Use of respiratory‐cardiovascular responses of rainbow trout (Salmo gairdneri) in identifying acute toxicity syndromes in fish: Part 2. malathion, carbaryl, acrolein and benzaldehyde

Abstract

AbstractAn in vivo fish model was used to monitor the respiratory‐cardiovascular responses of individual spinally transected rainbow trout exposed to acutely toxic aqueous concentrations of two acetylcholinesterase (AChE) inhibitors, malathion and carbaryl, and two mucous membrane irritants, acrolein and benzaldehyde. The most striking changes in respiratory‐cardiovascular physiology noted on malathion and carbaryl exposures were immediate decreases in oxygen utilization (U) and heart rate (HR). Ventilation volume (VG) increased to compensate for the lower U, but not enough to increase oxygen consumption (VO2). Blood responses in carbaryl‐exposed trout differed from those in the malathion group; there were increased hematocrit (Hct) and hemoglobin (Hb) values along with an extensive drop in arterial pH (pHa) and total arterial carbon dioxide (TaCO2). The overall respiratory‐cardiovascular responses of the rainbow trout to acrolein and benzaldehyde intoxication represent a direct effect of the chemical at the respiratory surface. A steady increase in cough rate (CR) was recorded for fish exposed to both chemicals throughout exposures. A moderate to low increase in VG and VO2 was followed at 50 to 60% survival time by sudden decreases in VG and VO2 until death. Ventilation rate (VR), U and HR showed a steady downward trend over the entire survival period. After the midpoint in survival time, total arterial oxygen (TaO2), (TaCO2) and pHa all decreased, while Hct increased steadily. Individual principal components analyses of the cardiovascular‐respiratory responses of fish exposed to the four chemicals showed that the variables were highly correlated and that the first two principal components explained 55 to 70% of the variation in the 18 parameters analyzed. A two‐dimensional diagram of the first two principal components illustrated this multivariate response and the increased variability in the responses of exposed fish as compared with the control fish. Sets of toxic responses were developed to describe two new fish acute toxicity syndromes (FATS), one for AChE inhibitors and one for respiratory irritants. These were combined with the FATS for respiratory uncouplers and narcotics from previous work prior to discriminant function analysis (DFA). DFA was used to predict the specific FATS for a chemical based on the cardiovascular‐respiratory responses observed during intoxication. DFA on these responses resulted in a 100% correct separation of four specific FATS for all 32 trout tested. Of the 18 responses monitored and used in the DFA, CR, VO2, TaO2, pHa and U were the best discriminators in predicting the correct FATS for each fish.