Laboratory ecotoxicity tests may not adequately evaluate the effects of pesticides, because they often do not include more environmentally relevant conditions, such as pulsed toxicant exposures and low food conditions. Therefore, we tested the effects of a pulse of the pyrethroid insecticide fenvalerate (FV) on the life history and population growth rate (r) of the cladoceran Daphnia magna. The daphnids were subjected to a 24-h pesticide pulse exposure (0.03, 0.1, 0.3, 0.6, 1.0, and 3.2 microg/L) under high and low food conditions and were monitored for 21 d. Chemical analysis showed that at t = 1 h, the nominal FV concentrations were reduced by 50 to 66%. Fenvalerate decreased survival and growth in the week following pulse exposure. Age at first reproduction increased, with consequent adverse effects on cumulative reproduction per living female and, therefore, on r. Thus, a short-term exposure of FV caused a long-term reduction on r as a result of increased mortality and a delay in development. Low food conditions exacerbated the effects of the FV exposure on juvenile survival and growth during the first week. This caused a much stronger reduction in r under low food conditions. We concluded that a pulsed FV exposure may result in long-term reduction of r that can be predicted only with more environmentally relevant toxicity tests, as described in the present study.
Feeding activity and maturation were investigated in Daphnia magna exposed to fenvalerate for 24 h. The feeding activity was monitored by measuring filtration rates and 15N-traced food assimilation. Exposure resulted in individuals with reduced feeding activity and smaller body size at concentrations of 0.3 microg/L or greater as well as delayed maturation at concentrations of 0.61microg/L or greater. Filtration rates recovered within 2 d of the exposure, but long-term effects of reduced feeding activity, such as growth retardation, occurred. Because D. magna needs to reach a minimum size to mature, growth retardation may explain the observed delay in maturity. The proposed causal relationships suggest that exposure to fenvalerate reduces feeding activity, resulting in growth retardation, which leads to delayed maturity. In cases of exposure to such toxicants, the monitoring of feeding activity may predict long-term effects on population parameters.
This study compares lethal and sublethal responses of Daphnia magna Straus exposed to fenvalerate continuously (21 d) and as a pulse (24 h). Survival was reduced more severely in the continuous- than in the pulse-exposure regime. Complete mortality occurred at 1 microg/L for continuous exposure and at 3.2 microg/L for pulse exposure. Regarding reproductive endpoints, fenvalerate delayed the age at first reproduction. At the beginning of the reproductive phase (day 10), this delay resulted in a reduction of the neonates per living female at similar concentrations in both exposure regimes (0.3 and 0.1 microg/L for continuous and pulse exposure, respectively). The population growth rate was inhibited in continuous and pulse exposure at 0.3 and 0.6 microg/L, respectively. However, the effects of fenvalerate in the pulse exposure were transient. After 21 d, a recovery to values close to the controls occurred with respect to the total neonates per female and the population growth rate over a broad range of concentrations from 0.1 up to 1 microg/L. In contrast, no substantial recovery occurred in the continuous-exposure regime.
The aim of this study was to determine the influence of exposure duration (1 h, 24 h, continuous) to paraoxon-methyl on the magnitude of lethal and sublethal effects, the shape of the concentration-response relationships and the recovery processes in Daphnia magna. Survival was more severely reduced in the continuous than in the pulse exposure regimes. The lethal concentrations (3d median lethal concentration [LC50] values) were 233, 2.33, and 1.14 microg/L after 1-h, 24-h, and continuous exposure, respectively. The shapes of the concentration-response relationships for survival were significantly different after 1 h of exposure than after 24-h and continuous exposure. Indeed, the slopes of the curves defined by the ratios LC90/LC10 (ratio of 90 and 10% lethal concentrations) were 100, 1.74, and 1.97 for 1-h, 24-h, and continuous exposure, respectively. The large difference between 1 h and longer durations of exposure shows that the population is partially affected (10-90%) over a much broader range of concentrations when exposure is short. Negative effects on reproductive outputs occurred mostly at concentrations affecting partly the survival and therefore also over a broad range of concentrations after 1 h of exposure. However, these effects were only transient in the pulse exposure regimes as individual performances recovered. By contrast, reproductive outputs of survivors exposed continuously remained impaired. These results suggest that a refined risk assessment should consider exposure duration because it influences the magnitude of effects and recovery.
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