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PCB's PagePolychlorinated Biphenyl Peterman, Paul H. (1983) Polychlorinated Biphenyl (PCB) Substitute Compounds In The Fox River System: Their Identification And Distribution. Master Thesis UWI-M "... the PCB substitutes (as well as PCB's themselves) have been released from waste paper during deinking-recycling by the B-G mill. The non-chlorinated PCB substitute compounds become chlorinated during bleaching operations within the mill. A leaching experiment with carbonless copy paper and a mild, aqueous chlorination experiment verified that the chemicals can be released from the paper and that they are able to become chlorinated." Peterman further "calculated log P values showed that all of the PCB substitutes were lipophilic and potentially able to bioaccumulate. He notes, "The non-chlorinated PCB substitute components of Isopropyl-biphenyl, Santosol 100 and Santosol 150 become chlorinted during their exposure to aqueous chlorinating agents in the mill's bleaching processes. Substituted derivatives contained one to three chlorine atoms." This should be a definite possibility at all recycling-deinking mills that use the process aformentioned process.See also:
Skin Damage and Absorption Summeries on PCB's http://www.foxriverwatch.com/dermal_skin_pcb_pcbs_1e.html A good summery on many PCB exposures. Plus much more information. The Fox River Watch is commended for their excellent site and information. See also TOXNET at http://toxnet.nlm.nih.gov PCB replacement, substitute chemical compounds from Mr. Peterman's AROCLOR, a PCB, made by Monsanto was used in CCP by several manufacturers. Aroclor 1242 Aroclor 1254 MSDS Environmental Health Perspectives EHP 104(1) Articles: Address
correspondence to P. E. Ganey, Department of Pharmacology and Toxicology,
Life Sciences Building, Michigan State University, East Lansing, MI 48824
USA. Received 25 July 1995; accepted 29 September 1995. "In conclusion, the results presented in this study are consistent with the hypothesis that neutrophils, upon exposure to Aroclor 1242, produce O2- by a mechanism that involves phospholipase A2-dependent release of arachidonic acid. The release of arachidonic acid by inflammatory cells upon exposure to PCBs may represent an additional mechanism of PCB-induced toxicity. Arachidonic acid and its metabolites have been implicated in a variety of inflammatory disease states including septicemia (36,37), rheumatoid arthritis (38), and systemic lupus erythematosus (39), as well as diseases characterized by cellular transformation such as hypertrophic transformation of the skin (40) and colon cancer (41). In addition, arachidonic acid has been implicated as a cytotoxicant in various models of tissue injury (42,43), and activation of phospholipase A2 is required for the cytotoxic effects of cytokines such as tumor necrosis factor (44). Therefore, the activation of phospholipase A2 and subsequent release of arachidonic acid from cells exposed to PCBs may be important in mechanisms of PCB toxicity." Environmental Health Perspectives Volume 106, Number 6, June 1998 Assessing the Cancer Risk From Environmental PCB's Vincent James Cogliano U.S. Environmental Protection Agency, National Center for Environmental Assessment, Washington, D.C. 20460 USA http://ehp.niehs.nih.gov/members/1998/106p317-323cogliano/cogliano-full.html "In the recent cancer study (1), groups of 50 male or female Sprague-Dawley rats were fed diets with 50, 100, or 200 ppm Aroclor 1016; 50 or 100 ppm Aroclor 1242; or 25, 50, or 100 ppm Aroclor 1254 or 1260. There were 100 controls of each sex. Exposure began when the rats were 6-9 weeks old, and the animals were killed 104 weeks later. Complete histopathologic evaluations were done for control and high-dose groups; for low- and mid-dose groups, evaluations were done for liver, brain, mammary gland, and male thyroid gland. Statistically significant increased incidences of liver tumors were found in female rats for all Aroclors and in male rats for Aroclor 1260 (Table 3). Fewer than a quarter of the tumors were malignant, but the proportion of tumors that were malignant increased with dose. In female rats, Aroclor 1254 appeared most potent, followed by Aroclors 1260 and 1242, with Aroclor 1016 markedly less potent. In male rats, only Aroclor 1260 caused liver tumors. " "To investigate tumor progression after exposure stops, this same study exposed groups of 24 female rats for 52 weeks; exposure was then discontinued for an additional 52 weeks before the rats were killed. For 52 weeks exposure to Aroclors 1242 or 1254, tumor incidences were approximately half those for 104 weeks exposure, that is, nearly proportional to exposure duration. In contrast, there were no tumors from 52 weeks exposure to Aroclor 1016, while for Aroclor 1260 incidences were generally greater than half those for 104 weeks exposure (Table 4). For 100 ppm Aroclor 1260, the incidence from 52 weeks exposure was greater than that from 104 weeks, 71 and 48%, respectively. " "Different patterns may hold for other cancers. In the study just described (1), thyroid gland follicular cell adenomas or carcinomas were increased in males for all Aroclors, and statistically significant trends were noted for Aroclors 1242 and 1254. The increases did not continue proportionately above the lowest dose, and no thyroid trends were apparent in females. " Endocrine Abstracts (2003) 5 P198 Effect of aroclor 1242 (PCB)
on the reproductive function of adult male rhesus monkey (Macaca mulatta)
MM Ahmad, SU Ahmad & S Tariq Department of Biological Sciences, Quaid-i-Azam University, Islamabad, Pakistan. "Adult male rhesus monkeys (Macaca mulatta) were given oral treatment of either Aroclor 1242 or vehicle (corn oil and glycerol) at a dose of 200 microgram/kg bw/day/animal for six months to investigate the effect of pollutant on plasma testosterone and morphology of testis and accessory glands. The animals used in this research have been treated humanely according to institutional guidelines, with due consideration to the alleviation of distress and discomfort. Aroclor 1242 treatment significantly decreased testicular size, declined testosterone levels in plasma and adversely affected spermatogenetic activity by disrupting epithelial organization. All the components of germinal epithelium reduced to a great extent. The spermatogonia were either hypertrophied or contained shrunken vesiculated cytoplasm containing distorted mitochondria and nuclei with variable degree of pyknosis. Sertoli cells were least affected by PCB treatment yet, nuclear infoldings were reduced to a considerable extent. Characteristic features of the treated Leydig cells were the presence of electron dense and electron opaque zones appearing as plaques, cell membrane abnormalities and high variability in nuclear shape and heterochromatin distribution. All the Aroclor 1242-treated accessory glands contained more connective tissue than their vehicle-treated counterparts. The epithelium contained many layers of irregular shaped necrotic cells that possessed stereocilia in the epididymides, either hypochromic and hypertrophied or hyperchromic and hypotrophied cells in the prostate and shrunken cuboidal cells with elongated nuclei in the seminal vesicles. It is concluded that Aroclor 1242 treatment cause severe structural alterations in gonads and accessory organs in adult male rhesus monkeys and these effects could have mediated through both estrogen and Ah receptors." Monsanto Hid Decades Of Pollution **** Aroclor 1248 used in Moore Patent 3,016,308. 3,016,308 is referenced in other ccp patents.
Environmental Health Prospectives Volume 113
Number 2
February 2005
Exposure to PCBs and p,p´-DDE and
Human Sperm Chromatin Integrity
Anna Rignell-Hydbom,1 Lars Rylander,1 Aleksander Giwercman,2 B.A.G. Jönsson,1 Christian Lindh,1 Patrizia Eleuteri,3 Michele Rescia,3 Giorgio Leter,3 Eugenia Cordelli,3 Marcello Spano,3 and Lars Hagmar1 1Department of Occupational and Environmental Medicine, Lund University Hospital, Lund, Sweden; 2Fertility Centre, Malmö University Hospital, Malmö, Sweden; 3Section of Toxicology and Biomedical Sciences, ENEA Casaccia Research Centre, Rome, Italy Abstract
Address correspondence to A. Rignell-Hydbom, Department of
Occupational and Environmental Medicine, Lund University, SE-221 85
Lund, Sweden. Telephone: 46-46-177280. Fax: 46-46-173669. E-mail:
Anna.Rignell-Hydbom@ymed.lu.se
This work was supported by grants from the European Commission,
Quality of Life and Management of Living Resources, Key Action Four
on Environment and Health (contract QLK4-CT-2001-00202), the Swedish
Research Council, the Swedish Research Council for Environment,
Agricultural Sciences and Spatial Planning, and the Medical Faculty,
Lund University.
The authors declare they have no competing financial interests.
Received 13 May 2004; accepted 22 November 2004.
Polychlorinated biphenyls (PCBs)"PCBs are synthetic
persistant organic pollutants which were manufactured between 1929 and
1977. Due to their non-flammability, chemical stability, high boiling
point and electrical insulating properties, PCBs were used in hundreds
of industrial and commercial applications including electrical, heat
transfer, and hydraulic equipment; as plasticizers in paints, plastics
and rubber products; in pigments, dyes and carbonless copy paper and
many other applications. Therefore, although the manufacture of PCBs
was banned in 1977, they are still found in older equipment and are
still being released in the environment.
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Last modified: July 21 2006, 05:02pm