal dealers suggests an ongoing source of lead exposure at the sites, other than the soil.


AU Flesch-Janys-D, Becher-H, Gurn-P, Jung-D, Konietzko-J, Manz-A, Paepke-O. TI Elimination of polychlorinated dibenzo-p-dioxins and dibenzofurans in occupationally exposed persons. SO Journal-of-Toxicology-and-Environmental-Health 47 (4). 1996. 363-378. ISSN 0098-4108. IN Med Cent Chemical Workers' Health, Fuhlsbuettler Str 401, 22309 Hamburg, Germany. AB The elimination of 2,3,7,8-substituted polychlorinated dibenzo-p- dioxins and dibenzofurans (PCDD/F) was investigated in a group of n = 43 exposed workers with 2 blood measurements and n = 5 workers with 3 measurements. Under the assumption of a one-compartment, first-order kinetic model the median half-life for 2,3,7,8-TCDD was 7.2 yr, while for the other dioxins the estimates were between 3.7 yr for 1,2,3,4,6,7,8-HpCDD (hepta-chlorinated) and 15.7 yr for 1,2,3,7,8- PCDD (penta-chlorinated). For the furans median half-lives between 3.0 yr for 1,2,3,4,6,7,8-HpCDF and 19.6 yr for 2,3,4,7,8-PCDF were observed. There was no indication for a deviation from a first-order kinetic. Increasing age and percent body fat were associated with increasing half-life for most of the congeners. Smokers in general had a faster decay than non- and ex-smokers. In summary, the higher chlorinated PCDD/F like TCDD appear to be highly persistent in humans with half-lives ranging between 4 and 12 yr.


AU Halperin-W, Kalow-W, Sweeney-M-H, Tang-B-K, Fingerhut-M, Timpkins-B, Wille-K. TI Induction of P-450 in workers exposed to dioxin. SO Occupational-and-Environmental-Medicine 52 (2). 1995. 86-91. ISSN 1351-0711. IN Div Surveillance Hazard Evaluations Field Studies, National Inst Occupational Safety Health, Cent Disease Control Prevention, 4676 Columbia Parkway, Cinicinnati, OH 45226, USA. AB Objectives: To examine the effects of occupational exposure to substances contaminated with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on cytochrome P-4501A2 activity in a cross sectional medical survey. Methods: The exposed workers had been employed at two chemical plants gt 15 years earlier in the manufacture of 2,4,5- trichlorophenol and its derivatives. The control group consisted of people with no occupational exposure to phenoxy herbicides and who lived within the communities of the exposed workers. A total of 58 workers and 125 unexposed controls participated in the analysis. Cytochrome P-450 activity was assessed with a test that measures caffeine metabolites in the urine. A ratio of metabolites of caffeine (CMR) constituted a measure of P-4501A2 activity. Results: Compared with the control group in multivariate logistic regression, raised non-significant associations were found for three of four categories of TCDD in exposed workers (TCDD lt 20 pg/g, odds ratio (OR) 1.7, 95% confidence interval (95% CI) 0.6 to 5.0, TCDD 20-66, OR 0.3, 95% CI 0.0 to 1.7; TCDD 67-147, OR 2.3, 95% CI 0.6 to 8.8; TCDD gtoreq 148, OR 3.1, 95% CI 0.8 to 12.5). We found a strongly significant association of CMR and urinary cotinine, a measure of smoking, and urinary free ethanol. We found weak non-significant associations between P-4501A2 activity and increased serum TCDD among workers. Conclusion: The absence of an association between serum TCDD and cytochrome P-4501A2 may be due to the size of the study, insensitivity of the CMR to assess cytochrome P-4501A2 activity, or inadequate levels of exposure, although these were among the highest in human groups tested.


AU Peltola-V, Mantyla-E, Huhtaniemi-I, Ahotupa-M. TI Lipid peroxidation and antioxidant enzyme activities in the rat testis after cigarette smoke inhalation or administration of polychlorinated biphenyls or polychlorinated naphthalenes. SO Journal-of-Andrology 15 (4). 1994. 353-361. ISSN 0196-3635. IN Dep Physiology, Univ Turku, Kiinamyllynkatu 10, SF-20520 Turku, FIN. AB Lipid peroxidation products and antioxidant enzyme activities were studied in the rat testis following exposures to cigarette smoke, polychlorinated biphenyls (PCBs), or polychlorinated naphthalenes (PCNs). Three hours after a single 1-hour period of smoke inhalation, the levels of fluorescent chromolipids and thiobarbituric acid- reactive species (TBARS) were markedly increased in the testis (+49%, P lt 0.01, and +43%, P lt 0.05, respectively). Twelve hours after daily smoking for 1 hour, for 1, 5, or 10 days, such an increase was not found. Activities of the antioxidant enzymes superoxide dismutase (SOD), catalase, glutathione peroxidase (GSH-Px), glutathione transferase (GSH-Tr), or hexose monophosphate shunt (HMS) were not affected immediately, 3 hours, or 12 hours after a single smoking session. Twelve hours after smoking for 5 days, the activity of catalase was decreased (-16%, P lt 0.05). Smoking exposures had no consistent effects on serum follicle-stimulating hormone (FSH), luteinizing hormone (LH), or testosterone concentrations. Single i.p. injections of PCB or PCN mixtures resulted in decreases in testicular SOD activity 1 day after the exposures (-14%, P lt 0.05, and -51%, P lt 0.01, respectively). Catalase activity also decreased after both exposures (-30 to -42%, P lt 0.05, at days 1-7 after PCB exposure, and -37 to -43%, P lt 0.05, at days 3-7 after PCN exposure). Ninety days after the PCN exposure, activities of GSH-Px and GSH-Tr were decreased in the testis (-20%, P lt 0.05, and -26%, P lt 0.05, respectively). The only statistically significant change in lipid peroxidation measurements in the testes of PCB- or PCN-treated rats was a decrease in TBARS by 13% (P lt 0.01) 1 day after PCN exposure. The main findings of this study were the increase in lipid peroxidation in the rat testis after cigarette smoke inhalation and the impairment of the function of the enzymatic antioxidant defense after exposures to PCBs or PCNs. These results suggest that free radical-dependent mechanisms may play an important role in the testicular toxicity of environmental chemicals.


AU HOVINGA-M-E, SOWERS-M, HUMPHREY-H-E-B. TI ENVIRONMENTAL EXPOSURE AND LIFESTYLE PREDICTORS OF LEAD CADMIUM PCB AND DDT LEVELS IN GREAT LAKES FISH EATERS. SO ARCH-ENVIRON-HEALTH 48 (2). 1993. 98-104. IN DEP EPIDEMIOL, SCH PUBLIC HEALTH, UNIV ALABAMA BIRMINGHAM, UAB STATION, BIRMINGHAM, AL 35294. AB A previously characterized cohort of 115 Great Lakes fish eaters and 95 non-fish-eating regional controls was reexamined in 1989. Levels of blood lead and cadmium and serum PCB and DDT were measured. Lifestyle characteristics, including recent and historic fish consumption, were evaluated as predictors of contaminant levels using multivariate regression analysis. Significantly elevated serum PCB and DDT levels were observed in fish eaters, compared with controls. Historic fish consumption, rather than recent consumption, was identified as the primary predictor of current serum levels. Mean blood lead and cadmium were also significantly higher in fish eaters than in controls. However, the primary predictors of lead and cadmium were behavioral exposures-specifically smoking and self-reported occupational and recreational exposure-rather than fish consumption. These findings illustrate the importance of evaluating a variety of possible sources when investigating human exposure to environmental contaminants.


AU ZOBER-M-A, OTT-M-G, PAEPKE-O, SENFT-K, GERMANN-C. TI MORBIDITY STUDY OF EXTRUDER PERSONNEL WITH POTENTIAL EXPOSURE TO BROMINATED DIOXINS AND FURANS I. RESULTS OF BLOOD MONITORING AND IMMUNOLOGICAL TESTS. SO BR-J-IND-MED 49 (8). 1992. 532-544. IN OCCUPATIONAL MED HEALTH PROTECTION DEP, BASF AKTIENGESELLSCHAFT, LUDWIGSHAFEN, GER. AB The potential for exposure of employees to polybrominated dibenzofurans (PBDFs) and dibenzo-p-dioxins (PBDDs) during extrusion blending of resins containing decabromodiphenyl ether was established through previous air monitoring (area samples) and biomonitoring studies. The findings presented herein are further biomonitoring results for 42 employees and immunological tests for exposed and referent employees. Among potentially exposed men, 2,3,7,8-TBDF and 2,3,7,8-TBDD concentrations in blood lipid ranged from non-detectable to 112 parts per trillion (ppt) and from non-detectable to 478 ppt respectively. Biomonitoring results correlated well with assignments in the extruder work area when adjusted for process changes and engineering improvements and provided biological half life estimates of between 1.1 and 1.9 years for 2,3,7,8-TBDF and between 2.9 and 10.8 years for 2,3,7,8-TBDD. Resuls for 16 measures of the immune system were examined in relation to exposure (exposed v referent group) and in relation to the biomonitoring data. Some individual trends in immunological parameters with exposure and covariates such as age and cigarette smoking were found (for example, an increase in complement C4 with increasing concentrations of PBDFs and PBDDs, increased lymphocyte subpopulation counts with cigarette smoking); however, the overall clinical assessment was that the immune system of exposed employees was not adversely impacted at these burdens of PBDFs and PBDDs.


AU HEUSSEN-G-A-H, HIKSPOORS-M-L-J, SPENKELINK-A, BROUWER-A, KOEMAN-J-H. TI INHIBITION OF BINDING OF THYROXINE TO TRANSTHYRETIN BY OUTDOOR AND INDOOR AIRBORNE PARTICULATE MATTER AND EFFECTS ON THYROID HORMONE AND VITAMIN A METABOLISM IN RATS. SO ARCH-ENVIRON-CONTAM-TOXICOL 23 (1). 1992. 6-12. IN DEP TOXICOL, AGRIC UNIV TUINLAAN 5, 6703 HE WAGENINGEN, NETH. AB Previous studies have indicated that chemicals, e.g., hydroxylated polychlorinated biphenyls (PCBs) decrease plasma thyroxin levels through interaction with transthyretin. As a consequence, plasma vitamin A and thyroxin are depleted. Both thyroxin and vitamin A are important regulators of normal epithelial differentiation and proliferation and might act in the promotion phase of carcinogenesis. In the present report, extracts of indoor and outdoor airborne particulate matter (APM), originating from different pollution sources, were tested for a possible interaction in vitro and in vivo with thyroxin and vitamin A. Results indicated that all APM extracts significantly interfered with thyroxin binding to transthyretin. In all cases, the more polluted samples inhibited binding more than the corresponding control samples. Exposure of rats to cigarette smoke extract induced clear changes in plasma thyroxin and triiodothyronin hormone levels. Triidothyronin levels were reduced most. Effects on plasma vitamin A levels were also found, but these were less clear. In addition a decrease in lung vitamin A levels was found, but this decrease was not statistically significant. Exposure of rats to an outdoor APM extract induced significant changes in plasma triiodothyronin levels. Effects on thyroxin levels were not significant, although the same trend was seen as for the cigarette smoke APM extract. No changes in plasma or liver vitamin A concentrations were induced by the outdoor APM extract. Lung vitamin A levels were decreased, but again this decrase was not statistically significant. Taken together, the present report shows that APM extracts have the potency to interfere with thyroid hormone metabolism both in vitro and in vivo and probably with vitamin A metabolism as well. As the thyroxin-transthyretin binding assay is rapid and sensitive, this parameter may be a useful new biomarker for assessing air quality.


AU DAGNELIE-P-C, VAN-STAVEREN-W-A, ROOS-A-H, TUINSTRA-L-G-M-T, BUREMA-J. TI NUTRIENTS AND CONTAMINANTS IN HUMAN MILK FROM MOTHERS ON MACROBIOTIC AND OMNIVOROUS DIETS. SO EUR-J-CLIN-NUTR 46 (5). 1992. 355-366. IN INSTITUTE OF INTERNAL MED, II, ERASMUS UNIV OF ROTTERDAM, PO BOX 1738, 3000 DR ROTTERDAM, NETHERLANDS. AB The effect of alternative dietary habits and prolonged lactation on the nutrient and contaminant concentrations in human milk was studied. The study sample consisted of mothers on macrobiotic diets, containing little or no dairy products and meat, at 2-3 months postpartum (n = 9) and 9-13 months postpartum (n = 12), and mothers of omnivorous diets at 2-3 months postpartum (n = 10). Protein and zinc concentrations in breast-milk from macrobiotic mothers decreased with stage of lactation. After adjustment for stage of lactation, milk from macrobiotic mothers contained less calcium, magnesium and saturated fatty acid C15:0-C20:0, and more polyunsaturated fatty acids. Observed tendencies for lower protein and fat and higher lactose concentrations in the macrobiotic group were not statistically significant. Concentrations of vitamin B12, HCB and polychlorinated biphenyls (PCB 118, PCB 138, PCB 153 and PCB 180) were lower in the macrobiotic group. After adjustment for confounding variables, meat and fish consumption, but not dairy products, contributed to vitamin B12 concentrations. Meat and dairy products strongly contributed to breast-milk concentrations of dieldrin and PCBs, fish to PCB 118, and smoking to DDT and dieldrin. Our findings suggest that breast-milk contamination could be reduced by abstinence from smoking and a moderate intake of animal products. However, risk of nutritional deficiencies rules out complete avoidance of meat, fish or dairy products. Quantitative research on the effects of a reduced consumption of animal products, as well as smoking, on breast-milk contamination is warranted.


AU COGGON-D, PANNETT-B, WINTER-P. TI MORTALITY AND INCIDENCE OF CANCER AT FOUR FACTORIES MAKING PHENOXY HERBICIDES. SO BR-J-IND-MED 48 (3). 1991. 173-178. IN MRC ENVIRON EPIDEMIOL UNIT, UNIV SOUTHAMPTON, SOUTHAMPTON GEN HOSP, SOUTHAMPTON SO9 4XY. AB To assess the possible carcinogenicity of phenoxy herbicides and related chlorophenols and dioxins, the International Agency for Research on Cancer is coordinating an international collaborative study of workers exposed to these compounds in their production or use. Four British cohorts of chemical manufacturers which have been recruited to the survey are described. They comprise a total of 2239 men employed during 1963-85. These subjects were traced to 31 December 1987 through the National Health Service Central Register and the National Insurance Index, and their mortality compared with that in the national population. Two deaths were from non-Hodgkin's lymphoma with 0.87 expected. Both deaths occurred more than 10 years after first exposure to phenoxy compounds. One further non-Hodgkin's lymphoma was registered in a living subject with probable exposure to phenoxy compounds. No cases of soft tissue sarcoma or Hodgkin's disease were recorded. A nonsignificant excess of lung cancer (19 deaths observed, 14.2 expected) is probably attributable to chance or a confounding effect of smoking. In one cohort only there was increased mortality from circulatory disease (34 deaths observed, 20.4 expected). A nested case-control study did not point to any occupational cause for this excess, but further evaluation will be needed during continued follow-up.


AU FINGERHUT-M-A, HALPERIN-W-E, MARLOW-D-A, PIACITELLI-L-A, HONCHAR-P-A, SWEENEY-M-H, GREIFE-A-L, DILL-P-A, STEENLAND-K, SURUDA-A-J. TI CANCER MORTALITY IN WORKERS EXPOSED TO 2 3 7 8 TETRACHLORODIBENZO-P- DIOXIN. SO N-ENGL-J-MED 324 (4). 1991. 212-218. IN INDUSTRYWIDE STUDIES BRANCH, DIVISION SURVEILLANCE, HAZARD EVALUATIONS, FIELD STUDIES, NATIONAL INSTITUTE OCCUPATIONAL SAFETY HEALTH, CENTERS DISEASE CONTROL, 4676 COLUMBIA PKY, CINCINNATI, OHIO 45226. AB Background: In both animal and epidemiologic studies, exposure to dioxin (2,3,7,8-tetrachlorodibenzo-p-dioxin, or TCDD) has been associated with an increased risk of cancer. Methods: We conducted a retrospective cohort study of mortality among the 5172 workers at 12 plants in the United States that produced chemicals contaminated with TCDD. Occupational exposure was documented by reviewing job descriptions and by measuring TCDD in serum from a sample of 253 workers. Causes of death were taken from death certificates. Results: Mortality from several cancers previously associated with TCDD (stomach, liver, and nasal cancers, Hodgkin's disease, and non- Hodgkin's lymphoma) was not significantly elevated in this cohort. Mortality from soft-tissue sarcoma was increased, but not significantly (4 deaths; standardized mortality ratio (SMR), 338; 95 percent confidence interval, 92 to 865). In the subcohort of 1520 workers with .gtoreq. 1 year of exposure and .gtoreq.20 years of latency, however, mortality was significantly increased for soft- tissue sarcoma (3 deaths; SMR, 922; 95 percent confidence interval, 190 to 2695) and for cancers of the respiratory system (SMR, 142; 95 percent confidence interval, 103 to 192). Mortality from all cancers combined was slightly but significantly elevated in the overall cohort (SMR, 115; 95 percent confidence interval, 102 to 130) and was higher in the subcohort with .gtoreq. 1 year of exposure and .gtoreq. 20 years of latency (SMR, 146; 95 percent confidence interval, 121 to 176). Conclusions: This study of mortality among workers with occupational exposure to TCDD does not confirm the high relative risks reported for many cancers in previous studies. Conclusions about an increases in the risk of soft-tissue sarcoma are limited by small numbers and misclassification on death certificates. Excess mortality from all cancers combined, cancers of the respiratory tract, and soft-tissue sarcoma may result from exposure to TCDD, although we cannot exclude the possible contribution of factors such as smoking and occupational exposure to other chemicals.


AU KOPPE-J-G. TI DIOXINS AND FURANS IN THE MOTHER AND POSSIBLE EFFECTS ON THE FETUS AND NEWBORN BREAST-FED BABY. SO ACTA-PAEDIATR-SCAND-SUPPL 0 (360). 1989. 146-153. IN DEP NEONATOLOGY, ACADEMIC MED CENTER, UNIVERSITY AMSTERDAM, MEIBERGDREEF 9, 1105 AZ AMSTERDAM, THE NETHERLANDS. AB Due to pollution of the environment with PCBs, dioxins and furans these highly poisonous chemicals have accumulated in the adipose tissue of human beings. In breast milk of 14 mothers concentrations of dioxins and furans were found in milk fat, close to or in the range of the concentrations necessary to induce enzymes in "in vitro" rat liver cells (80-132 ppt). The hypothesis is that the above mentioned chemicals can be responsible for a vitamin K deficiency in the babies resulting in a bleeding analogous with phenobarbital. Both the pure TCDD content in milk fat and the content of dioxins and furans expressed as toxic equivalents (Nordic model) were higher in milk given to babies that presented a bleeding (4 our of 14). However, the sample size is too small for statistical analysis. No relation with age, parity, overweight, fish eating or smoking of the mother and dioxin content of her breast milk was seen in our small sample size.


AU BRANDT-RAUF-P-W, NIMAN-H-L. TI SERUM SCREENING FOR ONCOGENE PROTEINS IN WORKERS EXPOSED TO PCBS. SO BR-J-IND-MED 45 (10). 1988. 689-693. IN OCCUPATIONAL MED, COLUMBIA-PRESBYTERIAN MED CENTER, NEW YORK, NY. AB A cohort of 16 municipal workers engaged in cleaning oil from old transformers was examined for possible health effects from exposure to polychlorinated biphenyls (PCBs). In addition to the evaluation of routine clinical parameters (history, physical examination, liver function tests, serum triglycerides, serum PCB values), a new screening technique for the presence of oncogene proteins in serum using monoclonal antibodies was used to ascertain the potential carcinogenic risk from exposure in these workers. Except for one individual, serum PCB concentrations were found to be relatively low in this cohort, probably due to the observance of appropriate protective precautions. The results of liver function test were within normal limits and serum triglyceride concentrations showed no consistent relation to PCB concentrations. Six individuals, all of whom were smokers, showed abnormal banding patterns for fes oncogene related proteins. The individual with the highest serum PCB concentration also exhibited significantly raised levels of the H-ras oncogene related P21 protein in his serum. These oncogene protein findings may be indicative of an increased risk for the development of malignant disease in these individuals.


AU EMMETT-E-A, MARONI-M, JEFFERYS-J, SCHMITH-J, LEVIN-B-K, ALVARES-A. TI STUDIES OF TRANSFORMER REPAIR WORKERS EXPOSED TO PCBS II. RESULTS OF CLINICAL LABORATORY INVESTIGATIONS. SO AM-J-IND-MED 14 (1). 1988. 47-62. IN NATL INST OCCUPATIONAL HEALTH SAFETY, GPO BOX 58 SYDNEY, NSW 2001, AUSTRALIA. AB Thirty-eight transformer repairmen currently exposed to polychlorinated biphenyls (PCBs), 17 former transformer repairmen, and 56 comparison workers not known to be exposed to PCBs were studied. Measurements were made of serum liver function tests, gamma- glutamyl transpeptidase (GGT), lipid profile, thyroid function tests, and other serum biochemistry; hemoglobin; white cell count; 24-hour excretion of delta-aminolevulinic acid, porphyrins, 17- hydroxycorticosteriods and 17-ketosteroids; sperm count; spirometry; and antipyrine half-life to evaluate microsomal mixed function oxidase inuction. The total exposed group differed significantly from the comparison group in albumin, LDH, T4, T4-RT3 index, and actual /predicted FEV1. Significant differences among all three exposure groups were seen for albumin, T4, T4-RT3 index, and 17- hydroxycorticosteroid excretion. Differences in FEV1 were attributable to smoking. Significant correlations between serum PCBs and serum lipids were removed by adjustment for confounding variables. After adjustment for confounding variables, there was a statistically significant positive correlation between serum PCBs and GGT and a negative correlation between adipose PCBs and 17- hydroxycorticosteroid excretion. These may reflect subtle metabolic effects of PCBs.


AU LUND-J, ANDERSSON-O, RIPE-E. TI CHARACTERIZATION OF A BINDING PROTEIN FOR THE POLYCHLORINATED BIPHENYL METABOLITE 4 4' BISMETHYLSULFONYL-2 2' 5 5'- TETRACHLOROBIPHENYL PRESENT IN BRONCHOALVEOLAR LAVAGE FROM HEALTHY SMOKERS AND NON-SMOKERS. SO TOXICOL-APPL-PHARMACOL 83 (3). 1986. 486-493. IN DEP MED NUTR, KAROLINSKA INST, HUDDINGE UNIV HOSP, F69, S-141 86 HUDDINGE, SWED. AB Bronchoalveolar lavage (BAL) was performed in a group of healthy subjects (10 smokers and 10 nonsmokers) and the recovered fluid was shown to contain specific binding sites for a metabolite of a polychlorinated biphenyl (PCB), 4,4'-bis((3H) methylsulfonyl)-2,2',5,5'-tetrachlorobiphenyl ((3H-MeSO2)2TCB). The sites seem to reside within a protein-like component and the apparent dissociation constant (Kd) for the binding was .apprx. 2 .times. 10-7 M regardless of the smoking status of the subject. However, the maximum number of binding sites (Bmax) was significantly lower for the smokers (p < 0.001). Competition studies indicated that some PCB methyl sulfones had similar affinities for the specific binding sites as (MeSO2)2TCB. Physicochemical characterization of the human (3H-Me SO2)2TCB-binding protein indicated a Stokes radius of 22 .ANG. and a sedimentation coefficient of 1.9 S, and on the basis of these parameters an apparent molecular weight of 17,700 was calculated. The binding protein had an apparent pI of 4.9. It is suggested that the specific binding protein for certain PCB methyl sulfones in bronchoalveolar lavage fluid from healthy subjects is responsible for the previously observed tendency of PCB metabolites to accumulate in human lung tissue.

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