Document KG926dDwY0jy9jb6jaoOkDdLr

Hydropericardium and Ascites in Chicks Fed a Chlorinated Hydrocarbon* E. L. McCune, J. E. Savace and B. L, O'Dell DrparIntents oj Veterinary Bacteriology, Poultry Husbandry and Agricultural Chemistry, University of Missouri, Columbia, Missouri (Received for publicfttiun Miy 3, 1961) AX epoxy-resin paintf lias been used in They were weighed weekly and examined - our laboratory to coat galvanized daily for gross symptoms. All chicks were batteries employed for trace mineraal utopsied at death and at least two indi studies. This paint was supplied as two viduals per group were selected during the separate 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 fat" syndrome meal 36%, yellow corn 59.5%, CaHPO described by Schmittle el al. (1958) and 2%, limestone 1.3%, iodized salt 0.5%, Sanger el al. (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 al., 1959; Friedman el al., paint fractions were dissolved in isopropyl 1959; Wooton and Alexander, 1959; Har alcohol and added to the mixed ration. man cl 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 closed 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, VantressWhitc 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 Missouri Agricultural Experiment Station, Journal Series No. 2295. t The paint (Epo- Floor Top) was obtained from the Steelcote Manufacturing Co., St. Louis, Mis souri. We gratefully acknowledge the assistance of Mr. A. G. Sternberg of this company who kindly supplied the various fractions 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, polyamid (made from diethylenetriamine and dimerized fatty acids), tri-dimethyl- 295 W'>"' :-f'- Vrv fM \*FX* ~'fa - ** t: VT;': d S > : v v-: H; ft '-m A./* 5 mm 'vytuc.; - `<-L : . '-.a V ' * j--.' V*-#*;'. -vAv* <y . X' "A-f. V'V. / -v , < - * . ;w-j DSW 025384 A- s<4?. STLCOPCB4009339 Tablf. l.---Toxicity oj various components of Hie amine hardener Substance fed Name Level Isopropyl Alcohol Amine Hardener % 2.0 0,1 Chlorinated Biphenyl Diethylenetriamine Tri-dimethylaminomelhylphenol Dimerized Tatty Acids Polyamid 0.1 0.1 0.1 0.1 0.1 3 weeks 4 weeks Weight Mortality Mortality Gross pathology g- % 290 0 219 20 106 90 288 0 234 0 336 0 318 0 % 0 None 60 Hydropcrcardiuni; lungs hemorrhagic and edematous; kidneys and liver swollen 90 Similar to amine hardener 0 Slight enteritis; kidneys slightly swollen 0 Liver and kidneys enlarged. No edema 0 None 0 None aminomethylphenol, 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. Diethylenetriamine, 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 diethylenetriamine. Tri-dimelhylaminomethylphenol caused some liver and kidney damage and de pressed the rate of gain, but was not severely toxic. The dimerized fatty acids 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 it was 4 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- Table 2.--Toxicity oj chlorinated biphenyl (Aroclor 1242) Substance fed Name Level Chlorinated Biphenyl Chlorinated Biphenyl Chlorinated Biphenyl % o.ot 0.02 0.04 Chlorinated Biphenyl 0.08 Polyamid Polyamid + Chlorinated Biphenyl 0.10 0.10 0.04 3 weeks 4 weeks Weight Mortality Mortality Gross pathology g- % 306 0 317 c 237 10 160 50 340 0 259 40 % 0 Slight 0 Hydropericardium 50 Hydropericardium; hemorrhage of in ternal organs; liver enlarged and mottled; enteritis 90 Hydropericardium; hydroperitoneum; enlarged heart; enteritis; kidney ami liver damage 0 No pathology 70 Hydropericardium DSW 025385 STLCOPCB4009340 I-lYUROPERICARDlUM AND ClILORIN-.ATED BlPJTENYL 297 drome such as distended abdomen 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 amine hardener fraction. Feeding the polyamid along with chlorinated biphenyl did not change the results appreciably. Gross 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 cases the abdominal cavity was dis tended with fluid. At necropsy the most Ion. I. Hyrlropericardiuin observed in a chick fed 0.02% of chlorinated biphenyl for 4 weeks. Fio. 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 w'erc hemorrhagic. The liver w'as 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. Histopathology. 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 wras concen trated largely in the smaller collecting tubules. The liver had a few areas of lymphocyt- DSW 025386 * ' .C; a: .vA A -A STLCOPCB4009341 298 E. L. McCvne, J. E. Savage and B. L. O'Deli. Fig. 3. Kidney from control chick. H and E stain (100 X). ic infiltration which was observed chiefly around the smaller blood vessels. The severity of the liver lesions varied with individual birds, but tended to be directly related to the level of chlorinated bi phenyl. The damage to liver and kidney observed in chicks fed the 0.01% level was of only questionable significance. The heart showed chiefly mechanical dilatation. A few areas of infiltration of lymphocytes and heterophils had occurred between the muscle fibers. The microscopic lesions produced by 0.1% of the amine hardener were similar to those produced by chlorinated biphenyl but additional lesions were observed. These included cellular casts in the renal convoluted tubules, glomerular atrophy, and mild tubular necrobiosis. Some kid neys showed glomerular congestion, glo merular vacuolization and hyaline infiltra tion, and small areas of interstitial ne phritis. The livers of chicks fed the amine hardener showed general toxic degenera tion. The most frequent lesion was bile duct proliferation with an increased num ber of reticular cells and heterophils. The parenchymal cells showed generalized fatty degeneration. Cord cell atrophy, reduced amounts of lymphoid tissue, and irregular accumulations of lymphocytes and heterophils were present in some chicks. The results suggest that the amine hardener was somewhat more toxic than the chlorinated biphenyl alone. The prod uct of dimerized fatty acids and diethylenetriamine (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 large basophilic cells commonly found in the kidney. DISCUSSION The symptoms and gross pathology observed in birds fed chlorinated bi phenyl can not be distinguished from those described for the "toxic fat'' syn drome (Schmittle el al., 1958). The micro scopic lesions were similar to those de scribed by Sanger cl al. (1958), but there were differences, at least in degree. In the case of chlorinated biphenyl the renal tubules and bile ducts were more severely damaged and less hepatic, necrosis had occurred. The lesions observed in this study bear a strong resemblance to those produced by coal-tar creosote (Bullis and Van Roekel, 1944). The fact that it is not possible to dis tinguish between the syndromes produced by "toxic fat" and chlorinated biphenyl suggests that the toxic compounds are similar in nature. On the other hand, it is recognized that many different toxic com pounds produce similar symptoms in the ichick. Tire chlorinated biphenyl fed in this investigation was far less toxic than the crystalline compound isolated by Harman cl til. (1960). It is possible that the 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 et al. (1958) 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 a syndrome resembling the "toxic fat" syndrome. Excess salt increased the incidence of the disease in the presence but not in the absence of the fat-soluble factor. Accumulation of fluid results when the kidney fails to maintain normal water balance either because of excess electrolytes or because of kidney damage. Chlorinated biphenyl causes estensive 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 was 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, hydroperiloneum, en larged heart, Iver and kidneys, and hemorrhage of internal organs. Micro scopically the kidneys showed marked tubular dilatation and numerous casts. REFERENCES Brew, W. B., J. B. Dore, J. H. Benedict, G. C. Potter and E. Sipos, 1959. Characterization of m type of unidentified compound producing edema in chicks. J. Assoc. Offic. Agr. Chemists. 42: 120-128. Bullis, K. L., and H. Van Roekel, 1944. Uncommon pathological conditions in chickens and turkeys. Cornell Vet. 34: 313-319. Friedman, L., D. Firestone, \V. Horwitz, D. Banes, M. Anstead and G. Shoe, 1959. Studies of the chick edema disease factor. J, Assoc. Oflfic. Agr. Chemists, 42: 129-140. Gordon, R. $., R. A. Mulholland, L. J. Machlin and K. H. Maddy, 1959. Hydropericardium and ascites caused by excess salt and a factor in blood meal. Poultry Sci. 38: 1209. Harman, R. E., G. E. Davis, W. H. Ott, N. G. Brink and F. A. Kuehl, 1960. The isolation and characterization of the chick edema factor. J. Am. Chem. Soc. 82: 2078. Pudelkiewicz, W. J., R. V. Boucher, E. W. Callenbach and R. C. Miller, 1958. Some physiological rcsi>onscs of Broad Breasted Bronze poults to chlorinated naplhalene, Poultry Sci. 37:185-187. Sanger, V. L., L. Scott, A. Hamdy, C. Gale and \V. D. Pounden, 1958. Alimentary toxemia in chickens. J. Am. Vet. Med. Assoc. 133: 172-176. Schmittle, S. C., H. M. Edwards and D. Morris, 1958. 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, 1959. Some 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 .;CV -,' /r/w. 4 .y. ,Vv'- Xr...Jw'v. !,`;-A' V/*<d'.^.*&vTv* v y Sve.K.j.A** DSW 025388 STLCOPCB4009343