Document 3JXgNYEBryDKD4Y8GQDBbQjwO

Hydropericardium and Ascites in Chicks Fed a Chlorinated Hydrocarbon* E. L. McCukk, J. E. Savage and B. L. O'Deli. Departments oj Veterinary Bacteriology, Poultry Husbandry and Agricultural Chemistry, University of Missouri, Columbia, Missouri <RK*lvt lot publication May J, 1M1) AX epoxy-resin paintf has been used in They were weighed weekly and examined - our laboratory to coat galvanised daily for gross symptoms. All chicks were batteries employed for trace mineraalutopsied at death and at least two indi studies. This paint was supplied as two viduals per group were selected during the sepurale fractions which were mixed just third and fourth weeks for histological prior to use. One portion contained the examination of liver, kidney, heart, lung epoxy monomer and the other the amine and spleen. The tissues were processed in hardener which catalyzed polymerization. the routine manner for histological exam On one occasion the paint did not harden ination and were stained with hematoxylin before chicks were placed in the battery and eosin. and within 3 weeks the chicks showed The basal ration-was a practical-type symptoms closely resembling those of the broiler ration composed of soybean oil "chick edema" or "toxic lat" syndrome meal 36%, yellow corn 59.5%, CaHPO< described by Schmittle tl al. (1958) and 2%, limestone 1.5%, iodized salt 0 5%, Sanger el ai. (1958). Because of the inter methionine 0.1%, a trace mineral mixture est in the chemical nature of the toxic and a vitamin supplement. The various factor (Brew el at., 1959; Friedman et al.t paint fractions were dissolved in isopropyl 1959; Wooton and Alexander, 1959; Har alcohol and added to the mixed ration. man el al., 1960) that has been observed Since some of the components were in feed-grade fats and the lipid origin of slightly volatile, the feeds were stored in certain components of the paint, it seemed dosed containers and kept under refriger worthwhile to investigate further the ation. Small portions were placed in the causative agent in the epoxy-resin paint. feeders daily. EXPERIMENTAL Groups of ten, straight-run, VantreasWhite Rock, cross-bred chicks were placed in electrically heated batteries at hatching and allowed to consume the experimental rations ad libitum for a four-week period. * Contribution from the Misaouri Agricultural Experiment Station, Journal Series No. 2295. t The paint (Epo- Floor Top) woe obtained fmm the Stcetane Manufacturing Co., St. Louie, MU* eouri. We gratefully acknowledge the eeeistance of Mr. A. G. Sternberg of tbU company who kindly supplied the verioue fraction* tested. RESULTS In a preliminary trial the two fractions of the paint, the amine hardener and the epoxy monomer, were tested at a level of 0.1%. One-half of the chicks that received the amine hardener died whereas the other group lived and grew at a normal rate. From this test it was clear that the toxic substance was associated with the amine hardener. According to the manufacturer this fraction contained isopropyl alcohol, poly&mid (made from diethylenctriamine and dimerized fatty acids), tri-dimethyl- 295 296 E. L. McCune, J. E. Savacf. and B, L. O'Dell TaBLR 1--Tffxiciiy of various components of the amine hardener Subsume* fed Nome Level Isopropyl Alcohol Amine Hardener 7o 2.0 0.1 Chlorinated Biphenyl Diethyleneirinmine Tri-dlmethylamino- methylphenol Dimerized Petty Acltlt Polyamid 0.1 0.1 0.1 Q.t 0.1 3 weeks 4 necks Weight Morte'ity Mortality Gros- paltiuldf^y 1 \ 20 106 90 288 0 234 0 336 0 318 0 % 0 None 60 Hydrojwrciinlmm; lungs bcmorrhupi; and edematous; kidneys and liver swollen 90 Similar to amine hardener 0 Slight enteritis; kidney* slightly swollen 0 Liver and kidney* enlarged. No edema 0 None 0 None anrinomethylphenol, and a chlorinated biphenyl (Aroclor 1242) which contains about 42% chlorine. The chlorinated bi phenyl was added as a plasticizer and is not an essential component of the paint. These fractions were tested and the results are summarized in Table 1. It is clear from these results that the major toxic agent was the chlorinated biphenyl. Dicthylenetriamine, which is considered to be highly toxic to man, had relatively little effect on the chick although it did cause slight liver and kidney damage. Feed consumption was not measured but it may be assumed that these chicks which had an average weight of 440 grams at 4 weeks consumed about 800 grams of feed and 0.8 grams of diethylenetriaraine. Tri-dimclhylaminomethylphtmd caused some liver and kidney damage and dc* pressed the rate of gain, but was not severely toxic. The dimerized fatty adds and the product (polyamid) that results from dimerized fatty acids and diethylenetriamine showed no gross evidence of toxicity. In order to determine the degree of toxicity of the chlorinated biphenyl jt was fed at graded levels. It was also fed with polyamid to determine whether or not there was a potentiating effect from this component. The results are summarized in Table 2. When chlorinated biphenyl was fed at 0.01% there was only slight evidence of toxicity. At the 0.02% level typical symptoms of the "toxic fat" syn- TaSLX 2.--Toxicity oj chlorinated biphenyl {Aroclor lltt) Substance (ed Name Level Chlorinated Biphenyl Chlorinated Biphenyl Chlorinated Biphenyl *\ 0.02 0.04 Chlorinated Biphenyl 0.08 Polyamid Polyamid+ Chlorinated Niphenyl 0.10 0.10 0.04 3 week* 4 weeks Weight Mortality Mortality - .. . 3&6 % 0 317 0 237 10 160 50 340 0 259 40 % 0 Slight 0 Hydrapericardium 50 Ilydropericarrfium; hemorrhage of in ternal organa; liver enlarged and mottled; enteritis 90 Hydtoperictrdium; hydropetitoneum; enlarged heart; enteriii*; kiJnc) anti liver damage 0 No pathology 70 Hydropcricardium MOMS 096117 IIVDUOPF.RICAKDIUM AND CHLORINATED BlPIfENYL 297 drome such as distended ubdomcn and labored respiration were evident, but there was no mortality during the fourweek test period. At necropsy hydroperi cardium was evident. The 0.04% level produced symptoms resembling those ob served among chicks fed 0.1% level of the utmne hardener fraction. Feeding the polyamid along with chlorinated biphenyl did not change the results appreciably. Grost Pathology. The gross pathology produced by chlorinated biphenyl closely resembled that observed in the "chick edema" syndrome. Losses usually started during the third week and reached major proportions during the fourth week. Be fore death the chicks exhibited symptoms of labored respiration with rales and in some cascs the abdominal cavity was dis tended with fluid. At necropsy the must Fin. t. Hyriroperlcariium observed In a chick fed 0.02% of chlorinated biphenyl for 4 weeks. Kio. 2. Tubular dilatation in kidney of a chick fed 0.1% of chlorinated biphenyl. H and E stain (100X). striking pathology was hydropericardium as illustrated in Figure 1. The crop of several birds contained bloody fluid. The kidneys were swollen and pale in most chicks but in the advanced stages many were hemorrhagic. The liver was some times enlarged and mottled in appear ance. The lungs were commonly hydropic and hemorrhagic. A yellow, jelly-like fluid was frequently found under the skin and within body cavities. A large amount of fibrin was often present in this fluid. HistopoMtology. Chlorinated biphenyl at the 0.1% level caused severe renal tubular dilatation with numerous casts especially near the surface of the kidneys. Figure 2 illustrates the typical kidney damage and Figure 3 is a photomicrograph from a control kidney. The majority of the casts were basophilic, but appeared to be made up of strands resembling fibrin. Many of these basophilic bodies contained smaller homogenous eosinophilic bodies sugges tive of amyloid. The damage was concen trated largely in the smaller collecting tubules. The liver had a few areas of lymphocyt- 298 E. L. McCune, J. E. Savage and B. L. 0'Di:u. ^er ^ ret'cu^ar ce^s HIK* heterophils. The ^ntiz\tymti\ cells showed generalized fty degeneration. Cord tell atrophy, \ f/4.: educed amounts of lymphoid tissue, and irregular accumulations o( lymphoeytea am* heterophils were present in some chicks. The results suggest that the umine hardener was somewhat more toxic than the chlorinated biphenyl alone. The prod uct of dimerized fatty acids and diethyl- enetriamine (Polyamid) produced micro scopic lesions similar to those caused by a low level of the amine hardener. These consisted of hepatic cord cell vacuoliza tion and a few dilated renal tubules con taining faintly eosinophilic casts. There was a slight increase in the groups of Urge basophilic cells commonly found in the kidney. lc infiltration which was observed chiefly around the smaller blood vessels. The DISCUS5ION severity of the liver lesions varied with The symptoms and gross pathology individual birds, but tended to be directly observed in birds fed chlorinated bi related to the level of chlorinated bi phenyl can not be distinguished from phenyl. The damage to liver and kidney those described for the "toxic fat" syn observed in chicks fed the 0.01% level drome (Schmittle el a}., 1958). The micro was of only questionable significance. scopic lesions were similar to those de The heart showed chiefly mechanical scribed by Sanger el al. (1958), but there dilatation. A few areas of infiltration of were differences, at least in degree. In the lymphocytes and heterophils had occurred case of chlorinated biphenyl the renal between the muscle fibers. tubules and bile ducts were more severely The microscopic lesions produced by damaged and less hepatic necrosis had 0.1% of the amine hardener were similar occurred. The lesions observed in this to those produced by chlorinated biphenyl study bear a strong resemblance to those but additional lesions were observed. produced by coal-tar creosote (Bullis and These included cellular casts in the renal Van Roekel, 1944). convoluted tubules, glomerular atrophy, The fact that it is not possible to dis and mild tubular necrobiosis. Some kid tinguish between the syndromes produced neys showed glomerular congestion, glo by "toxic fat" and chlorinated biphenyl merular vacuolization and hyaline infiltra suggests that the toxic compounds are tion, and small areas of interstitial ne similar in nature. On the other hand, it is phritis. recognized that many different toxic com The livers of chicks fed the amine pounds produce similar symptoms in the hardener showed general toxic degenera chick. The chlorinated biphenyl fed in tion. The most frequent lesion was bile this investigation was far less toxic than duct proliferation with an increased num- the crystalline compound isolated by HONS 096119 mm Hydropericardium and Chlorinated Biphenyl 299 Harman el al. (1960). It is possible that lh toxic component of the chlorinated biphenyl product used here is a contami nant rather than the major component. Although the toxicity of some chlori nated hydrocarbons has been studied in poultry, the pathology involved has re ceived little attention. Pudelkiewicz tt al. (1938) observed that a mixture of pentaand hexa-chloronaphthalenes caused high mortality in poults but there was no accumulation of fluid in body cavities. Hydropericardium and ascites in chicks can be caused by a variety of compounds, the most common cause under practical conditions being excessive amounts of sodium chloride. Gordon el al. (1959) observed that a fat-soluble substance in blood meal caused n syndrome resembling the "toxic fat" syndrome. Excess salt increased the incidence of the disease in tho presence but not in the absence of the fat-soluble factor. Accumulation of fluid resuils when the kidney fails to maintain normal water balance either because of excess electrolytes or because of kidney damage. Chlorinated biphenyl causes es(cn*ive kidney damage and ascites is probably a secondary result. SUMMARY Chicks fed fractions of an epoxy-resin paint developed hydropericardium and ascites. These symptoms were similar to those observed in the "toxic-fat" syn drome. The toxicity wax found to be caused by a chlorinated biphenyl product used as a plasticizer in the paint. Chlorinated biphenyl was moderately toxic when fed at a level of 0.02% and caused high mortality and extensive pathology within 4 weeks at a dietary level of 0.04%. Gross pathology included hydropericardium, hydroperitoneum, en larged heart, 'ver and kidneys, and hemorrhage of internal organs. Micro scopically the kidneys showed marked tubular dilatation and numerous casts. REFERENCES Brew, \V. B., J. B. Dore, J. H. Benedict, G. C. Potter and E. Slpos, 1959. Characterization of a type of unidentified compound producing edema in chicks. J. Asaoc. Offic. Agr. Chemists, 42: 120-128. Dullls, K. L., and H. Van Roekel, 1944. Uncommon pathological conditions in chickens and turkeys. Cornell Vet. 54: 515- 519. Friedman, L., D. Firestone, W. Horwitt, D. Banes, M. Anstead and G. Shoe, 1959. Studies of tha chick edema disease (actor. J. Assoc. Offic. Agr. Chemists, 42: 129-140. Gordon, R. S,, R. A. Mulholiand, L. J. Machlin and K. H. Middy, 1959. Hydropericardium and aadtes caused by excess salt and a factor in blood meal. Poultry Sci. 58: 1209. Harman, R. E., G. E. Davis, W. H. Ott, N. G. Brink and F. A. KuehJ, 1960. The isolation and characterisation of the chick edema factor. J. Am. Chem. Soc. 82: 2078. Pudelkiewicx, W. J., R. V. Boucher, E. W. Callenbach and R. C. Miller, 1958, Some physiological res|wnses of Broad Breasted Bronxe poults to chlorinated napthalene. Poultry Sd. 57:185-187. Sanger, V. L,, L. Scott, A. Hamdy, C. Gale and W. D. Pounden, 1958. Alimentary toxemia in chickens. J. Am. Vet. Med. Assoc. 153: 172-176. Schmittle, S. C., H. M. Edwards and D. Morris, 1956. A disorder of chickens probably due to a toxic feed-preliminary report. J. Am. Vet. Med. Assoc. 132: 216-219. Wooton, J. C., and J. C. Alexander, I9S9. Soma chemical characteristics of the chick edema dis ease factor; J. Assoc. Offic. Agr. Chemists, 42: 141-148. AUGUST 10-18. TWELFTH WORLD'S POULTRY CONGRESS SYDNEY, AUSTRALIA SEPTEMBER 18-21. FIRST INTERNATIONAL CONGRESS OF FOOD SCIENCE AND TECHNOLOGY, IMPERIAL COLLEGE OF SCIENCE AND TECHNOLOGY, LONDON, ENGLAND MOMS 09612U