Physiological toxicity of low-chlorine bleached pulp and paper mill effluent on whitefish (Coregonus lavaretus L. s.l.): a laboratory exposure simulating lake pollution.
In order to validate previous field observations by the authors on whitefish, Coregonus lavaretus L. s.l., a 30-day laboratory experiment with concentrations (0, 1.3, 2.3, 3.5, and 7 vol%) of bleached kraft pulp and paper mill effluent (BKME) simulating those occurring in a polluted lake was conducted. Chlorine dioxide had almost entirely replaced chlorine gas in the bleaching of pulp. As a consequence, the concentrations of adsorbable organic halogens and chlorinated phenolics (CPs) in BKME were significantly lowered compared to earlier studies. This reduction was also seen in the concentrations of CPs in the bile and CPs and extractable organic halogens in the intestinal lipids: the concentrations were low and did not depend on the dilution of BKME. In contrast, the resin acid content of bile decreased with decreasing BKME concentration. The growth of fish was speeded up in all BKME concentrations. However, at the highest BKME concentration (7 vol%) the increase was lowest. The induction of hepatic ethoxyresorufin O-deethylase (EROD) activity revealed strong dose-response relationship with BKME. At 3.5 vol% BKME (corresponding to a distance of 3.3 km from the mill sewer in the field) the EROD activity increased 12-fold. There was a tendency for lower activity of uridinediphosphate glucuronosyltransferase in the liver, but the decrease (34%; P < 0.05) was statistically significant only at 7 vol% BKME. The activity of liver glutathione S-transferase remained unchanged. All dilutions of BKME significantly depressed the concentrations of plasma immunoglobulin M (IgM). Erythrocytic concentrations of nucleotide triphosphates decreased and of sodium increased as the BKME concentration increased. Also some other blood parameters (hematocrit, hemoglobin, plasma glucose, and aspartate aminotransferase) were changed in all BKME exposures, although without obvious dependence on effluent concentration. In conclusion, there was a good agreement between field studies and laboratory experiments using BKME concentrations occurring in the field, confirming close or similar causes for responsive toxicity endpoints.
D000818:Animals; D001711:Biotransformation; D002713:Chlorine / Q000633:toxicity*; D019363:Cytochrome P-450 CYP1A1; D003577:Cytochrome P-450 Enzyme System / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D004912:Erythrocytes / Q000187:drug effects / Q000201:enzymology / Q000378:metabolism; D005618:Fresh Water; D007075:Immunoglobulin M / Q000097:blood; D007220:Industrial Waste; D008099:Liver / Q000187:drug effects / Q000201:enzymology; D010088:Oxidoreductases / Q000378:metabolism; D010209:Paper; D012487:Salmonidae / Q000097:blood / Q000502:physiology*; D014874:Water Pollutants, Chemical / Q000633:toxicity*
D007075:Immunoglobulin M; D007220:Industrial Waste; D014874:Water Pollutants, Chemical; D002713:Chlorine; D003577:Cytochrome P-450 Enzyme System; D010088:Oxidoreductases; D019363:Cytochrome P-450 CYP1A1