Risk mitigation measures for pesticide runoff: How effective are they?

BACKGROUND: One of the most important sources of pesticide pollution of surface waters is runoff and erosion from agricultural fields after rainfall. This study analyses the efficacy of different risk mitigation measures to reduce pesticide runoff and erosion inputs into surface waters from arable land excluding rice fields. RESULTS: Three groups of risk mitigation measures were quantitatively analyzed: vegetative filter strips, micro-dams in row crops and soil conservation measures. Their effectiveness was evaluated based on a meta-analysis of available experimental data using statistical methods such as classification and regression trees, and exploratory data analysis. Results confirmed the effectiveness of vegetative filter strips and micro-dams. Contrary to common assumption, the width of vegetative filter strips alone is not sufficient to predict their effectiveness. The effectiveness of soil conservation measures (especially mulch-tillage) varied widely. This was in part due to the heterogeneity of the available experimental data, probably resulting from the inconsistent implementation and the inadequate definitions of these measures. CONCLUSION: Both vegetative filter strips and micro-dams are effective and suitable, and can therefore be recommended for quantitative assessment of environmental pesticide exposure in surface waters. However, the processes of infiltration and sedimentation in vegetative filter strips should be simulated with a mechanistic model like Vegetative Filter Strip Modeling System, VFSMOD. The reduction effect of micro-dams can be modelled by reducing the runoff curve number, e.g., in the pesticide root zone model, PRZM. Soil conservation measures are in principle promising, but further well-documented data are needed to determine under which conditions they are effective. © 2023 The Authors. Pest Management Science published by John Wiley & Sons Ltd on behalf of Society of Chemical Industry.

Toxic Mixtures in Time-The Sequence Makes the Poison.

"The dose makes the poison". This principle assumes that once a chemical is cleared out of the organism (toxicokinetic recovery), it no longer has any effect. However, it overlooks the other process of re-establishing homeostasis, toxicodynamic recovery, which can be fast or slow depending on the chemical. Therefore, when organisms are exposed to two toxicants in sequence, the toxicity can differ if their order is reversed. We test this hypothesis with the freshwater crustacean Gammarus pulex and four toxicants that act on different targets (diazinon, propiconazole, 4,6-dinitro-o-cresol, 4-nitrobenzyl chloride). We found clearly different toxicity when the exposure order of two toxicants was reversed, while maintaining the same dose. Slow toxicodynamic recovery caused carry-over toxicity in subsequent exposures, thereby resulting in a sequence effect-but only when toxicodynamic recovery was slow relative to the interval between exposures. This suggests that carry-over toxicity is a useful proxy for organism fitness and that risk assessment methods should be revised as they currently could underestimate risk. We provide the first evidence that carry-over toxicity occurs among chemicals acting on different targets and when exposure is several days apart. It is therefore not only the dose that makes the poison but also the exposure sequence.

Relative importance of microplastics as a pathway for the transfer of hydrophobic organic chemicals to marine life.

It has been hypothesised that, if ingested, plastic debris could act as vector for the transfer of chemical contaminants from seawater to organisms, yet modelling suggest that, in the natural environment, chemical transfer would be negligible compared to other routes of uptake. However, to date, the models have not incorporated consideration of the role of gut surfactants, or the influence of pH or temperature on desorption, whilst experimental work has shown that these factors can enhance desorption of sorbed contaminants several fold. Here, we modelled the transfer of sorbed organic contaminants dichlorodiphenyltrichloroethane (DDT), phenanthrene (Phe) and bis-2-ethylhexyl phthalate (DEHP) from microscopic particles of polyvinylchloride (PVC) and polyethylene (PE) to a benthic invertebrate, a fish and a seabird using a one-compartment model OMEGA (Optimal Modelling for EcotoxicoloGical Applications) with different conditions of pH, temperature and gut surfactants. Environmental concentrations of contaminants at the bottom and the top of published ranges were considered, in combination with ingestion of either 1 or 5% by weight of plastic. For all organisms, the combined intake from food and water was the main route of exposure for Phe, DEHP and DDT with a negligible input from plastic. For the benthic invertebrate, predictions including the presence of contaminated plastic resulted in very small increases in the internal concentrations of DDT and DEHP, while the net change in the transfer of Phe was negligible. While there may be scenarios in which the presence of plastic makes a more important contribution, our modelling study suggests that ingestion of microplastic does not provide a quantitatively important additional pathway for the transfer of adsorbed chemicals from seawater to biota via the gut.

Review of the partitioning of chemicals into different plastics: Consequences for the risk assessment of marine plastic debris.

Marine plastic debris are found worldwide in oceans and coastal areas. They degrade only slowly and contain chemicals added during manufacture or absorbed from the seawater. Therefore, they can pose a long-lasting contaminant source and potentially transfer chemicals to marine organisms when ingested. In order to assess their risk, the contaminant concentration in the plastics needs to be estimated and differences understood. We collected from literature plastic water partition coefficients of various organic chemicals for seven plastic types: polydimethylsiloxane (PDMS), high-density, low-density and ultra-high molecular weight polyethylene (LDPE, HDPE, UHMWPE), polystyrene (PS), polypropylene (PP), and polyvinyl chloride (PVC). Most data was available for PDMS (1060) and LDPE (220), but much less for the remaining plastics (73). Where possible, regression models were developed and the partitioning was compared between the different plastic types. The partitioning of chemicals follows the order of LDPE≈HDPE≥PP>PVC≈PS. Data describing the impact of weathering are urgently needed.

Death Dilemma and Organism Recovery in Ecotoxicology.

Why do some individuals survive after exposure to chemicals while others die? Either, the tolerance threshold is distributed among the individuals in a population, and its exceedance leads to certain death, or all individuals share the same threshold above which death occurs stochastically. The previously published General Unified Threshold model of Survival (GUTS) established a mathematical relationship between the two assumptions. According to this model stochastic death would result in systematically faster compensation and damage repair mechanisms than individual tolerance. Thus, we face a circular conclusion dilemma because inference about the death mechanism is inherently linked to the speed of damage recovery. We provide empirical evidence that the stochastic death model consistently infers much faster toxicodynamic recovery than the individual tolerance model. Survival data can be explained by either, slower damage recovery and a wider individual tolerance distribution, or faster damage recovery paired with a narrow tolerance distribution. The toxicodynamic model parameters exhibited meaningful patterns in chemical space, which is why we suggest toxicodynamic model parameters as novel phenotypic anchors for in vitro to in vivo toxicity extrapolation. GUTS appears to be a promising refinement of traditional survival curve analysis and dose response models.

Including carrier-mediated transport in oral uptake prediction of nutrients and pharmaceuticals in humans.

Most toxicokinetic models consider passive diffusion as the only mechanism when modeling the oral uptake of chemicals. However, the overall uptake of nutrients and xenobiotics, such as pharmaceuticals and environmental pollutants, can be increased by influx transport proteins. We incorporated carrier-mediated transport into a one-compartment toxicokinetic model originally developed for passive diffusion only. The predictions were compared with measured oral uptake efficiencies of nutrients and pharmaceuticals, i.e. the fraction of the chemical reaching systemic circulation. Including carrier-mediated uptake improved model predictions for hydrophilic nutrients (RMSE=10% vs. 56%, Coefficient of Efficiency CoE=0.5 vs. -9.6) and for pharmaceuticals (RMSE=21% vs. 28% and CoE=-0.4 vs. -1.1). However, the negative CoE for pharmaceuticals indicates that further improvements are needed. Most important in this respect is a more accurate estimation of vMAX and KM as well as the determination of the amount of expressed and functional transport proteins both in vivo and in vitro.

Predicting the oral uptake efficiency of chemicals in mammals: combining the hydrophilic and lipophilic range.

Environmental risk assessment requires models for estimating the bioaccumulation of untested compounds. So far, bioaccumulation models have focused on lipophilic compounds, and only a few have included hydrophilic compounds. Our aim was to extend an existing bioaccumulation model to estimate the oral uptake efficiency of pollutants in mammals for compounds over a wide K(ow) range with an emphasis on hydrophilic compounds, i.e. compounds in the lower K(ow) range. Usually, most models use octanol as a single surrogate for the membrane and thus neglect the bilayer structure of the membrane. However, compounds with polar groups can have different affinities for the different membrane regions. Therefore, an existing bioaccumulation model was extended by dividing the diffusion resistance through the membrane into an outer and inner membrane resistance, where the solvents octanol and heptane were used as surrogates for these membrane regions, respectively. The model was calibrated with uptake efficiencies of environmental pollutants measured in different mammals during feeding studies combined with human oral uptake efficiencies of pharmaceuticals. The new model estimated the uptake efficiency of neutral (RMSE=14.6) and dissociating (RMSE=19.5) compounds with logK(ow) ranging from -10 to +8. The inclusion of the K(hw) improved uptake estimation for 33% of the hydrophilic compounds (logK(ow)<0) (r(2)=0.51, RMSE=22.8) compared with the model based on K(ow) only (r(2)=0.05, RMSE=34.9), while hydrophobic compounds (logK(ow)>0) were estimated equally by both model versions with RMSE=15.2 (K(ow)&K(hw)) and RMSE=15.7 (K(ow) only). The model can be used to estimate the oral uptake efficiency for both hydrophilic and hydrophobic compounds.

Significance of xenobiotic metabolism for bioaccumulation kinetics of organic chemicals in Gammarus pulex.

Bioaccumulation and biotransformation are key toxicokinetic processes that modify toxicity of chemicals and sensitivity of organisms. Bioaccumulation kinetics vary greatly among organisms and chemicals; thus, we investigated the influence of biotransformation kinetics on bioaccumulation in a model aquatic invertebrate using fifteen (14)C-labeled organic xenobiotics from diverse chemical classes and physicochemical properties (1,2,3-trichlorobenzene, imidacloprid, 4,6-dinitro-o-cresol, ethylacrylate, malathion, chlorpyrifos, aldicarb, carbofuran, carbaryl, 2,4-dichlorophenol, 2,4,5-trichlorophenol, pentachlorophenol, 4-nitrobenzyl-chloride, 2,4-dichloroaniline, and sea-nine (4,5-dichloro-2-octyl-3-isothiazolone)). We detected and identified metabolites using HPLC with UV and radio-detection as well as high resolution mass spectrometry (LTQ-Orbitrap). Kinetics of uptake, biotransformation, and elimination of parent compounds and metabolites were modeled with a first-order one-compartment model. Bioaccumulation factors were calculated for parent compounds and metabolite enrichment factors for metabolites. Out of 19 detected metabolites, we identified seven by standards or accurate mass measurements and two via pathway analysis and analogies to other compounds. 1,2,3-Trichlorobenzene, imidacloprid, and 4,6-dinitro-o-cresol were not biotransformed. Dietary uptake contributed little to overall uptake. Differentiation between parent and metabolites increased accuracy of bioaccumulation parameters compared to total (14)C measurements. Biotransformation dominated toxicokinetics and strongly affected internal concentrations of parent compounds and metabolites. Many metabolites reached higher internal concentrations than their parents, characterized by large metabolite enrichment factors.

Toxicokinetic-toxicodynamic modeling of quantal and graded sublethal endpoints: a brief discussion of concepts.

We report on the advantages and problems of using toxicokinetic-toxicodynamic (TKTD) models for the analysis, understanding, and simulation of sublethal effects. Only a few toxicodynamic approaches for sublethal effects are available. These differ in their effect mechanism and emphasis on linkages between endpoints. We discuss how the distinction between quantal and graded endpoints and the type of linkage between endpoints can guide model design and selection. Strengths and limitations of two main approaches and possible ways forward are outlined.