Sewage effluent biomonitoring. I. Survival, growth, and histopathological effects in channel catfish.
A 17-day, in situ, biomonitoring study using caged, juvenile channel catfish (Ictalurus punctatus) was conducted at five sites along a 9-km section of the Flint River at the Anthony Ragnone Wastewater Treatment Plant near Montrose, Michigan. Effects on survival, growth, and gill and liver histopathology were examined. No differences in growth, measured as wet weight gain, were observed between upstream control (UP) and experimental fish located 9 km downstream from the outfall (Down 4). Acute, 100% mortality occurred at study sites 300 and 500 m downstream from the outfall (Down 1 and Down 2, respectively). Mortality was probably due to excessive mean total residual chlorine concentration (0.24 and 0.30 mg/liter at Down 1 and Down 2, respectively). No mortality was observed at the remaining study sites. Forty percent of the fish at UP had slight hyperplasia and hypertrophy of the respiratory epithelium. All fish at Down 4 had two or more moderate to severe histopathological damages to the gills, including severe hyperplasia of the epithelial cells, clubbing and fusion of the secondary lamellae, moderate to severe edema in the secondary lamellae, and multiple, blood-filled aneurysms. Thirty-eight percent of livers from the UP fish were extremely vacuolated compared to 60% of the Down 4 fish livers. Both the vacuolated and less vacuolated (dense) liver sections stained negatively for lipids with oil red O. The vacuolated liver sections were qualitatively more intense than the dense sections when stained with Best's carmine. Vacuolated liver sections stained negatively with Best's carmine when pretreated with amylase, thereby indicating that the vacuolation represented glycogen storage. There was no correlation between the histopathological changes and any deleterious effects on growth or survival during the 17-day exposure. However, the gill histopathological changes would likely increase susceptibility to bacterial gill disease, and cause a reduction in the scope for activity due to impaired oxygen diffusion in the gills.
D000818:Animals; D005393:Fish Diseases / Q000139:chemically induced* / Q000473:pathology; D005399:Fishes / Q000254:growth & development / Q000502:physiology*; D005880:Gills / Q000473:pathology; D008099:Liver / Q000473:pathology; D012722:Sewage / Q000009:adverse effects* / Q000032:analysis; D013696:Temperature; D014873:Water Pollutants / Q000633:toxicity*; D014874:Water Pollutants, Chemical / Q000633:toxicity*
D012722:Sewage; D014873:Water Pollutants; D014874:Water Pollutants, Chemical