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Per- and polyfluoroalkyl substances (PFASs) such as perfluorooctanoic acid (PFOA) and perfluorooctanesulfonic acid (PFOS) are persistent in the environment and bioaccumulate in wildlife and humans, potentially causing adverse health effects at all stages of life. Studies from human pregnancy have shown that exposure to these contaminants are associated with placental dysfunction and fetal growth restriction; however, studies in humans are confounded by genetic and environmental factors. Here, we synthesize the available results from mouse models of pregnancy to show the causal effects of prenatal exposure to PFOA and PFOS on placental and fetal development and on neurocognitive function and metabolic disorders in offspring. We also propose gaps in the present knowledge and provide suggestions for future research studies. Summary Sentence Using mouse models of pregnancy, maternal exposure to perfluoroalkyl substances has been shown to have significant impact on placental development, fetal growth, neurocognitive function, and risk for disease in both mother and offspring.

While microplastics have been recently detected in human blood and the placenta, their impact on human health is not well understood. Using a mouse model of environmental exposure during pregnancy, our group has previously reported that exposure to polystyrene micro- and nanoplastics throughout gestation results in fetal growth restriction. While polystyrene is environmentally relevant, polyethylene is the most widely produced plastic and amongst the most commonly detected microplastic in drinking water and human blood. In this study, we investigated the effect of maternal exposure to polyethylene micro- and nanoplastics on fetal growth and placental function. Healthy, pregnant CD-1 dams were divided into three groups: 10 6  ng/L of 740–4990 nm polyethylene with surfactant in drinking water ( n  = 12), surfactant alone in drinking water ( n  = 12) or regular filtered drinking water ( n  = 11). At embryonic day 17.5, high-frequency ultrasound was used to investigate the placental and fetal hemodynamic responses following exposure. While maternal exposure to polyethylene did not impact fetal growth, there was a significant effect on placental function with a 43% increase in umbilical artery blood flow in the polyethylene group compared to controls (p < 0.01). These results suggest polyethylene has the potential to cause adverse pregnancy outcomes through abnormal placental function.

Microcystins are cyclic heptapeptide hepatotoxins produced by cyanobacteria in freshwater. Sample preparation for the analysis of these cyanotoxins in water from algal blooms can take up to several days due to the matrix complexity and the low detection limits required to comply with current legislation. Moreover, there is a large number of unknown microcystins that could potentially exist in the environment resulting from different amino acid substitutions into the microcystin skeletal structure. To tackle these problems, the present study involved the development of a high throughput method based on on-line solid phase extraction coupled to liquid chromatography that could provide quantitative results for 12 microcystin variants (LR, YR, RR, HtyR, HilR, WR, LW, LA, LF, LY, Dha 7 -LR, and Dha 7 -RR) and anatoxin-A in less than 3 h with detection limits between 0.004 and 0.01 μg L −1 and expanded uncertainty between 4 and 14%. Data-dependent acquisition was employed for the non-targeted analysis of these cyanotoxins. Filtering the data based on structure diagnostic fragments, two unknown microcystin variants not previously reported in the literature were detected. The structures Leu 1 -microcystin-Met(O)R and Leu 1 -microcystin-LY were fully characterized by accurate mass measurement, collision-induced dissociation, and fragmentation prediction software.

Gas chromatography–high-resolution mass spectrometry (GC–HRMS) is a powerful nontargeted screening technique that promises to accelerate the identification of environmental pollutants. Currently, most GC–HRMS instruments are equipped with electron ionization (EI), but atmospheric pressure ionization (API) ion sources have attracted renewed interest because: (i) collisional cooling at atmospheric pressure minimizes fragmentation, resulting in an increased yield of molecular ions for elemental composition determination and improved detection limits; (ii) a wide range of sophisticated tandem (ion mobility) mass spectrometers can be easily adapted for operation with GC–API; and (iii) the conditions of an atmospheric pressure ion source can promote structure diagnostic ion–molecule reactions that are otherwise difficult to perform using conventional GC–MS instrumentation. This literature review addresses the merits of GC–API for nontargeted screening while summarizing recent applications using various GC–API techniques. One perceived drawback of GC–API is the paucity of spectral libraries that can be used to guide structure elucidation. Herein, novel data acquisition, deconvolution and spectral prediction tools will be reviewed. With continued development, it is anticipated that API may eventually supplant EI as the de facto GC–MS ion source used to identify unknowns.

Maternal exposure to microplastics and nanoplastics has been shown to result in fetal growth restriction in mice. In this study, we investigated the placental and fetal hemodynamic responses to plastics exposure in mice using high-frequency ultrasound. Healthy, pregnant CD-1 dams were given either 106 ng/L of 5 µm polystyrene microplastics or 106 ng/L of 50 nm polystyrene nanoplastics in drinking water throughout gestation and were compared with controls. Maternal exposure to both microplastics and nanoplastics resulted in evidence of placental dysfunction that was highly dependent on the particle size. The umbilical artery blood flow increased by 48% in the microplastic-exposed group and decreased by 25% in the nanoplastic-exposed group compared to controls (p < 0.05). The microplastic- and nanoplastic-exposed fetuses showed a significant decrease in the middle cerebral artery pulsatility index of 10% and 13%, respectively, compared to controls (p < 0.05), indicating vasodilation of the cerebral circulation, a fetal adaptation that is part of the brain sparing response to preserve oxygen delivery. Hemodynamic markers of placental dysfunction and fetal hypoxia were more pronounced in the group exposed to polystyrene nanoplastics, suggesting nanoplastic exposure during human pregnancy has the potential to disrupt fetal brain development, which in turn may cause suboptimal neurodevelopmental outcomes. Summary Sentence Exposure to polystyrene micro- and nanoplastics during pregnancy causes placental dysfunction, leading to fetal blood flow redistribution and growth restriction in mice. Graphical Abstract

IntroductionThe rapid growth in the worldwide use of plastics has resulted in a vast accumulation of microplastics in the air, soil and water. The impact of these microplastics on pregnancy and fetal development remains largely unknown. In pregnant mice, we recently demonstrated that exposure to micro- and nanoplastics throughout gestation resulted in significant fetal growth restriction. One possible explanation for reduced fetal growth is abnormal placental metabolism.ObjectivesTo evaluate the effect of maternal exposure to microplastics on placental metabolism.MethodsIn the present study, CD-1 pregnant mice were exposed to 5 μm polystyrene microplastics in filtered drinking water at one of four concentrations (0 ng/L (controls), 102 ng/L, 104 ng/L, 106 ng/L) throughout gestation (n = 7–11/group). At embryonic day 17.5, placental tissue samples were collected (n = 28–44/group). Metabolite profiles were determined using 1 H high-resolution magic angle spinning magnetic resonance spectroscopy.ResultsThe relative concentration of lysine (p = 0.003) and glucose (p < 0.0001) in the placenta were found to decrease with increasing microplastic concentrations, with a significant reduction at the highest exposure concentration. Multivariate analysis identified shifts in the metabolic profile with MP exposure and pathway analysis identified perturbations in the biotin metabolism, lysine degradation, and glycolysis/gluconeogenesis pathways.ConclusionMaternal exposure to microplastics resulted in significant alterations in placental metabolism. This study highlights the potential impact of microplastic exposure on pregnancy outcomes and that efforts should be made to minimize exposure to plastics, particularly during pregnancy.

Environmental metabolomics provides insight into how anthropogenic activities have an impact on the health of an organism at the molecular level. Within this field, in vivo NMR stands out as a powerful tool for monitoring real-time changes in an organism’s metabolome. Typically, these studies use 2D 13C-1H experiments on 13C-enriched organisms. Daphnia are the most studied species, given their widespread use in toxicity testing. However, with COVID-19 and other geopolitical factors, the cost of isotope enrichment increased ~6–7 fold over the last two years, making 13C-enriched cultures difficult to maintain. Thus, it is essential to revisit proton-only in vivo NMR and ask, “Can any metabolic information be obtained from Daphnia using proton-only experiments?”. Two samples are considered here: living and whole reswollen organisms. A range of filters are tested, including relaxation, lipid suppression, multiple-quantum, J-coupling suppression, 2D 1H-1H experiments, selective experiments, and those exploiting intermolecular single-quantum coherence. While most filters improve the ex vivo spectra, only the most complex filters succeed in vivo. If non-enriched organisms must be used, then, DREAMTIME is recommended for targeted monitoring, while IP-iSQC was the only experiment that allowed non-targeted metabolite identification in vivo. This paper is critically important as it documents not just the experiments that succeed in vivo but also those that fail and demonstrates first-hand the difficulties associated with proton-only in vivo NMR.

IntroductionPlastics used in everyday materials accumulate as waste in the environment and degrade over time. The impacts of the resulting particulate micro- and nanoplastics on human health remain largely unknown. In pregnant mice, we recently demonstrated that exposure to nanoplastics throughout gestation and during lactation resulted in changes in brain structure detected on MRI. One possible explanation for this abnormal postnatal brain development is altered fetal brain metabolism.ObjectivesTo determine the effect of maternal exposure to nanoplastics on fetal brain metabolism.MethodsHealthy pregnant CD-1 mice were exposed to 50 nm polystyrene nanoplastics at a concentration of 106 ng/L through drinking water during gestation. Fetal brain samples were collected at embryonic day 17.5 (n = 18–21 per group per sex) and snap-frozen in liquid nitrogen. Magic angle spinning nuclear magnetic resonance was used to determine metabolite profiles and their relative concentrations in the fetal brain.ResultsThe relative concentrations of gamma-aminobutyric acid (GABA), creatine and glucose were found to decrease by 40%, 21% and 30% respectively following maternal nanoplastic exposure when compared to the controls (p < 0.05). The change in relative concentration of asparagine with nanoplastic exposure was dependent on fetal sex (p < 0.005).ConclusionMaternal exposure to polystyrene nanoplastics caused abnormal fetal brain metabolism in mice. The present study demonstrates the potential impacts of nanoplastic exposure during fetal development and motivates further studies to evaluate the risk to human pregnancies.

Mass defect is the difference between the nominal and exact mass of a chemical element or compound. An intrinsic property of polyhalogenated molecules is a uniquely negative mass defect, which readily distinguishes halogenated from non-halogenated compounds in a complex mass spectrum and can be visualized by constructing a mass defect plot. This study demonstrates the utility of the mass defect plot as a powerful tool to screen gas-chromatography (ultra)high-resolution mass spectrometry data for potentially toxic and bioaccumulative halogenated compounds in a Lake Ontario lake trout, an apex species in the Great Lakes environment. Our results indicate that the sample is contaminated with polychlorinated biphenyls, terphenyls, diphenylethers, as well as other chlorinated pesticides and flame retardants that are regulated and routinely analyzed by traditional target analyses. However, the mass defect plot also displays peaks which could be traced to the presence of as yet undiscovered contaminants. These include chlorinated polycyclic aromatic hydrocarbons as well as mixed halogenated analogues of the flame retardant Dechlorane 604. The identity of the latter class of compounds is supported by experiments with genuine standards. Fig The mass defect plot provides an informative picture of the halogenated contaminants in a sample of Lake Ontario lake trout.

Bisphenols are used in the production of polycarbonate plastics and epoxy resins. Bisphenol A (BPA) has been widely studied and is believed to act as an endocrine disruptor. Bisphenol F (BPF) and bisphenol S (BPS) have increasingly been employed as replacements for BPA, although previous studies suggested that they yield similar physiological responses to several organisms. Daphnia magna is a common model organism for ecotoxicology and was exposed to sub-lethal concentrations of BPA, BPF, and BPS to investigate disruption to metabolic profiles. Targeted metabolite analysis by liquid chromatography-tandem mass spectrometry (LC-MS/MS) was used to measure polar metabolites extracted from D. magna, which are linked to a range of biochemical pathways. Multivariate analyses and individual metabolite changes showed similar non-monotonic concentration responses for all three bisphenols (BPA, BPF, and BPS). Pathway analyses indicated the perturbation of similar and distinct pathways, mostly associated with protein synthesis, amino acid metabolism, and energy metabolism. Overall, we observed responses that can be linked to a chemical class (bisphenols) as well as distinct responses that can be related to each individual bisphenol type (A, F, and S). These findings further demonstrate the need for using metabolomic analyses in exposure assessment, especially for chemicals within the same class which may disrupt the biochemistry uniquely at the molecular-level.