Toxicity models of pulsed copper exposure to Pimephales promelas and Daphnia magna

Abstract

Semiempirical models are useful for interpreting the response of aquatic organisms to toxicants as a function of exposure concentration and duration. Most applications predict cumulative mortality at the end of the test for constant exposure concentrations. Summary measures, such as the median lethal concentration, are then estimated as a function of concentration. Real-world exposures are not constant. Effects may depend on pulse timing, and cumulative analysis based only on integrated exposure concentration is not sufficient to interpret results. We undertook a series of pulsed-exposure experiments using standard toxicological protocols and interpreted the results (mortality, biomass, and reproduction) using a dynamic generalization of a Mancini/Breck--type model that includes two compartments, one for internal concentration as a function of exposure and one for site-of-action concentration or accumulated damage as a function of the internal dose. At exposure concentrations near the effects level, the model explained approximately 50% of the variability in the observed time history of survival, 43% of the change in biomass, and 83% of the variability in net reproduction. Unexplained variability may result from differences in organism susceptibility, amplified by the effects of small sample sizes in standard tests. The results suggest that response is sensitive to prior conditions and that constant-exposure experiments can underestimate the risk from intermittent exposures to the same concentration. For pulsed exposures, neither the average nor the maximum concentration alone is an adequate index of risk, which depends on both the magnitude, duration, and timing of exposure pulses. Better understanding about the impacts of pulsed exposures will require use of experimental protocols with significantly greater numbers of replicates.

Bayesian multilevel discrete interval hazard analysis to predict dichlorodiphenyldichloroethylene mortality in Hyalella azteca based on body residues

“…2). These data confirm the data from Zhao and Newman [12] that show toxicity continues even after the end of exposure, indicating that the total damage continues consistent with the damage assessment model [6] and other models that represent similar processes [10,11]. 2).…”

“…In the field, exposure is often pulsed, creating differing durations and intervals of exposure. Advances in the accumulation and response models can now incorporate both the toxicokinetics and the toxicodynamics to address hazard (response) for any known exposure condition using the internal concentration as the dose metric [10,11]. In cases where the exposure and toxicokinetics are known, the toxicity can be determined as any combination that exceeds an internal threshold, as found in a study with pentachlorophenol [9].…”

Toxicokinetic-toxicodynamic modelling of survival of Gammarus pulex in multiple pulse exposures to propiconazole: model assumptions, calibration data requirements and predictive power

“…Previously it has been claimed that TK is an essential part of understanding survival patterns over time (Ashauer et al 2010; Butcher et al 2006), which might suggest that TK may also be essential for predicting survival over time. Here we compared the goodness of fit between reduced and full models (Fig.…”

“…The models have been calibrated using long term pulsed toxicity experiments (Ashauer et al 2007a, b; Ashauer et al 2010; Butcher et al 2006; Meyer et al 1995) or constant exposure experiments (Mancini 1983; Meyer et al 1995). Using the toxicity data from constant exposures for model calibration would allow applying these models widely in risk assessment because this type of data has been and is generated in standard toxicity experiments.…”

Review of toxicological effects caused by episodic stressor exposure

“…Examples of natural variation include fluctuations in physicochemical water quality (temperature, dissolved oxygen, pH, electrical conductivity, etc.) The concentration of pollutants in water resources will fluctuate depending on the quantity released in to the environment as well as the dilution rate and the potential degradation of the pollutant within the environment [3]. Episodic stressor exposure originating from anthropogenic activities can be because of accidental or deliberate releases of pollutants from the following four main sources: urban stormwater runoff, agricultural activities, sewage treatment works, and industrial activities [1].…”