Environmental Pollution

Perfluorooctane sulfonic acid (PFOS), a per- and polyfluoroalkyl substance (PFAS), is a widespread persistent environmental pollutant that has been implicated in various human health conditions, including infertility and cancer. Here, we investigate the effects of acute exposure to PFOS on human fallopian tube epithelial (FNE) cells that are essential for fertility and increasingly recognized as the origin site for high-grade serous ovarian cancer. We show that acute PFOS exposure changes morphology, arrests proliferation, impairs adhesion, and compromises epithelial integrity of FNE cells. Using transcriptomic profiling of FNE cells exposed to PFOS, we found increased expression of genes associated with stress-response signal transduction, including KRAS, and decreased expression of genes related to cholesterol transport and lipid homeostasis. We show that inhibition of MEK/ERK or cholesterol supplementation rescued changes in cell morphology. Further, we performed membrane fluidity measurements of cells exposed to PFOS and found elevated membrane disorder and fluidity. Our results are consistent with a model in which PFOS perturbs plasma membrane, activates stress-response signaling pathways, and impairs epithelial cell function. These studies establish a framework for understanding the effects of PFAS on cell physiology.

The global industrialization and rapid urbanization elevated the risk of toxic pollutant exposure, which affects human health specially during pregnancy. Pregnant mothers are daily exposed to bisphenol-A (BPA), which is a common plastic leachate and a prominent toxic pollutant present in our environment. BPA act as an endocrine disrupting chemical (EDCs) by altering feto-placental homeostasis. This persistent and potent exposure of BPA during gestation can trigger placental damage affecting trophoblast cell function and survival. BPA even disrupts specific signalling cascades by altering post translational protein phosphorylation. However, this BPA mediated dysregulation of signalling nodes in early trimester placenta is still unexplored. Therefore, this study investigates the global proteome changes in post-BPA exposed extravillous trophoblast (EVTs) cells, which revealed a BPA mediated dynamic regulation of phosphoproteome-signatures and their associated kinases. Further inspection showed that the altered phosphorylation of c-JUN (S63) and GSK3 (Y279) is associated with BPA toxicity in EVTs and placenta. This altered phosphorylation affects the cellular signalling downstream, imparting damage upon the growing feto-placental unit. This highlights an altered phosphorylation mediated mechanism of BPA toxicity in placenta which can cause an onset of adverse pregnancy outcome. Data are available via ProteomeXchange with the identifiers PXD074780.

Microbially induced concrete corrosion (MICC) is a significant issue that reduces the service life of sewer systems. Bacteriostatic agent in concrete can inhibit microbial activity and the process of MICC to some extent. However, a systematic comparison of the inhibition effects of various bacteriostatic agents on MICC remains lacking. In this study, three bacteriostatic agents (copper oxide, nickel, and sodium tungstate) were investigated for their inhibitory effects on MICC. For each inhibitor, the cement mortar coupons with 0.05 wt%, 0.1 wt%, and 0.2 wt% of the inhibitor were prepared. The coupons were partially submerged in sewage of a controlled laboratory corrosion chamber (20 {+/-} 5 ppm H2S) to simulate the tidal region of gravity sewer. During the 56 days of exposure, the intensification of pores, cracks, surface erosion, and spalling was observed on all coupons. After 56 days of exposure, the sulfate concentration and adenosine triphosphate (ATP) content of coupons without inhibitor were 10.65 mg/cm2 and 30.17 {+/-} 3.87 mol/cm2, respectively. They were higher than those of coupons containing 0.05 wt%, 0.1 wt%, and 0.2 wt% of copper oxide and 0.05wt% of nickel. The temporal profiles of ATP of coupons without inhibitor was similar to those of coupons containing sodium tungstate. After exposure for 28 days, the surface pH of coupons without inhibitor was 7.45, meanwhile of those coupons containing 0.2 wt% of copper oxide and 0.05 wt% of nickel were 9.42 and 9.93, respectively. Those results indicated that the bacteriostatic effect of copper oxide and nickel (0.05 wt %) was found to be the most prominent. The findings indicate that a single bacteriostatic agent is only effective during specific corrosion stages, suggesting that a combination of multiple agents may be a promising strategy to combat the multi-stage MICC process over the long term. This study provides a theoretical basis for the selection and development of protective materials against concrete corrosion in sewer networks.

Azoxystrobin is a widely used fungicide that has been associated with to reproductive, neurological, and developmental defects. This chemical also disrupts gut microbial communities; however, if these perturbations contribute to the harms associated with exposure to azoxystrobin, this remains unclear. In this study, we investigated the effects of acute exposure to a series of concentrations (5-500 mg/kg) of azoxystrobin on the host and gut microbiota in zebrafish. Fecal amplicon and shotgun metagenomic sequencing was integrated with liver gene expression to quantify associations between microbiome disruption azoxystrobin toxicity in the host. Azoxystrobin exposure resulted in significant alteration in microbiome composition and functional potential in a dose- and sex-dependent manner. Microbial communities in exposed animals exhibited an increased abundance of xenobiotic metabolism pathways and decreased bacterial motility and lipopolysaccharide biosynthesis pathway metabolism. At the host level, histopathology identified increased biliary proliferation, most evident in medium- and high-dose fish. We also observed hepatic transcriptional changes consistent with a stress response, including altered redox-associated genes and reduced expression of lipid and small-molecule metabolic genes, with sex-stratified differences. Importantly, alterations in host transcriptional programming correlated with the compositional changes in exposed microbiota. Together, these results suggest concurrent impacts of azoxystrobin on gut microbiota and the liver implicate the microbiome as a potential contributor to changes in liver gene expression during exposure. ImportanceWidespread fungicide use contaminates ecosystems worldwide, but the biological pathways underlying their effects on humans and other animals are not well understood. Using zebrafish (Danio rerio), we found that short-term exposure to the fungicide azoxystrobin was associated with changes in the gut microbiome, liver gene activity, and liver changes. Exposure produced dose- and sex-dependent shifts in microbial communities, including changes in predicted microbial functions involved in chemical metabolism, bacterial motility and defense. Compositional changes in the microbiome correlated with gene-expression changes consistent with stress and altered metabolism in exposed fish, suggesting that exposure induced disruption may contribute to exposure impact to the host. These results highlight a potential role for the microbiome in mediation of the impacts of azoxystrobin on host physiology. As such microbial based interventions could be a viable strategy to mitigate exposure impacts on health.

Tropical coastal ecosystems in Southeast Asia are facing rapid warming and increasing pollution. Shallow coastal waters now frequently exceed 34 {degrees}C during marine heatwaves, potentially pushing tropical ectotherms beyond their thermal optimum while they are simultaneously exposed to copper (Cu) contamination, especially from aquaculture and shipping activities. However, how warming alters Cu toxicity in dominant tropical zooplankton remains poorly understood. We examined the effects of Cu (0 - 40 {micro}g L-{superscript 1}) across a realistic temperature gradient (26 - 35 {degrees}C) on the calanoid copepod Pseudodiaptomus annandalei, a dominant grazer of coastal plankton communities. Adult survival, cumulative faecal pellet production (as a proxy for energy intake), and cumulative nauplii production were quantified over seven days. No significant effects of temperature or Cu on adult survival were detected, likely reflecting age-dependent variability among wild-collected individuals. In contrast, temperature strongly structured feeding and reproductive performance, which peaked at 29 - 32 {degrees}C and declined at 35 {degrees}C. Cu exposure alone had no significant effects at 26 - 32 {degrees}C due to high variability in responses. At 35 {degrees}C, however, cumulative nauplii production decreased significantly at 30 {micro}g Cu L-{superscript 1} but increased at 20 {micro}g Cu L-{superscript 1}, while faecal pellet production was reduced in Cu-exposed copepods. These findings indicate that warming can modify contaminant effects in tropical zooplankton and highlight the importance of incorporating realistic thermal regimes and natural population variability into ecological risk assessments under climate change.

Bats are exposed to a variety of pollutants, including cadmium (Cd), that can impair immune function and potentially increase viral shedding and burden. Despite this, little is known about the impacts of heavy metals on bats. This study aimed to determine the impacts of Cd exposure on bat T and B cell immune responses in naive and coronavirus infected bats and determine the impact of Cd on viral replication in Jamaican fruit bat (JFB; Artibeus jamaicensis) cells. To determine the impact of Cd exposure on adaptive immune responses, splenocyte cultures from naive and BANAL-52 coronavirus infected JFB were treated with 0, 1, and 10 {micro}M Cd and stimulated overnight with concanavalin A. RNA was extracted, a SYBR Green qPCR was used to assess gene expression. To determine if Cd exposure increased viral replication, two JFB kidney cell clones were treated with 0, 1, 10, and 50 {micro}M of CdCl2 overnight and then infected with Cedar virus (CedV). Supernatants were collected and viral titers determined. Several transcripts were upregulated in both naive and virus infected JFB splenocytes treated with Cd. B cell transcripts were significantly upregulated in a dose-dependent manner and T cell transcripts were also increased in Cd treated splenocytes. Assessment of transcripts associated with T cell subsets suggest a predominant Th2 response in Cd treated splenocytes. Viral replication was not significantly different in Cd treated kidney clones compared to the non-treated cells. These studies provide evidence that JFB adaptive immune responses are altered when exposed to low Cd concentrations.

Urbanization-driven environmental change has significant implications for human health and well-being. However, studies have found differing patterns in microbial diversity along urbanization gradients; and it remains unknown whether this reflects methodological limitations or genuine ecological complexities. Resolving these inconsistencies requires innovative, reproducible methods that accurately reflect human contact with environmental microbiota. In this study, we have validated a new method for assessing environmental microbial exposure by measuring microbiota from particulate matter collected from shoe soles and studied the influence of vegetation at different proximities. Through repeated walks on routes along an urbanization gradient in Finland, we show that left and right shoe sole dust from the same walk and same route represent more similar microbial communities compared to different walks and routes. We found that bacterial biomass and diversity were best predicted by Normalized Difference Vegetation Index (NDVI, as a measure of greenness) immediately surrounding the walking path, whereas fungal communities responded to broader landscape-scale greenness (100m-1km), suggesting that bacteria and fungi are governed by different dispersal processes. Importantly, NDVI explained these differences in diversity more effectively than simple classifications of the path based on its substrate and whether it was in a rural or urban setting. Shoe sole dust sampling offers a simple, effective, and reliable approach for evaluating microbial exposures, capturing scale-dependent microbial responses to vegetation, and enabling more robust epidemiological studies on the health effects of greenness and environmental biodiversity.

Micro and nanoplastics are pollutants which concentration in different biotopes increases continuously over time, which poses the question of their potential effects on health. In animals, these micro and nanoplastics are recognized as particulate materials and thus handled by macrophages, which are therefore a key cell type to study. Most studies have used an experimental scheme in which the cells are exposed to a single dose of plastics, with a readout made immediately after exposure. However, this classical experimental scheme does not take into account the impact of biopersistence, nor the potential cellular adaptation that may take place when cells are exposed repeatedly to a low dose of plastics. We thus used a repeated exposure scheme, in order to better take into account these phenomena. Within this frame, we compared the macrophages responses to a persistent nanoplastic, i.e. polystyrene nanoparticles and to a biodegradable nanoplastic, i.e. polylactide, by a combination of proteomic and targeted experiments. Our results show that under this repeated exposure scheme, the proteome changes were of a lesser (for PS) or similar (for PLA) extent than under the acute exposure mode, indicating cell adaptation. However, PLA particles induced mitochondrial dysfunction and depression of response to bacterial molecules perceived as danger signals, such as lipopolysaccharide. Polystyrene nanoparticles also induced a slight alteration of the immune functions of macrophages. This indicates harmful effects even in the repeated exposure scheme.

Microplastics (MPs), resulting from plastic objects and waste degradation, are increasingly abundant, particularly in marine environments. They exhibit a hydrophobic surface on which biofilms form easily. Metagenomic analyses of these biofilms have revealed that they often contain bacterial species potentially pathogenic to humans or animals. For this reason, MPs are suspected to present a risk for public health by acting as a vector for pathogenic bacteria species. To better understand this hazard, we studied different factors potentially affecting the bacterial attachment rate to MPs. Focusing on the fish pathogen Vibrio anguillarum, a collection of 16 strains was assembled and GFP-labelled. Their attachment rates were measured using fluorescence microscopy on three types of MPs (milled polypropylene and polyethylene terephthalate particles and commercially available polystyrene beads). A strong effect of the particle type was found, likely linked to both the chemical composition of the particles and the surface characteristics, with higher attachment rates on rough particles. Our results also revealed a strong intra-specific variation in attachment rate, highlighting the need of testing several strains of the same species to assess attachment rate and related hazards. Finally, it was observed that when a biofilm already formed on the MPs (by field-incubation of the MPs along the Mediterranean French coast), differences in attachment rates between particle types were erased. It was concluded that the attachment rate of V. anguillarum depends on a combination of biotic and abiotic factors, which makes risk assessment of MPs as vectors of pathogenic bacteria species a very complex task.

Biofilms in the built environment (BE) can harbor pathogens and have been linked with negative health outcomes, particularly in hospital environments. The formation of biofilms requires bacterial cell attachment on surfaces, such as hospital plumbing, which can have varying properties, including roughness, wettability, chemistry, and charge. Despite the importance of bacterial attachment to surfaces, the role of multiple surface properties has been minimally investigated. Using seven materials with differing surface characteristics, this work considers the initial attachment of Escherichia coli, Pseudomonas aeruginosa, Bacillus subtilis, and Staphylococcus aureus to investigate the impact of several surface characteristics. Initial attachment was evaluated using column experiments and compared to batch experiments in which bacterial growth on coupons was monitored. The attachment of all bacterial species was not influenced by material surface properties, with similar attachment seen across materials tested. Bacterial cell envelope morphology affected attachment, with gram-negative species displaying greater attachment than gram-positive species. Attachment efficiency () was found to be a good predictor of bacterial attachment, with greater sensitivity than batch tests. Establishment of commensal communities should be the focus for limiting pathogens in the BE, as engineering surfaces to reduce microbial attachment appears to offer limited benefit.

O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=112 SRC="FIGDIR/small/708170v1_ufig1.gif" ALT="Figure 1"> View larger version (51K): org.highwire.dtl.DTLVardef@4c2513org.highwire.dtl.DTLVardef@116256corg.highwire.dtl.DTLVardef@f30846org.highwire.dtl.DTLVardef@1a44e00_HPS_FORMAT_FIGEXP M_FIG O_FLOATNOGraphical abstractC_FLOATNO C_FIG The extensive use of herbicides and antibiotics in aquaculture has led to compounded pollution of coastal waters, marked by the co-occurrence of herbicides, antibiotic residues, and antibiotic resistance genes (ARGs). Plasmid-mediated conjugative transfer is a major driver of the dissemination and evolution of ARGs, yet the influence of herbicides alone or in combination with antibiotics on this process in aquatic bacterial communities remains unclear. In this study, we demonstrated that triazine herbicides, alone and in combination with a fluoroquinolone antibiotic, significantly promote the conjugative transfer of the broad-host-range RP4 plasmid. Using Escherichia coli DH5 as a donor, we observed increased plasmid transfer to multiple recipients, including E. coli HB101, Pseudomonas putida KT2440, and a natural coastal seawater microbial community. The enhanced transfer under co-exposure was associated with several interacting mechanisms, including elevated intracellular reactive oxygen species (ROS) and adenosine triphosphate (ATP) levels, increased cell membrane permeability, altered extracellular polymeric substance (EPS) composition, and upregulated expression of conjugation-related genes. Overall, this work underscores the potential role of combined herbicide and antibiotic contamination in shaping the microbial resistome of coastal ecosystems and provides insights to inform strategies for mitigating the spread of antibiotic resistance.

BackgroundMicroplastics and nanoplastics (MNP) are an increasingly recognized component of airborne particulate matter, yet their impact on respiratory health is unclear. This study aimed to develop a job exposure matrix (JEM) for occupational exposure to airborne MNP (PlastiXJEM(R)) and examine its association with respiratory outcomes in the Lifelines cohort. MethodsFour experts scored occupational airborne MNP exposure levels (none, low, high) for all ISCO-08 occupations based on documented sources and published evidence. After consensus, the PlastiXJEM(R) was applied to baseline current or last-held jobs of 136,928 adult Lifelines participants. Cross-sectional and longitudinal associations with lung function, respiratory symptoms, and asthma were assessed using linear and logistic regression models adjusted for age, sex, smoking, height, BMI, and co-exposure to organic dust, gasses and fumes, pesticides, metals, solvents and silica. ResultsHigh exposure was associated with lower FEV (-43 ml; 95% CI:-61;-25), lower FVC (-47 ml(-69;-26)), lower FEV1%FVC (-0.26 % (-0.51;-0.00) and higher odds of airway obstruction, respiratory symptoms and asthma (e.g. dyspnea OR=1.58; 1.34-1.87). Low exposure was associated with lower FEV1 and FVC in women only. Associations were attenuated after adjustment for socio-economic status but remained for FEV, airway obstruction and dyspnea. MNP exposure was not associated with accelerated lung function decline or with the development of airway obstruction, respiratory symptoms, or asthma. ConclusionOccupational exposure to airborne MNP is associated with lower lung function and a higher prevalence of respiratory symptoms in this cohort. These findings warrant further investigation with complete occupational histories.

BackgroundWhile coal mine fire smoke has been linked to short-term increases in cardiovascular events, there is little evidence on long-term risks. We investigated longer-term risk of major adverse cardiovascular events (MACE) following the 2014 Hazelwood coal mine fire in regional Victoria, Australia. MethodsIn this cohort study, combined administrative data on ambulance attendances, emergency department presentations, hospital admissions, and mortality from March 2014 to June 2022, with survey data from 2016/17. Time-location diaries for the mine-fire period were combined with modelled fire-related particulate matter [≤]2.5{micro}m in diameter (PM2.5) to estimate individual exposures. We analysed the association between PM2.5 exposure and time to MACE using a recurrent event survival analysis, adjusting for key confounders. Outcomes were examined over 8 years of follow-up and stratified by time. ResultsN = 2,725 cohort members agreed to linking their survey responses to administrative data. There was no detectable effect of fire-related PM2.5 exposure on overall risk of MACE during 8-year follow-up. However, there was weak evidence suggesting increase in MACE risk in the first 3 years post-fire, with hazard ratios ranging from 1.05-1.18 per 10{micro}g/m3 of daily average PM2.5 exposure. Nearly all analyses of cardiovascular death detected an increased risk across the entire follow-up period, with hazard ratios ranging from 1.19-1.25 per 10{micro}g/m3. ConclusionsWe found smoke exposure predicted an increase in cardiovascular health service use in the three years after the mine fire. There was additional evidence that the mine fire increased risk of cardiovascular death over the entire 8-year follow-up. This suggests that cardiovascular screening should be a routine component of planning recovery after landscape fires.

The East Asian region, known for its high levels of human and fishery activities, experiences serious plastic pollution in the marine environment, especially in seawater and along coastlines. Wharf roaches (Ligia spp.) collected from the coast of western Japan frequently ingest expanded polystyrene (EPS), which is then excreted as microplastic through their feces. However, the impact of EPS exposure and ingestion on the gut microbiome of wharf roaches remains unclear. Thus, this study aimed to investigate the effects of EPS ingestion on the gut microbiota of wharf roaches by examining their gut microbiota and gene expression. The expression levels of more than 400 genes, including those associated with xenobiotic metabolism, and the abundance of gut microbial community were altered. Microbial analysis revealed that at least five archaeal types, two to four bacterial types, three to seven eukaryotic types, and three viral types were involved in a correlation network composed of strong associations. Among them, Haloquadratum, Halalkalicoccus, and Methanospirillum (archaea); Volvox (eukaryote); and Varicellovirus and T4-like viruses showed significantly increased abundance. Furthermore, covariance structure analysis indicated that the viruses and methanogens played key causal roles as characteristic factors related to EPS administration. In conclusion, EPS disrupts the intestinal environment of wharf roaches and serves as a potential material for viral activation and methane production. Building on our previous field study that identified wharf roaches as potential indicators of coastal EPS pollution, this study provides novel insights into the ecological impacts of EPS ingestion and consequences of plastic pollution.

Promyelocytic leukemia (PML) proteins are known to form phase-separated nuclear punctate structures called PML-nuclear bodies (PML-NBs). The integrity disruption of PML-NBs is linked with the pathogenesis of acute promyelocytic leukemia (APL), and trivalent arsenic (As3+) has been used for the clinical treatment of APL to restore normal PML-NBs. As3+ is considered to bind to cysteine residues and enhances modification of PML with small-ubiquitin-like protein (SUMO). We exposed U-2OS and CHO-K1 cells stably overexpressing PML-VI to As3+ and found that the solubility of PML decreased and SUMOylation of PML increased after 2 h-exposure to 3 M As3+. Contrary to As3+-induced remarkable biochemical changes including the solubility change and SUMOylation of PML, microscopic observation of PML-NBs was not changed clearly after a short-term exposure to As3+. The number of PML-NBs decreased and extranuclear PML bodies (EnPBs), which are remniscences of PML-NBs after nuclear membrane breakdown at mitosis, increased after exposure to As3+ for 24 - 72 h. The amount of SUMOylated PML decreased after prolonged exposure to As3+ while the solubility of PML was kept low, suggesting that As3+ stabilized EnPB without SUMOylation. The effects of As3+ on EnPBs were clearly observed at as low as 0.3 M As3+ which corresponds to inorganic arsenic level in drinking water worldwide.

Carbon dioxide (CO2), methane (CH4) and nitrous oxide (N2O) are the main greenhouse gases (GHGs) contributing to the ongoing climate crisis. Among those N2O has the highest global warming potential and is mainly of microbiological origin. Tropical rainforests are considered the primary natural source, although in recent years fluxes of N2O from polar ecosystems have been reported at comparable levels. In this study we aimed to identify High Arctic terrestrial habitats with the highest potential to become sources of N2O emissions. A microbiological and geochemical analysis was performed on soil procured from the biologically and geomorphologically diverse South Spitsbergen region in search of biotic and abiotic determinants of a N2O emission hotspot. Terrestrial sites within this High Arctic area vastly differed in their potential to emit substantial N2O amounts. External organic matter inputs were pivotal in maintaining a pool of inorganic nitrogen compounds for microbially-mediated N2O-generating processes such as denitrification. The examined planktivorous seabird colony presented a unique, potential N2O emission hotspot as it featured persistent acidification of the surrounding soil, a steady ammonia release and nitrate presence even after breeding season closure. Soils of the majority of analyzed sites did not display detectable nitrate and/or ammonia levels, with some areas having the characteristics of a N2O-sink rather than an emitter, especially postglacial moraine deposits. The presented data encourage further, more targeted investigations of High Arctic N2O emission hot- and coldspots to progressively improve N2O emission estimates for permafrost affected regions worldwide.

Stress Granules (SGs) are cytoplasmic biomolecular condensates that form in response to a variety of stress conditions, though their function remains unclear. "Canonical" SGs - caused by stressors like sodium arsenite - are dynamic and cytoprotective, allowing cells to evade cell death during periods of stress. Ultraviolet (UV) irradiation is known to elicit a "non-canonical" SG subtype, lacking canonical SG components such as eukaryotic initiation factor 3 and polyadenylated mRNAs. The exact function of UV SGs, and the mechanisms driving their formation, remain unknown. Here we report the findings of a comparative analysis of UVA, UVB and UVC exposures on SG formation in three cell types: osteosarcoma (U2OS), keratinocytes (HaCaT), and mouse embryonic fibroblasts (MEF). We observed that SG formation in response to UV is highly cell type dependent. UVB and UVC induce robust SG formation in U2OS cells. However, only UVC exposure induced modest SG formation in MEFs, and none of the wavelengths caused SGs in HaCaT. While UVC-induced SGs in U2OS cells appear to be cell cycle dependent and specific to G1, UVB induced SG formation regardless of cell cycle stage. We tested the hypothesis that oxidative stress triggered by UV may be driving UV SG formation, and that keratin may buffer this effect, by overexpressing keratin in U2OS. Interestingly, we found that keratin and antioxidant treatment efficiently suppressed arsenite-induced SGs but had no effect on UV SGs. Our work confirms that UV SG formation is cell type specific and is not driven by oxidative stress.

Ocean Alkalinity Enhancement (OAE) is a marine carbon dioxide removal (mCDR) strategy that involves adding alkaline substances to surface waters to enhance CO2 uptake and storage. The dispersal of alkaline materials such as sodium hydroxide (NaOH) into seawater can cause rapid increases in pH and total alkalinity (TA) that substantially exceeds natural variability in marine environments. Such fluctuations may negatively affect marine life, especially small animals like copepods who cannot avoid OAE plumes and whose physiological processes could be disrupted by large and rapid shifts in seawater pH. To address knowledge gaps regarding potential biological impacts of OAE, we studied these effects in Calanus finmarchicus, a keystone copepod species in the Northwest Atlantic Ocean. We exposed C. finmarchicus from the late juvenile copepodite stages and adult females to NaOH-dosed seawater at pH 10.5 ([~]5,000 {micro}mol kg-1 TA) and pH 9.0 ([~]3,150 {micro}mol kg-1 TA) for durations that reflect expected short-term exposure times during field OAE deployments (pH 10.5: 1, 5, 10 minutes; pH 9.0: 1, 15, 30 minutes). None of the treatment combinations resulted in mortality immediately after the initial exposure. Individuals were monitored for survival for 72 hours post-exposure (hpe), and only one treatment group (juveniles exposed to pH 10.5 for 10 minutes) showed a significant reduction in final survival; no other pH-duration combination showed increased mortality. Effects on the ability to initiate an escape response were more substantial. Adult females treated with pH 10.5 for 5 or 10 minutes showed a significant reduction in escape response immediately after exposure. In contrast, juveniles showed no immediate change in escape response following exposure to pH 10.5 or pH 9.0, although juveniles exposed to pH 10.5 for 10 minutes exhibited reduced escape response at 24 hpe. Using microrespirometry, we measured oxygen consumption following a 10-minute exposure to pH 10.5 and detected no effect on routine metabolic rate immediately post-exposure or at 12 hpe. Overall, our results suggest that C. finmarchicus is relatively tolerant to short-term exposures to very high pH and alkalinity. Future work should prioritize longer-term exposure under more moderate ocean OAE conditions.

Diatoms significantly contribute to aquatic primary productivity and biogeochemical cycles, with motility playing a crucial role in their ecological success. While several factors influence their motility, the effect of water flow remains poorly understood. This study used a digital holographic microscope to investigate the locomotion of the pennate diatom Navicula cf parapontica under varying flow rates. It demonstrates, for the first time, that Navicula perceives and actively counteracts water flows. As flow rates increased up to 500 nL/s, cells consistently moved against the current and frequently adjusted their orientation to maximize resistance. This behaviour allowed the diatoms to maintain a stable locomotion velocity despite a 6.7-fold increase in flow rate. This active rheotaxis likely serves as a strategy to resist resuspension and passive dispersal. These findings reveal a behavioural trait that might play significant role in the way benthic diatom communities maintain their position in the sediments, influencing bentho-pelagic coupling and biogeochemical processes.

Wildfires have become more frequent and intense worldwide. Wildfire emitted particulate matter (WFPM) can be more toxic than urban background PM due to its greater content of nanoscale size (WFPM0.1) and presence of more polar organic compounds, including polycyclic aromatic hydrocarbons (PAHs). While exposure to WFPM has been linked to cardiovascular and respiratory diseases, its impact on female reproduction remains elusive. Here, we used an in vivo mouse intratracheal exposure model and a 3D ovarian follicle culture system, together with molecular, transcriptomic, and computational approaches, to examine the female reproductive effects of lab-synthesized (LS-WFPM0.1) and real-world Canadian WFPM0.1 (C-WFPM0.1), collected from the New York City and New Jersey metropolitan area during the June 2023 wildfire events. Intratracheal exposure to environmentally relevant dose of LS-WFPM0.1 disrupted mouse estrous cycles and elevated serum concentrations of estradiol and testosterone. RT-qPCR and single-follicle RNA-sequencing (RNA-seq) analysis revealed altered steroidogenic genes, transcriptomic changes, and activation of aryl hydrocarbon receptor (AhR) in antral follicles from mice treated with LS-WFPM0.1. LS-WFPM0.1 consistently increased testosterone secretion and stimulated genes related to androgen synthesis and AhR in vitro. Single-follicle and single-oocyte RNA-seq analysis identified differentially expressed genes related to inflammation in somatic cells and mitochondrial respiratory chain in oocytes. Both C-WFPM0.1 and benzo[a]pyrene, a high-molecular-weight PAH, reproduced these ovarian defects. Mechanistically, AhR inhibition reversed hyperandrogenism induced by WFPM0.1. Together, our findings suggest that WFPM0.1, an increasingly pervasive environmental exposure, adversely impacts female reproductive functions by disrupting ovarian steroidogenesis and inducing hyperandrogenism through AhR activation, highlighting an urgent unmet need for further mechanistic studies and epidemiological investigations to define the reproductive risks of wildfire smoke exposure in human populations.