Document 4Jko1MKjnj8Qq3n3dnzLwV87G

Possible health hazards of the pol y chlo r na l cd biphcnyJa. M. Berlin. Department of Environmental Health, University of Lund, Sweden Since the 1930s it has been Known that technical products contai ning polychlorinated biphenyls (PCD) can cause skin changes, socalled chlor-acne, and inflammatory conditions of the eyelids. Liver damage caused by occupational exposure to PCB has been reported from industry, and recently, in 1%S, an extensive epi demic of food poisoning in Japan caused by rice oil contaminated with PCB has been reported, in which neurological signs were ob served (1). To evaluate health hazard* in connection with a substance which is distributed in the environment, it i j vjecssary to consider St least three factors: 1. The extent of exposure. 2. The risk of accumulation of the substance or its meta bolites in the tissue. 3. The toxicity of the substance of its metabolites, ' In the following, I will discuss what la known for PCB in relation to these three factors. The earlier speakers have already described the common use of PCBe and their spread In the whole cco-system, especially in the aquatic environment. This widespread occurrence causee man to be exposed to PCB by food, water and air pollution. The larger part of the population, in the developed countries at least, is ex posed to PCB, and this exposure varies between groups of diffe- i rent occupation and of different food consumption habits. " Is there then any risk for accumulation of PCB or its metabolites in the human tissue? The answer is undoubtedly yes. PCB has^ HONS In-fit i 1 nt i fi r d in Imm.iti fat in scvor.il wcslcrn counl ri*s . Conc ( nl r.iliuns around b pprn have i.ccn reported in human fat tissue from West Germany (2), and around 1 ppm in 45% of an examined population in USA ('>). Similar figure* have been reported from Norweigan autopsy material (4), in which values ranging from 0-5 ppm were found in brain tissues. Two eases in USA have been found to have 200 and GOO ppm in fat tissue (5). Analysts of human breast milk has shown mean concentration* of around 0. 1 ppm in West Germany (2). WestrtO and N'ordn (6) in Sweden conducted si milar investigations and found a mean concentration in the Stock holm area of about 0. 025 ppm. Their investigation wa* conducted during the period between 1 967-1 972, and from their results it cannot be excluded that there has been a continuous increase of the concentration of PCD in mother's milk during this period in the Stockholm area. In Japan, not less than a thousand persons were poisoned by POO contaminated rice oil in 1968 (7). In seve ral of these cases with chronic disease, high concentrations of PCB were found in the tiosun eight months after exposure had ceased. Available data thus strongly indicate a risk of accumulation of PCB in human tissue on prolonged exposure. Present data also give reasons to believe that there is a major difference between diffe rent cnlorinated biphenyl1? in this respect. Those that have been identified in human fat ar- -.'nerally the more highly chlorinated ones, pcntachlorobiphcnyl.i and up to dccachlorobiphenyls (5), while the less chlorine.' 1 biphenyls have not been shown to have the same tendency for accumulation and retention in human tissue. The tendency of PCB to be retained on prolonged exposure does not in itself Imply a health hazard. A health hazard will not occur until the concentrations of PCB in critical organs or critical tissue have risen to a toxic level. Our knowledge about the toxicity of the PCDs is very limited and uncertain. Most data concerning the toxicity of PCB is derived from experiments and clinical observelion* after exposure to technical products of undefined composition with regard to their content of different PCDs as well as to possible Impurities originating during manufacture. Vos et al (8) has shown that at least two technical products contain chlorinated dibriw.o- *ons Ob^*5 inruns, compounds of high toxicity which cause signs similar to those described with so called PCD intoxication, as (or instance liver damage and skin manifestations. It has not been possible from the literature to find out whether KaneeMor. the technical preparation that caused the Japanese epidemic, also contains chlorinated dibenzofurans. However, the fact that this product also gave rise to an epidemic of chick oedema disease in Japan (7) indicates that this may have been the case. So far, no studies on the toxicology of a single defined PCB have been published in the literature. Judged from published observations on the toxicity of technical PCB preparations in mammals and clinical observations from the Japanese poison epidemic, and reported cases of occupa* tional diaeasc caused by PCB containing products, the following effects may arise if a sufficient doje of PCB is retained. 1. induction and stimulation of liver microtomes. Expert* mental observations indicate that higher chlorinated biphenyls are more effective than lower (9). 2. Liver damans (7). 3. Interference in fat ?..id ."ccnod metabolism with an in* crease in triglycerides in plasma, and excretion of 1 7*kctostevoido in urine (10). 4. Interference in porphyrin metabolism with an Increased excretion of porphyrins (! 1). 5. Acneiform dermat'ti`1 (71 6. Changes in the conduction velocity of peripheral nerves and interference ir. '.he corebrai cortical function (1). 7. poeto-toxlc effects causing foetal dfcath or congenital abnormalities as well as retarded development (12). 8. Immunodepression (1 3). It cannot be excluded that the PCB products used in experimental studies, and those to which cases of poisoning have been exposed, have contained impurities like chlorinated bentofurans. Thus, uome of the above listed effect* rv.y, partly or entirely, have been caused by such impurities. Epidemiological investigation'! in Japan indicate that ll dose of Kanechlor in affected personj was .m average around 2 g, and HONS 069926 varied from 0. b g mil upwards (7). Other data. elucidotin . doso response relation for toxic effects caused by PCBs in man, are not available. It lias to bo pointed out, however, that the Japa nese figures relate to K im-chlur and do not permit conclusions about different types of chlorinated biphenyls and the occurrence of toxic impurities in Kanechlor cannot be excluded. CONCLUSION The conclusion is that \t is today impossible to estimate the health hazards to man due to long term exposure to PCB, as we lack knowledge about their toxicity. There is an appreciable exposure to these compounds in our communities and there is an evident tendency to accumulation of chlorinated biphenyls in human tissue. It cannot be excluded that the present spread of PCB in the envi ronment can involve significant health hazards in the long rung, and it cannot be excluded 'hat there is a continuous increase of ex posure. It is questional1 l- whether steady state between pollution and distribution in th; eca-aysiem is obtained at present. *0NS 069927 RE* KRENCl.S 1. Yoshiyuki Murni and Yoshigoro Kuroiwa, Peripheral neuro pathy in chlorobiphenyi poisoning. Neurology, Vol. 21, Nov. 1971. 2. L. Acker und E. Schulte, Uber das Vorkommeti von chlo* ricrtcn Biphcnylen und Hcxachlorbcnzol neben chlorierten Insektiziden in Humanmilch und menschjichcm f ttgowcbe, Naturwissenschaffen 57, 497, 1970. 3. Harold A. Price and Robert L. Welch. Occurrence of Poly, chlorinated Biphenyls in Hum.rns, Env. Health Perspective*, Experimental Issue no, 1, 73-73, 1 972. 4. John Erik Bjerk. Renter ;iv DDT og polyklorcrle bi/enylcr i norsk human', matcriale, T. norske Largeforcn. , 92, 15*19, 1972. 5. Francis J. Biros, Anr.ila C. Walker and Angela Wedbcry. Polychlorinated Biphenyls In Human Adipose Tissue, Bulls* ,tin of Env. Contamination it Toxicology, Vol. 5, No. 4 1 970. 6. Gunnel WestOO and Koidu Nordn. Levels of organochlorine pesticides and polychlorinated tiphonyl* In Swedish human milk, Vir fdda, vol. 24, nr 4, 1972. 7. Masanori Kuratsune, Takcsumi Yoshimura, Junichi Matsu* xaka, and Atsuko Yamaguchi, Epidemiologic Study on Yusho, a Poisoning Caused by Ingestion of Rice Oil Contaminated with a Commercial Brand of Polychlorinated Biphenyls, Env, Health Perspectives, Experimental Issue no. 1, 119* 1 28, 1972. HONS Q6992B Noi'Vtr tK: Biuuw ,iml R. II. dr Vo*. Jdentific.ition *iu| Toxicological Evaluation of Chlorinated Dibensofur.m and Chlorinated Naphthalene in Two Commercial Polychlori nated Biphenyls, Pd Cosmet. Toxicol-, Vol. 8, 625-633, 1 970. David R. Dickers., Leonard C. Harbcr, Atlul'.a.i K.t ppa a and Alvito P. Alvarej. Polychlorinated biphenyls: Com parative effects of high and low chlorine containing Aroclors^on h c pa tic mixed function oxidase, Research Communications in Chemical Pathology and Pharmacology, Vol. 3, No. 3, 1972. Masanori Kurat3unc. An Abstract of Results of Laboratory Examinations of Palioi.tc with Vm.ho and of Animal Kxperimenta, r.'nv. Il.-al.h Perspective-*, Experimental i,:,,uo no. 1, 129-136, 1972. J.C. Vos and R.3. Be ins. Dermal Toxicity Studies of Technical Polychlorinated Biphenyls and Fractions Thereof in Rabbits, Toxicology ina'tPnTirvnacology, 19, 617-63 3, 1 97 !. lichiro Fur.nlau, Fuiviio Yan.'tshita, Yushi ito, Shin Ti igawa, Takako Funatsu, 'ink >hi Yushikane, Masao Unyushi, Toshi Kato, Mtchlaki Yakusuijl, Gen Okamoto, Selichiro Yamasaki, Tadashi Arima, Tsu'.jko Kuno, Hayami Ide and Ichiro lae. Polychlorbiphenyla (PCD) induced Fetopathy, The Kurume Medical Journal, Vol. 19. No. 1, 1972. J.G. Vos. Toxicology of PCBs for Mammals and for Birds, Env, Health Perspectives, Experimental Issue no. 1, 105-117, 1972. HONS 069929