Document O3z5n2wwXRzekjMdqK7j2317M

PCB - Effects on Birds by J. BUckstrOm '. . Dept. oX Pharmacology, Royal Veterinary College, Stockholm National Poisons and Pesticides Board, Stockholm Polychlorinated biphenyls (PCB) are widely distributed in the environment and, according to many investigators, they seem to be ubiquitous as DDT (Riscbrough ct al. 1968; Koe- man et al, 1969; Jensen etal. 1969; Prestt 1970; Jensen 1966), Many observations concern high levels of PCBs in the avian fauna,, particularly in marine birds which are at the top of a food chain in the sea. Larger residues have been found in predatory birds than in omnivorous or herbivorous species, . '. . There is very little work published on the avian toxicity of the PCBs. No observations concern any acute effects of these compounds.in the avian fauna. As regards the sublethal effects, however, the situation may be different and there are indi cations that the PCBs may be responsible for certain repro duction disturbances. There are a few works on experimental toxicology. Koeman et al. (1969) fed adiet,containing 2000 ppm of Phenochlor DP6, a technical PCB mixture, to Japanese quails, all of which died betv/een day 6 and 55 after dosing had started. Gas chromatographic analysis of the residues in liver and brain of these birds indicated that some of the more lightly bhlorinatcd PCBs present in the original mixture, had been metabolized. Autopsy of the quails demonstrated large amounts of fluid in the pericardial sac. Hydropericard has also been observed in cockerels dosed with 400 ppm of PCB (Arochlor 1242) in their diet (Flick et al. 1965) and in Bengalese finch- HONS 0 3 4 6 7 3 / G o L *> l 9 * e o SNOW cs fed with a diet containing various amounts of Arochlor 54 (Prestt et al. 1970). . 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 et al, (1955) fed Arochlor 1242 to dayold cockerels (200 or 400 ppm in the diet) and reported, besides hydropericard, 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 defeathering. They also discussed the similarity between the symptoms elicited by PCBs and those of the chick .edema disease. Certain differen ces, however, exist and the possibility that the chick edema factor (today known to be a mixture of chlorinated dioxincs) might be present in PCB-preparations was not supported by gas chromatographic analyses performed by McCune et al. (1962), McCune e` al. (1962) also fed a chlorinated bi phenyl to chicks (100 ppm) and observed symptoms similar to those of chick edema disease (hydropcricard, subcutaneous and abdominal edema, hemorrhages of internal organs and enteritis). The toxicity of PCB as compared with othor chlorinated hydro carbons, is somewhat difficult to establish, because, whereas e.g. DDT presents a relatively steep mortality curve, the curve for a PCB is much more gradual. This means that at low dose rates, PCB may have a comparatively greater toxi city than similar amounts of DDT, but at higher dose rated the toxicity of DDT is considerably higher. In the experiment:* of Prestt et al. (1970) with Bengalese finches, the estimated dose rate for 50 % mortality at 56 days was 254 mg/kg/day. At low doses, PCB was more toxic than DDT; at highex doses PCB was about 10 times less toxic than DDT. ' ^restt et al. (1970) also gave s ne values of the concentra tions of PCB in .some organs of the birds. One,bird, killed after 8 weeks daily feeding with 367 >tg of PCB, showed 14 ppm in the brain, 25 ppm in the liver, 574 ppm in fat and 61 ppm as a mean 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 were starved prior to analysis. Starvation resulted in a redistribution o 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 drop in reproduction. The symptoms observed in connection with this decline have included late breedingr failure to lay eggs, a remarkable * thinning of the shell's and much breakage of the eggs that are laid, eating of broken eggs by the parents, failure to Jay more eggs after earlier clutches have been lost, reduced c.lutch else and a high mortality of the embryos and among fledglings. The regions o:* population decline coincide with o areas where chlorinated hydrocarbons arc widely applied. The pato-physiological mechanisms behind these symptoms are uncertain, but may to some 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 PCBs, like DDT end DDE, Have the capacity to induce steroid hydroxylating liver enzymes to increase their breakdown of estradlol(Risebrogh et al. 1968). . The PCBs are more powerful inducers of these enzymes than DDT or DDE. The breakdown of estradiol in pigeon liver was increased 2.5 times by DDE. 3.5 times by DDT and 5. 5 times by PCB, in spite of that only half as much HONS 0 3 4 6 7 5 PCB as DDT or DDE was used (Risebrough et al, 1968). 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 is involved in the stimulation and maintenance of the sex organs and breeding behaviour. A delayed laying may be very serious for certain species 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. The failure to lay at all could also bo caused by decreasod hormone concentrations resulting from hepatic enzyme indue, tion or apparent failure to lay could be 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 whose populations were decreasing (Risebrough 1968 and others). Thin eggshells were found in avian species who accumulated high concentrations of chlorinated hydrocarbons. In uncon taminated populations of these species the production of egg shells was normal. Extremely thin eggshells have been found in the brown pelican in California where the average percen tage thinning was 53 % and the extreme was 95 %. In North American peregrines, contaminated with DDT as well as PCBs, a decrease in eggshell thickness of 34 % from the mean has been demonstrated. The reduction in eggshell thick ness increases the chances of egg breakage. Water reten tion, which affects a successful hatching, might also be im paired. The PCBs cause thinning of the eggshells but this thinning seems not to be as,effective as that caused by DDT or its metabolites. / The formation of thin egg-shells could bo explained by two HONS 0 3 4 6 7 6 fferent mechanisms. The dsp *tion 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 this hormone caused by hepatic ensyme induction as mentioned above* might influence the thickness of the egg shell. However, it seems unlikely that a reduction of the calcium reeerve 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 o skeleton. Furthermore* birds on a very low calcium diet have been found tocease egg-laying rather than laying thin- shelled 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 anhydrase in shell glands produ cing soft-shelled eggs or no eggs than in glands producing normal eggs. Inhibition of this enzyme by DDT and DDE tos been demonstrated and the close similarity between these compounds suggests that PCD might have a similar offect. Its interesting to note that no threshold value has been found for the effect of DDE on egg-shell thickness. Very small doses will cause some thinning of the shell. MONS 0 3 4 6 7 7 Eggs from several species of birds have been demonstra ted to contain large amounts of PCB (Risebrough 1968; 1970). This might contribute to explain the decreased hatchability. Chick embryo experiments have also shown that injection of small amounts of PCB in the eggs will cause a high mor tality. Certain signs also indicate teratogenic effects. (Me Laughling et al. 1963). rinsiw * *. I 6. be mentioned. It has been demonstrated in Hie* that vari ous PCJBs significantly may increase the toxic effects of dieldrin and DDT (Lichtenstein et 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 these com pounds in many populations. HONS 034678 ( 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 Sclent. _32, 612. Jensen, S. , A.G. Johuds, M. Olsson and G. Otterlind (1969). DDT and PCB in marine animals from Swedish waters. Na ture, Lond.. 224, 247 - 250. Koeman, J.H.. M.C. Ten Noever de Brauw and R.H. da Vox (1969). Chlorinated biphenyls in fish, mussels .and birds from the river Rhine and the Netherlands coastal area. Na ture, Lond., 22^, 1126 - 1128. Lichtenstein, E.P., K.R. Schulz, T.W. Fuhremann and T.T. Liang (1969). Biological interaction between plasticlzers and insecticides. J. Econ, Enlomol. bZ, 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., 4t_. 295 - 299. McLaughling, Jr. J., J.P. Marliac, M.J. Vcrrett, M.K. ` . Mutchlcr and O. G. Fitzhugh (1963). Toxicology and Appl. ' Pharmacol., S . 760 - 766. ' Prestt, J., D.J. Jefferies and N.W. Moore (1970). Poly chlorinated biphenyls in wild birds in.Britain and their avian toxicity. Environ. Pollut. , 3 - 26. Rigebrough, R.W., P. Rieche, D.B. Peckall, S.G. Kerman and M.N. Kirven (1968). Polychlorinated biphenyls in the global ecosystem. Nature, Lond., 220. 1098 - 1102. HONS 036679