Document Ed6XYqMy02y6NDZq3XwxEpnb4

PCB - Effects or, Bird s by J , B&ckslrOm Dept, of Pharmacology, Royal Veterinary College, Stockholm National Poisons and Pesticides Board, Stockholm Polychlorinated biphenyls (PCB) are widely distributed ir. O the environment and, according to many investigators, they a $/ toem to be ubiquitous as DDT (Risebrough el al. 19o: Koe- man ei a 1. 1969; Jensen el a 1. 1969; Presttl970; Jer sen O 1 966). Many observations concern high levels of PCBs ir. the avian fauna,, particularly in marine birds which aic at the top of a food chain in the sea. Larger residues have be en found in predatory birds than in omnivorous or herbivorous specie s, ' There is very little work, published on the avian toxicity of the PCBs. No observations concern any acute effects of these compound s .in the avian faunr. As regards the sublcthol effects, however, the situation may be different and there arc indi cations that the PCBs may be responsible for certain repro duction disturbances. There arc a few works on experimental toxicology. Koenun el al. (1969) fed a diet containing 2000 ppm of Phcnochlor DP6, a technical PCB mixture, to Japanese qua.Is, ail of which died between day 6 and 56 after dosing had started. Gas chromatographic analysis of the residues in liver and brain of these birds indicated that some of the more lightly chlorinated PCDs present in thu original mixture, had been mciaoohzed. Autopsy of the cuails demonstrated larte amount?, of fluid in the pericardial sac. Hy b rope n ca r b has been observed in cockerels do6ed with *S0G nnm of PCii (Arocdcr [2.42) in their diet fPliek et al. 1965) and m Ber.gaK-sc Preb- DSW 026679 STLCOPCB4010640 es fed with a diet containing various- amounts of Arochlor 1254 (Prosit ei al. J 970}, In the latter experiment were observed signs of acute poi soning including balance disturbance at perching, paralysis in the legs and trembling with shaking wings. At the autop sy was also observed enlarged kidneys. Flick el al, (1 965) fed Arochlor 1242 to dayold cockerels (200 or 400 ppm in the diet) p-nd reported, besides hyd.-opcricard, growth depression, abdominal and subcutaneous edema, hemorrhagic and enlarged kidneys and adrenals, a small spleen, a cream-coloured pale pancreas, decreased hemoglobin values, dermatitis and dc'feathering. They also discussed the similarity between the symptoms elicited by PCB s and those of the cluck edema disease, Certain difft rcnccs, however, exist and the possibility that the chick edema factor (today known to be c. mixture cf chlorinated dioy.incs) might be present in PC B - n i opa rations was not supported by gas chromatographic, ar-.nlyses performed by h'cCune c i al, (1962). McCune e', al. (19o2) alto fed a chlorinated bi phenyl to chicks (100 ppm) ar.d observed symptoms similar to those of chick edema di;-oa.se (hydropc ricard, subcutaneous and abdominal edema, hemorrha.gec of internal organs and enteritis). The toxicity of PCB as compared with other chlorinated hydro carbons, is somewhat difficult to establish, because, whereas e.g. DDT presents a relatively steep mortality curve, thecurve for a PCB ifc much more gradual. This means that at low dose rales. PCB may have a comparatively greater toxi city than similar amounts of DDT, but at higher dose ratur the toxicity of DDT is considerably higher. In the expe rimof Prcstt et al, (!970) with Bengalese finches . the e s tin':\e \ dose rate for 50 % mortality at 56 days was 254 mg/kg/d y. At low doses, PCB was more toxic than DDT; at higher <\r PCB was about 10 times less toxic than DDT. DSW 026680 STLCOPCB4010641 Prestt et al. (1970) also gave some values of the concentra tions of PCB in some organs of the birds. One bird, killed after 8 weeks daily feeding with 367 ng oJf PCB, showed H ppm in the brain, 25 ppm in the liver, 574 ppm in fat and 61 ppm as a moan in the rest of the body, 9 % of the inges ted amount remained in the body, and was stored mainly in the depot and organ fa , Some of the birds v/cre starved prior to analysis. Starvation resulted in a redistribution of PCB with an increase of the brain concentration. The population declines of many avian species in Europe and North America has been attributed to the use of chlori nated hydrocarbons. This decline has been traceable not to the death of adults, but to a drastic ^rop in reproduction, The symptoms observed in connection with this decline have included late breeding, failure to lay eggs, a remarkable thinning of the shells and much breakage of the eggs that are laid, eating of broken eggs; by the parent's, failure to lay more eggs after earlier clutchc:.*; have hen; lost, reduced clutch size and a high mortality of the embryos arid anion;' fledglings. The regions of population decline co:r.cicie w.ih areas where chlorinated hydrocarbons are widely applied. The pato-phy siological mcchani sms behind these symptoms are uncertain, but may to sonic parts be attributed to the capacity of the chlorinated hydrocarbons to disturb the hor mone balance and the function of enzymes. It has been demonstrated in pigeons, that PCDs, like POT and DDE, have the capacity lo induce steroid hybroxvlating liver enzymes to increase their breakdown of c s l rad iol (ID sc brogh et al. 1 968). The PCB s arc more powerful inducers of these e.u uy rr. than DDT or DDE. The breakdown of estradiol i.\ p:ge^. livcr was increased 2,5 times by DDE, 3.5 times by DDT and 5. 5 times by PCB, in spite of that only half in much . DSW 026681 STLCOPCB4010642 PCB as DDT or DDE was used (Risebrough el a] , 1 968). The late breeding, the delayed egg-laying and the failure to lay again after early loss of eggs could be explained in this way because estradiol 16 involved in the stimulation and maintenance of the sex organs ar.d breeding behaviour, A delayed laying may be very serious for certain spec es because this reduces the chances for the young to get opti mum of feed and consequently reduces the optimal chance for survival. Concerning this risk it appears that the PCBs are greater threats to birds than DDT, V The failure to lay at all could also be caused by decreased hormone concentrations resulting from hepatic enzyme indue* tion or apparent failure to lay could ue caused by early break age and eating of eggs. A reduced clutch size could also be caused by the breakage of eggs. Since about 1947, there has been a sharp decrease in the thickness of the* egg shell of Certain predatory birds who-c populations were decreasing (Risebrough 1968 and others). Thin eggshells were found in avian species who accumulated high concentrations of chlorinated hydroca rbons. In ur.ccnlaminated populations of these species the production of egg shells was normal, idxirernely thin eggshells have been found in the brown pelican in California where the average percen tage thinning was 53 % and the extreme was 95 `To. In North American peregrines, contaminated with DDT as well as PCBs, a decrease in eggshell thickness of 3-J Tj from the mean has been demonstrated. The reduction in eggshell thick ness increases the chances of egc breakage. Water rcur.tion, which affects a successful hatching, might also be im paired. The PCBs cause thinning of the eggSnelis hut tk.s thinning seems not to be as effective as that caused by Df'T or its metabolite:;. The formation of thin egg-shells could be explained by tv o OSW 026682 STLCOPCB4010643 different mechanisms. The deposition of calcium in the me dullary bone, a storage necessary for the egg-shell produc tion, is under control of estradiol. A decreased concentra tion of tli i s hormone caused by hepatic enzyme induction as mentioned above, might influence the thickness of the egg shell. However, it seems unlikely that a reduction of the calcium reserve in the medullary bone, alone could be re sponsible for the marked thinnings often observed. The birds could compensate this lack by drawing calcium from the skeleton. Furthermore, birds on a very low calcium diet have been found locease egg-laying rather than laying thinshelled eggs. An acute hypocalcemia might also result in flight disturbances since the muscle* and the nervous sys tems would be affected. Another mechanism therefore seems to play the major role in the thinning of the shells. Carbonic anhydrase is neces sary to supply the carbonate ions required for calcium depo sition in the shell. Several investigations have shown a lower concentration of carbonic anhydrasc in shell glands produ cing soft-shelled eggs or no eggs than in glands producing normal eggs. Inhibition of lhi6 enzyme by DDT and DDE ha.s been demonstrated and the close similarity between those compounds suggests that PCD might have a similar effect. Us interesting to note that no threshold value has been found for the effect of DDE on egg-shell thickness. Very small doses will cause sonic thinning of the shell, Eggs from several species of birds have been demonstra ted to contain large amounts of PCD (Risebrougn 1966; 1970). This might contribute to explain the decreased hatchubihty , Chick embryo experiments have also shown that injection of small amounts of PCD in the eggv will caus-.c a high mor tality. Certain signs also indicate teratogen:^ effects. (Me Laughling ct al. 1963). Finally, another interesting aspect of those compound*. e ild DSW 026683 STLCOPCB4010644 o. be mentioned. It has been demonstrated in flies that vari ous PCBs significantly may increase the toxic effects of dieldrin and DDT (.Lichtenstein el al. 1969). No information has been found on such an interaction in the tissues of higher animals. However, the potential risks should not be disre garded in view of the synchronous occurrence of those com pounds in many populations. DSW 026684 STLCOPCB4010645 References Flick, D. F. , R. G. O'Dell and V. A. Childs (1965). Studies of the chick edema disease. 3. Similarity of symp toms produced by feeding chlorinated biphenyl. Poult, Sci. 44, 1460 - 1465. Jensen, S. (1966) Report of a new chemical hazard, New Scient. ^2 , 612. Jensen, S., A.C. Johuds, M. Olssonand G. Ottc-rlind (1969). DDT and PCB in marine animals from Swedish waters. Na ture, Lond.. 2 2-1, 247 - 250. Koeman, J , H . . M . C. Ten Noever de Brauw and R.H. d e Vox (1969). Chlorinated biphenyls in fish, mussels and birds from the river Rhine and the Netherlands coastal area. Na ture, Lond., 221, 1126 - 1128. Lichtenstein, E.P., K.R. Schulz, T.W. Fuhremaan and T.T. Liang (1 969). Biological interaction between plaf.ticizers and insecticides. J. Econ. Entomol. 6^2, 761 - 765. McCune, E.L., J.E. Savage and B.L. O'Dell (1962). Hydro pericardium and ascites in chicks fed a chlorinated hydro carbon, Poultry sci., 295 - 299. MeLaughling, Jr. J., J. P. Marliac, M.J. Vcrrctt, Ni. is. Mulchler and O. C. Fi l sjhugh (1963), To xi colog y and Appl , Pharmacol,, 5 . 7o0 - 766. . Pr e stl, J . , D. J . Jeffe r ie s and N . W . Moor e (1 97 0). Poly - chlorinated biphenyls in wild birds in Britain and their avian toxicity. Environ. Pollut., 3 - 26. Risebrough, R. W. , p, Riecht, D.13. Peckall, S.C. Kerman and M.N. Kirven (1968). Polychlorinated biphenyls in the global ecosydem. Nature, Lond. , 22 0, 1098 - 1102, DSW 026685 STLCOPCB4010646