Document RJ1qmYDD7LD7y7ZVkvwJLKqBB

Zitko, V. and P. M. K. Choi. j973L Oral toxicity of chlorinated dibenzofurans to Juvenile Atlantic Salmon. Bulletin of Environ mental Contamination & Toxicology 10(2): 120-122. t MOMS 200606 Oral Toxicily of Chlorinated Dibenzofiirnntt to Juvenile Atlantic Salmon hr V. Zitko nd I'.M.K. Choi FithrUt Httnrrh Hamnl af Itiolofical Sutiaa, St. Anjratn, NJi. McMvttr Vaimanitr. Ttamihan,jhlirii Chlorinated dlbenzofurans, finmpt In some poly chlorinated biphenyl (PCS) preparations, are highly toxic compounds, often lethal In rabbits after a single oral dose of 0.5-1.0 mg/k (VOS et al. 1970). Chlorin ated dlbenzofurans were not detectable In high trophiclevel aquatic animals which accumulated significant quantities of PCS (ZITKO 1972). The tissue levels of these compounds, associated with toxic effects are not known. The present Investigation was undertaken to deter mine the tissue levels of chlorinated dlbenzofurans causing mortality In juvenile Atlantic salmon (Salmo talar). Dry fish food (trout chow, Purina) was spiked wlch dl-, trl-, tetra-, and octachlorodlbenzofuran. The compounds were dissolved In a small volume of benzene, the solution was diluted with pesticide-grade hexane and mixed thoroughly with the food. The solvent was evaporated on a rotatory evaporator at 22*C, and the food was kept In vacuum (27 psl) overnight at room tem perature to remove last traces of the solvent. A con trol batch of food was treated under the same condi tions with the solvent only. Food and fish tissues were analysed as described (ZITKO 1972). The concentration of dl-, trl-, tetra-, and octachlorodlbenzofuran In the food, calculated and (determined) was 2.7 (2.1), 5.7 (4.4), 2.8 (2.2), and 9.1 (9.7) ug/g. respectively. * Juvenile Atlantic salmon (35 fish) were kept In a 20-11ter fiberglass tank In running water (500 ml/mln) at 10*C, 16-h light, 8-h dark photoperiod, and fed the spiked food several times a day. A control experiment using the solvent-treated food was carried out under the same conditions. Average length of the fish was 10.9 cm, average weight was 10.7 g. Fish In the control experiment suffered no mortal ities whereas median mortality (LTSO) of 120 t 30 days occurred among fish on the diet containing chlorinated dlbenzofurans. The experiment was terminated after 140 days and fish still alive (20X) were sacrificed. $ m Vollrti* of gevinmiwmitri fwsema^arfvM A TaiWen. \vi. 10. N*. J O kv Nrw York, **e. . -rz ***#* vr**. Muscle and gut of fish that died between the 81st and 135th day of the experiment, and of fish surviving for 140 days were analysed and the results are pre sented in Table 1. The levels of PCB and 00E in the control fish were not significantly different from those reported in Table 1. The concentration of lipid In the control fish was 2.85X (whole fish). TABLE 1 Analyses of fish tissues (data on wet weight basis). Lipid Number Pt&* O'CBF**' X Samp 1e analysed Mean SO Mean SO Mean 50 Mean SO Muscle Dead 5 0.1S 0.03 0.040.00 0.03 0.01 0.8S 0.17 Live 3 0.14 0.02 0.05 0.02 0.01 0.00 0.77 0.06 Gut Dead 4 0.52 0.10 0.10 0.01 0.21 0.14 1.21 0.27 i Live 3 0.66 0.13 0,20 0.0S 0.02 0,04 2.02 0.31 *45 Aroclor* 1254 **octachlorodibenzofuran D1-, trl-, and tetrachlorodlbenzofuran were not detectable In any of the samples. The detection limit ^or these compounds Is approximately 0.02 ug/g on wet weight basis (ZITXO et al. 1972). The dead fish con tained about 10 times higher concentration of octachlorodlbenzofuran In the gut and 3 times higher con centration In the muscle than the fish alive after 140 days. Octachlorodlbenzofuran Is less readily absorbed from food than PCB. Juvenile Atlantic salmon fed a diet containing Aroclor* 1254 at a level of 10 ug/g had a PCB concentration of 3.5 ug/g In whole body after 120 days (ZITXO and HUTZINGEA 1972). It Is possible that as In the case of chlorinated dlbenzodloxlns (ROME et al. 1971), dlbenzofurans with Intermediate degress of chlorination are the most toxic compounds. The observed levels of octechlorodlbenzo- furan may be only a measure of the amount of Ingested food, not associated with the toxic effects. It Is In teresting to note that the lipid level In the gut Is higher in the live fish than In the dead fish. 121 V\- V-*} w -% .. . ^ c.-i* * .. .. -r. lr ^r",1 Mr<1 - V-'V.^-y -W.Jy-4 ' >5`. 1*hicF ... ...__ .-r. .wi a, fv \% -JSf. '*&i foV;*'* .i*i--. Jki3 V-- y) V-!A nO*., ^*?8&a 3V, V Vt. T llW, The presented data Indicate that In fish, as well as mammals, chlorinated dlbenzofurans are much more toxic than PCS. Nothing Is known about the Input and possible formation of chlorinated dlbenzofurans In the environment. Thus far, we were not able to detect these compounds In Aroclor* preparations. The results Indicate that fcagfl^jpt of the high toxicity and low residual leveTt #&thlor1nated dibenzofurans, a more sensitive analytfc#f%ethod Is required. The mechanism and kinetics of the formation of these compounds should be determined and toxicological studies of dibenzofurans with known chlorine substitution oat* terns should be carried out. ACKNOWLEDGMENTS Chlorinated dlbenzof.urans were a gift from Or. 0. Firestone, FDA, Washington, O.C. Mr. W.6. Carson carried out the feeding experiment. REFERENCES ROWE, V.K., J.M. NORRIS, G.L. SPARSCHU, B.A. SCHWETZ, and P.J, GEHRING: Paper presented at 162nd National Meeting, American Chemical Society, Washington, D.C., September (1971). VOS, J.G., J.H. KDEMAN, H.L. VAN OER MAAS, H.C. TEN NOEVER OE GRAllM, and R.H. OE VOS: Food Cosmet. Toxicol. S, 625 (1970), ZITKD. V.$ Bull, Environ. Contam. Toxicol. 7, 105 (1972). ZITKO, V., and 0. HUTZINGER: American Chemical Society, Division of Water, Air and Waste Chemistry, Preprints of papers presented at 164th National Meeting, 12(2), 157 (1972). ZITKO, V., 0. HUTZINGER, and P.M.IC. CHOI: Environmental Health Perspectives 1, 47 (1972). 'W'J'VctT a l -R'N. ' : \ i-1 m .i!** 200609 .r.'r.T-f( T-r