No abstract

Despite the rapid rise in diversity and quantities of engineered nanomaterials produced, the impacts of these emerging contaminants on the structure and function of ecosystems have received little attention from ecologists. Moreover, little is known about how manufactured nanomaterials may interact with nutrient pollution in altering ecosystem productivity, despite the recognition that eutrophication is the primary water quality issue in freshwater ecosystems worldwide. In this study, we asked two main questions: (1) To what extent do manufactured nanoparticles affect the biomass and productivity of primary producers in wetland ecosystems? (2) How are these impacts mediated by nutrient pollution? To address these questions, we examined the impacts of a citrate-coated gold nanoparticle (AuNPs) and of a commercial pesticide containing Cu(OH) nanoparticles (CuNPs) on aquatic primary producers under both ambient and enriched nutrient conditions. Wetland mesocosms were exposed repeatedly with low concentrations of nanoparticles and nutrients over the course of a 9-month experiment in an effort to replicate realistic field exposure scenarios. In the absence of nutrient enrichment, there were no persistent effects of AuNPs or CuNPs on primary producers or ecosystem productivity. However, when combined with nutrient enrichment, both NPs intensified eutrophication. When either of these NPs were added in combination with nutrients, algal blooms persisted for >50 d longer than in the nutrient-only treatment. In the AuNP treatment, this shift from clear waters to turbid waters led to large declines in both macrophyte growth and rates of ecosystem gross primary productivity (average reduction of 52% ± 6% and 92% ± 5%, respectively) during the summer. Our results suggest that nutrient status greatly influences the ecosystem-scale impact of two emerging contaminants and that synthetic chemicals may be playing an under-appreciated role in the global trends of increasing eutrophication. We provide evidence here that chronic exposure to Au and Cu(OH) nanoparticles at low concentrations can intensify eutrophication of wetlands and promote the occurrence of algal blooms.

The use of novel pesticides containing nanomaterials (nanopesticides) is growing and is considered a promising approach to reduce the impacts of agriculture on the environment and human health. However, the environmental effects of these novel agrochemicals are not fully characterized, and more research is needed to determine the benefits and risks they confer. Here, we assessed the impacts of repeated exposures to a Cu(OH) 2 nanopesticide on the soil and sediment biodiversity of target (terrestrial) and nontarget (wetland) ecosystems by performing long-term outdoor mesocosm experiments. As pesticides are often used concomitantly with other agrochemicals, we also tested for interactive effects between nanopesticide exposure and fertilization treatments in both ecosystems. We used high-throughput sequencing on three marker genes to characterize effects on bacterial, fungal, and total eukaryotic community structure and diversity. Interestingly, we found limited effects of nanopesticide exposure on the terrestrial soil communities. Conversely, we found significant shifts in the sediment communities of the wetland mesocosms, especially for eukaryotes (protists, fungi, and algae). In the absence of fertilization, fungal and total eukaryotic community compositions exposed to nanopesticides for long periods of time were distinct from unexposed communities. We identified 60 taxa that were significantly affected by nanopesticide exposure, most of which were microeukaryotes affiliated to cercozoans, Gastrotricha, or unicellular algal taxa. Our study suggests that this nanopesticide has limited effects on the soil biodiversity of a target terrestrial agroecosystem, while nontarget aquatic communities are more sensitive, particularly among protists which are not targeted by this bactericide/fungicide.

The environmental fate and potential impacts of nanopesticides on agroecosystems under realistic agricultural conditions are poorly understood. As a result, the benefits and risks of these novel formulations compared to the conventional products are currently unclear. Here, we examined the effects of repeated realistic exposures of the Cu(OH)2 nanopesticide, Kocide 3000, on simulated agricultural pastureland in an outdoor mesocosm experiment over 1 year. The Kocide applications were performed alongside three different mineral fertilization levels (Ambient, Low, and High) to assess the environmental impacts of this nanopesticide under low-input or conventional farming scenarios. The effects of Kocide over time were monitored on forage biomass, plant mineral nutrient content, plant-associated non-target microorganisms (i.e., N-fixing bacteria or mycorrhizal fungi) and six soil microbial enzyme activities. We observed that three sequential Kocide applications had no negative effects on forage biomass, root mycorrhizal colonization or soil nitrogen fixation rates. In the Low and High fertilization treatments, we observed a significant increase in aboveground plant biomass after the second Kocide exposure (+14% and +27%, respectively). Soil microbial enzyme activities were significantly reduced in the short-term after the first exposure (day 15) in the Ambient (-28% to -82%) and Low fertilization (-25% to -47%) but not in the High fertilization treatment. However, 2 months later, enzyme activities were similar across treatments and were either unresponsive or responded positively to subsequent Kocide additions. There appeared to be some long-term effects of Kocide exposure, as 6 months after the last Kocide exposure (day 365), both beta-glucosidase (-57% in Ambient and -40% in High fertilization) and phosphatase activities (-47% in Ambient fertilization) were significantly reduced in the mesocosms exposed to the nanopesticide. These results suggest that when used in conventional farming with high fertilization rates, Kocide applications did not lead to marked adverse effects on forage biomass production and key plant–microorganism interactions over a growing season. However, in the context of low-input organic farming for which this nanopesticide is approved, Kocide applications may have some unintended detrimental effects on microbially mediated soil processes involved in carbon and phosphorus cycling.

Freshwater ecosystems are exposed to engineered nanoparticles through municipal and industrial wastewater-effluent discharges and agricultural nonpoint source runoff. Because previous work has shown that engineered nanoparticles from these sources can accumulate in freshwater algal assemblages, we hypothesized that nanoparticles may affect the biology of primary consumers by altering the processing of two critical nutrients associated with growth and survivorship, nitrogen and phosphorus. We tested this hypothesis by measuring the excretion rates of nitrogen and phosphorus of Physella acuta, a ubiquitous pulmonate snail that grazes heavily on periphyton, exposed to either copper or gold engineered nanoparticles for 6 months in an outdoor wetland mesocosm experiment. Chronic nanoparticle exposure doubled nutrient excretion when compared to the control. Gold nanoparticles increased nitrogen and phosphorus excretion rates more than copper nanoparticles, but overall, both nanoparticles led to higher consumer excretion, despite contrasting particle stability and physiochemical properties. Snails in mesocosms enriched with nitrogen and phosphorus had overall higher excretion rates than ones in ambient (no nutrients added) mesocosms. Stimulation patterns were different between nitrogen and phosphorus excretion, which could have implications for the resulting nutrient ratio in the water column. These results suggest that low concentrations of engineered nanoparticles could alter the metabolism of consumers and increase consumer-mediated nutrient recycling rates, potentially intensifying eutrophication in aquatic systems, for example, the increased persistence of algal blooms as observed in our mesocosm experiment.

No abstract

Mitochondria are central players in host immunometabolism as they function not only as metabolic hubs but also as signaling platforms regulating innate immunity. Environmental exposures to mitochondrial toxicants occur widely and are increasingly frequent. Exposures to these mitotoxicants may pose a serious threat to organismal health and the onset of diseases by disrupting immunometabolic pathways. In this study, we investigated whether the Complex I inhibitor rotenone could alter C. elegans immunometabolism and disease susceptibility. C. elegans embryos were exposed to rotenone (0.5 µM) or DMSO (0.125%) until they reached the L4 larval stage. Inhibition of mitochondrial respiration by rotenone and disruption of mitochondrial metabolism were evidenced by rotenone-induced detrimental effects on mitochondrial efficiency and nematode growth and development. Next, through transcriptomic analysis, we investigated if this specific but mild mitochondrial stress that we detected would lead to the modulation of immunometabolic pathways. We found 179 differentially expressed genes (DEG), which were mostly involved in detoxification, energy metabolism, and pathogen defense. Interestingly, among the down-regulated DEG, most of the known genes were involved in immune defense, and most of these were identified as commonly upregulated during P. aeruginosa infection. Furthermore, rotenone increased susceptibility to the pathogen Pseudomonas aeruginosa (PA14). However, it increased resistance to Salmonella enterica (SL1344). To shed light on potential mechanisms related to these divergent effects on pathogen resistance, we assessed the activation of the mitochondrial unfolded protein response (UPRmt), a well-known immunometabolic pathway in C. elegans which links mitochondria and immunity and provides resistance to pathogen infection. The UPRmt pathway was activated in rotenone-treated nematodes further exposed for 24 h to the pathogenic bacteria P. aeruginosa and S. enterica or the common bacterial food source Escherichia coli (OP50). However, P. aeruginosa alone suppressed UPRmt activation and rotenone treatment rescued its activation only to the level of DMSO-exposed nematodes fed with E. coli. Module-weighted annotation bioinformatics analysis was also consistent with UPRmt activation in rotenone-exposed nematodes consistent with the UPR being involved in the increased resistance to S. enterica. Together, our results demonstrate that the mitotoxicant rotenone can disrupt C. elegans immunometabolism in ways likely protective against some pathogen species but sensitizing against others.

No abstract