Persistent Organic Pollutants released from decomposed adipose tissue affect mitochondrial enzyme function in the brain and eyes other than the liver.

Persistent organic pollutants (POPs) are toxic chemicals that can accumulate in the human body, and particularly in adipose tissue. POPs can induce metabolic diseases via mitochondrial dysfunction and can also cause cancer, obesity, and cardiovascular and neurodegenerative diseases. Although the effects of POPs were studied by evaluating mitochondrial function, which is fundamental in investigating the etiologies of various metabolic diseases, the physiological impact of POPs released by the decomposition of fat in adipose tissue is barely understood. Therefore, to investigate the mitochondrial dysfunction caused by POPs released from adipose tissue to other organs, zebrafish were exposed to POPs and placed into four groups: control (C), obesity control (OC), obesity control with POPs (OP), and POP exposure with obesity and caloric restriction (OPR). Next, the activities of the mitochondrial respiratory complexes and the levels of ATP production, reactive oxygen species/reactive nitrogen species (ROS/RNS), and antioxidants, such as glutathione and superoxide dismutase, were measured in the brain, eyes, and liver, as these are the major organs most susceptible to metabolic diseases. POPs released from adipose tissue showed a stronger effect than the direct effects of obesity and POPs on mitochondrial enzyme activity in the brain and eye. Released POPs increased mitochondrial complex I activity and decreased mitochondrial complex II activity compared with normal, obesity, and POP-treated conditions in the brain and eyes. However, the mitochondrial complexes' activities in the liver were affected more by obesity and POPs. In the liver, the mitochondrial enzyme activities of the OPR group seemed to recover to the control level, but it was slightly lowered in the OC and OP groups. Independently, the ROS/RNS and antioxidant levels were not affected by obesity, POPs, or the released POPs in the brain, eye, and liver. The results indicate that POPs stored in adipose tissue and released during fat decomposition did not affect oxidative stress but could affect mitochondrial respiratory enzymes in organ dependent manner. This study is meaningful in that it provides experimental evidence that stored POPs affect specific organs for prolonged periods and can be linked to various diseases in advance.

The role of extracellular polymeric substances (EPS) in chemical-degradation of persistent organic pollutants in soil: A review.

Persistent organic pollutants (POPs) in soil show high environmental risk due to their high toxicity and low biodegradability. Studies have demonstrated the degradation function of microbial extracellular polymeric substances (EPS) on POPs in various matrices. However, the degradation mechanisms and the factors that influence the process in soil have not been clearly illustrated. In this review, the characteristics of EPS were introduced and the possible mechanisms of EPS on degradation of organic pollutants (e.g., external electron transfer, photodegradation, and enzyme catalysis) were comprehensively discussed. In addition, the environmental conditions (e.g., UV, nutrients, and redox potential) that could influence the production and degradation-related active components of EPS were addressed. Moreover, the current approaches on the application of EPS in biotechnology were summarized. Further, the future perspectives of enhancement on degradation of POPs by regulating EPS were discussed. Overall, this review could provide a new thought on remediation of POPs by widely-existing EPS in soil with low-cost and minimized eco-disturbance.

Varying temporal trends in the levels of six groups of legacy persistent organic pollutants (POPs) in liver of three gadoid species from the North Sea.

From 2005 to 2019, three gadoid species, Atlantic cod (Gadus morhua), haddock (Melanogrammus aeglefinus) and saithe (Pollachius virens), were sampled approximately every third year in the northeastern part of the North Sea. Liver samples were analyzed to investigate levels and temporal trends of six groups of persistent organic pollutants (POPs): polychlorinated biphenyls (PCBs), dichlorodiphenyltrichloroethane (DDT) and its degradation products, hexachlorocyclohexanes (HCHs), hexachlorobenzene (HCB), trans-nonachlor (TNC), and polybrominated diphenyl ethers (PBDEs). Some of the highest average concentrations were found in cod, the levels otherwise being similar between the three species and mostly below established threshold values. The levels of all the contaminants except HCB and TNC were higher than previously reported for cod and haddock in the Barents Sea. Significantly decreasing levels were found for Σ7PCBs, ΣDDTs, ΣHCHs and Σ15PBDEs in all three species, and for TNC in haddock and saithe, while there was no significant trend for TNC in cod. HCB levels increased significantly in cod and haddock and showed only a minor decrease in saithe. The observed time trends of legacy POPs demonstrate the persistence of some of the studied pollutants despite efforts to eliminate them from the marine environment.

Differential gene expression and developmental pathologies associated with persistent organic pollutants in sentinel fish in Troutman Lake, Sivuqaq, Alaska.

Persistent organic pollutants (POPs) are lipophilic compounds that bioaccumulate in animals and biomagnify within food webs. Many POPs are endocrine disrupting compounds that impact vertebrate development. POPs accumulate in the Arctic via global distillation and thereby impact high trophic level vertebrates as well as people who live a subsistence lifestyle. The Arctic also contains thousands of point sources of pollution, such as formerly used defense (FUD) sites. Sivuqaq (St. Lawrence Island), Alaska was used by the U.S. military during the Cold War and FUD sites on the island remain point sources of POP contamination. We examined the effects of POP exposure on ninespine stickleback (Pungitius pungitius) collected from Troutman Lake in the village of Gambell as a model for human exposure and disease. During the Cold War, Troutman Lake was used as a dump site by the U.S. military. We found that PCB concentrations in stickleback exceeded the U.S. Environmental Protection Agency's guideline for unlimited consumption despite these fish being low trophic level organisms. We examined effects at three levels of biological organization: gene expression, endocrinology, and histomorphology. We found that ninespine stickleback from Troutman Lake exhibited suppressed gonadal development compared to threespine stickleback (Gasterosteus aculeatus) studied elsewhere. Troutman Lake stickleback also displayed two distinct hepatic phenotypes, one with lipid accumulation and one with glycogen-type vacuolation. We compared the transcriptomic profiles of these liver phenotypes using RNA sequencing and found significant upregulation of genes involved in ribosomal and metabolic pathways in the lipid accumulation group. Additionally, stickleback displaying liver lipid accumulation had significantly fewer thyroid follicles than the vacuolated phenotype. Our study and previous work highlight health concerns for people and wildlife due to pollution hotspots in the Arctic, and the need for health-protective remediation.

Advanced biotechnology strategies for detoxification of persistent organic pollutants and toxic elements in soil.

This paper aims to comprehensively examine and present the current state of persistent organic pollutants (POPs) and toxic elements (TEs) in soil. Additionally, it seeks to assess the viability of employing advanced biotechnology, specifically phytoremediation with potent microbial formulations, as a means of detoxifying POPs and TEs. In the context of the "global treaty," which is known as the Stockholm Convention, we analyzed the 3D chemical structures of POPs and its prospects for living organisms which have not been reviewed up to date. The obstacles associated with the phytoremediation strategy in biotechnology, including issues like slow plant growth and limited efficiency in contaminant uptake, have also been discussed and demonstrated. While biotechnology is recognized as a promising method for detoxifying persistent organic pollutants (POPs) and facilitating the restoration of contaminated and degraded lands, its full potential in the field is constrained by various factors. Recent advances in biotechnology, such as microbial enzymes, designer plants, composting, and nanobiotechnology techniques, have opened up new avenues for mitigating persistent organic pollutants (POPs) and toxic elements (TEs). The insights gained from this review can contribute to the development of innovative, practical, and economically viable approaches for remediating and restoring soils contaminated with persistent organic pollutants (POPs) and toxic elements (TEs). The ultimate aim is to reduce the risks to both human and environmental health.

Concentrations and biomagnification of persistent organic pollutants in three granivorous food chains from an abandoned e-waste recycling site.

The distinct accumulation patterns of persistent organic pollutants (POPs) among granivorous groups and the biomagnification of POPs from crops to granivorous species are still unclear. In this study, occurrence and biomagnification of POPs in three granivorous species including spotted dove (Spilopelia chinensis), scaly-breasted munia (Lonchura punctulata), and reed vole (Microtus fortis Buechner) from a former e-waste recycling site were investigated. Concentrations of polychlorinated biphenyls (PCBs) and polybrominated diphenyl ethers (PBDEs) in granivorous species ranged from 41.5 to 1370 and 21.1 to 3890 ng/g lipid weight, respectively. PCBs and PBDEs were the main POPs in birds and vole, while decabromodiphenyl ethane (DBDPE) and PBDEs were predominant POPs in crops. The dominance of BDE 209 was observed in samples, with few exceptions. Biomagnification factors (BMFs) of POPs in birds and vole were measured. BMFs of most POPs in vole were higher than those in birds, indicating that POPs had greater biomagnification potential in vole. Species-specific biomagnification of POPs might be affected by many factors, such as physiochemical properties and metabolic capability of POPs. There was significant correlation between concentration ratios of POPs in muscle/air and log KOA, which demonstrated that respiratory elimination to air affects biomagnification of POPs in granivorous birds and vole.

Exposure to the aryl hydrocarbon receptor agonist dioxin disrupts formation of the muscle, nerves, and vasculature in the developing jaw.

Human exposure to environmental pollutants can disrupt embryonic development and impact juvenile and adult health outcomes by adversely affecting cell and organ function. Notwithstanding, environmental contamination continues to increase due to industrial development, insufficient regulations, and the mobilization of pollutants as a result of extreme weather events. Dioxins are a class of structurally related persistent organic pollutants that are highly toxic, carcinogenic, and teratogenic. 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is the most potent dioxin compound and has been shown to induce toxic effects in developing organisms by activating the aryl hydrocarbon receptor (AHR), a ligand activated transcription factor targeted by multiple persistent organic pollutants. Contaminant-induced AHR activation results in malformations of the craniofacial cartilages and neurocranium; however, the mechanisms mediating these phenotypes are not well understood. In this study, we utilized the optically transparent zebrafish model to elucidate novel cellular targets and potential transcriptional targets underlying TCDD-induced craniofacial malformations. To this end, we exposed zebrafish embryos at 4 h post fertilization to TCDD and employed a mixed-methods approach utilizing immunohistochemistry staining, transgenic reporter lines, fixed and in vivo confocal imaging, and timelapse microscopy to determine the targets mediating TCDD-induced craniofacial phenotypes. Our data indicate that embryonic TCDD exposure reduced jaw and pharyngeal arch Sox10+ chondrocytes and Tcf21+ pharyngeal mesoderm progenitors. Exposure to TCDD correspondingly led to a reduction in collagen type II deposition in Sox10+ domains. Embryonic TCDD exposure impaired development of tissues derived from or guided by Tcf21+ progenitors, namely: nerves, muscle, and vasculature. Specifically, TCDD exposure disrupted development of the hyoid and mandibular arch muscles, decreased neural innervation of the jaw, resulted in compression of cranial nerves V and VII, and led to jaw vasculature malformations. Collectively, these findings reveal novel structural targets and potential transcriptional targets of TCDD-induced toxicity, showcasing how contaminant exposures lead to congenital craniofacial malformations.

Environmentally realistic concentrations of chlorinated, brominated, and fluorinated persistent organic pollutants induce the unfolded protein response as a shared stress pathway in the liver of Atlantic cod (Gadus morhua).

In the North Sea and North Atlantic coastal areas, fish experience relatively high background levels of persistent organic pollutants. This study aimed to compare the mode of action of environmentally relevant concentrations of mixtures of halogenated compounds in Atlantic cod. Juvenile male cod with mean weight of 840 g were exposed by gavage to dietary mixtures of chlorinated (PCBs, DDT analogs, chlordane, lindane, and toxaphene), brominated (PBDEs), and fluorinated (PFOS) compounds for 4 weeks. One group received a combined mixture of all three compound groups. The results showed that the accumulated levels of chemicals in cod liver after 4 weeks of exposure reflected concentrations found in wild fish in this region. Pathway analysis revealed that the treatment effects by each of the three groups of chemicals (chlorinated, brominated, and fluorinated) converged on activation of the unfolded protein response (UPR). Upstream regulator analysis predicted that almost all the key transcription factors (XBP1, ERN1, ATF4, EIF2AK3, and NFE2L2) regulating the UPR were significantly activated. No additive effect was observed in cod co-treated with all three compound groups. In conclusion, the genome-wide transcriptomic study suggests that the UPR pathway is a sensitive common target of halogenated organic environmental pollutants in fish.

α-Galactosidase interacts with persistent organic pollutants to induce oxidative stresses in rice (Oryza sativa L.).

Persistent organic pollutants (POPs) in agricultural soil often triggered metabolic alterations and phytotoxicity in plants, ultimately threatening crop quality. Unraveling the phytotoxic mechanisms of POPs in crops is critical for evaluating their environmental risks. Herein, the molecular mechanism of POP-induced phytotoxicity in rice (Oryza sativa L.) was analyzed using metabolic profile, enzyme activity, and gene expression as linkages, including polycyclic aromatic hydrocarbons, polybrominated diphenyl ethers, polychlorinated biphenyls, and phthalate esters. Despite no observable changes in phenotypic traits (e.g., biomass and length of aboveground), the levels of reactive oxygen species (ROS) were promoted under stresses of the tested POPs, particularly 2,2',4,4'-tetrabromodiphenyl ether (BDE-47), dibutyl phthalate (DBP), and di(2-ethylhexyl) phthalate (DEHP). Metabolomics analysis revealed that ROS contents positively correlated with metabolic perturbation levels (r = 0.83), among which the galactose metabolism was significantly inhibited when exposed to DBP, DEHP, or BDE-47. The α-Galactosidase (α-Gal) involved in galactose metabolism was targeted as the key enzyme for the phytotoxicity of DBP, DEHP, and BDE-47, which was revealed by the inhibition of saccharide levels (45.5-82.1%), the catalytic activity of α-Gal (18.5-24.3%), and the gene expression (28.5-34.5%). Molecular docking simulation suggested that the three POPs occupied the active sites of α-Gal and formed a stable protein-ligand complex, thus inhibiting the catalytic activity of α-Gal. Partial least-squares regression analysis indicated that α-Gal activity was negatively associated with hydrogen bond acceptor, rotatable bond, and topological polar surface area of POPs. The results offered novel insights into the molecular mechanisms of phytotoxicity of POPs and provided important information for evaluating the environmental risk of POPs.

Microbiota dysbiosis associated with type 2 diabetes-like effects caused by chronic exposure to a mixture of chlorinated persistent organic pollutants in zebrafish.

Mixtures of chlorinated persistent organic pollutants (C-POPs-Mix) are chemically related risk factors for type 2 diabetes mellitus (T2DM); however, the effects of chronic exposure to C-POPs-Mix on microbial dysbiosis remain poorly understood. Herein, male and female zebrafish were exposed to C-POPs-Mix at a 1:1 ratio of five organochlorine pesticides and Aroclor 1254 at concentrations of 0.02, 0.1, and 0.5 µg/L for 12 weeks. We measured T2DM indicators in blood and profiled microbial abundance and richness in the gut as well as transcriptomic and metabolomic alterations in the liver. Exposure to C-POPs-Mix significantly increased blood glucose levels while decreasing the abundance and alpha diversity of microbial communities only in females at concentrations of 0.02 and 0.1 µg/L. The majorly identified microbial contributors to microbial dysbiosis were Bosea minatitlanensis, Rhizobium tibeticum, Bifidobacterium catenulatum, Bifidobacterium adolescentis, and Collinsella aerofaciens. PICRUSt results suggested that altered pathways were associated with glucose and lipid production and inflammation, which are linked to changes in the transcriptome and metabolome of the zebrafish liver. Metagenomics outcomes revealed close relationships between intestinal and liver disruptions to T2DM-related molecular pathways. Thus, microbial dysbiosis in T2DM-triggered zebrafish occurred as a result of chronic exposure to C-POPs-Mix, indicating strong host-microbiome interactions.

Biomagnification and elimination effects of persistent organic pollutants in a typical wetland food web from South China.

This study investigated the quantitative sources of persistent organic pollutants (POPs), their biomagnification factors, and their effect on POP biomagnification in a typical waterbird (common kingfisher, Alcedo atthis) food web in South China. The median concentrations of polychlorinated biphenyls (PCBs) and polybrominated diphenyl ethers (PBDEs) in kingfishers were 32,500 ng/g lw and 130 ng/g lw, respectively. The congener profiles of PBDEs and PCBs showed significant temporal changes because of the restriction time points and biomagnification potential of different contaminants. The concentrations of most bioaccumulative POPs, such as CBs 138 and 180 and BDEs 153 and 154, decreased at lower rates than those of other POPs. Pelagic fish (metzia lineata) and benthic fish (common carp) were the primary prey of kingfishers, as indicated by quantitative fatty acid signature analysis (QFASA) results. Pelagic and benthic prey species were the primary sources of low and high hydrophobic contaminants for kingfishers, respectively. Biomagnification factors (BMFs) and trophic magnification factors (TMFs) had parabolic relationships with log KOW, with peak values of approximately 7. Significant negative correlations were found between the whole-body elimination rates of POPs in waterbirds and the log-transformed TMFs and BMFs, indicating that the strong metabolism of waterbirds could potentially affect POP biomagnification.

Exposure to the persistent organic pollutant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD, dioxin) disrupts development of the zebrafish inner ear.

Dioxins are a class of highly toxic and persistent environmental pollutants that have been shown through epidemiological and laboratory-based studies to act as developmental teratogens. 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), the most potent dioxin congener, has a high affinity for the aryl hydrocarbon receptor (AHR), a ligand activated transcription factor. TCDD-induced AHR activation during development impairs nervous system, cardiac, and craniofacial development. Despite the robust phenotypes previously reported, the characterization of developmental malformations and our understanding of the molecular targets mediating TCDD-induced developmental toxicity remains limited. In zebrafish, TCDD-induced craniofacial malformations are produced, in part, by the downregulation of SRY-box transcription factor 9b (sox9b), a member of the SoxE gene family. sox9b, along with fellow SoxE gene family members sox9a and sox10, have important functions in the development of the otic placode, the otic vesicle, and, ultimately, the inner ear. Given that sox9b is a known target of TCDD and that transcriptional interactions exist among SoxE genes, we asked whether TCDD exposure impaired the development of the zebrafish auditory system, specifically the otic vesicle, which gives rise to the sensory components of the inner ear. Using immunohistochemistry, in vivo confocal imaging, and time-lapse microscopy, we assessed the impact of TCDD exposure on zebrafish otic vesicle development. We found exposure resulted in structural deficits, including incomplete pillar fusion and altered pillar topography, leading to defective semicircular canal development. The observed structural deficits were accompanied by reduced collagen type II expression in the ear. Together, our findings reveal the otic vesicle as a novel target of TCDD-induced toxicity, suggest that the function of multiple SoxE genes may be affected by TCDD exposure, and provide insight into how environmental contaminants contribute to congenital malformations.

Persistent organic pollutants affect steroidogenic and apoptotic activities in granulosa cells and reactive oxygen species concentrations in oocytes in the mouse.

CONTEXT: The destruction of granulosa cells (GCs), the main functional cell type in the ovary, prevents steroid hormone production, which in turn may damage oocytes, resulting in ovarian failure. The accumulation of a number of persistent organic pollutants (POPs) in the ovarian follicular fluid (FF) has been documented, which raises serious questions regarding their impact on female fertility. AIMS: We aimed to determine whether a mixture of POPs reflecting the profile found in FF influences mouse GCs or oocyte function and viability. METHODS: A mixture of POPs, comprising perfluorooctanoate, perfluorooctane sulfonate, 2,2-dichlorodiphenyldichloroethylene, polychlorinated biphenyl 153, and hexachlorobenzene, was used. In addition to using the exact concentration of POPs previously measured in human FF, we tested two other mixtures, one with10-fold lower and another with 10-fold higher concentrations of each POP. KEY RESULTS: Steroidogenesis was disrupted in GCs by the POP mixture, as demonstrated by lower oestradiol and progesterone secretion and greater lipid droplet accumulation. Furthermore, the POP mixture reduced GC viability and increased apoptosis, assessed using caspase-3 activity. The POP mixture significantly increased the number of oocytes that successfully progressed to the second meiotic metaphase and the oocyte reactive oxygen species (ROS) concentration. CONCLUSIONS: Thus, a mixture of POPs that are typically present in human FF has detrimental effects on ovarian function: it reduces the viability of GCs, and increases the oocyte concentrations of ROS. IMPLICATIONS: These results indicate that chronic exposure to POPs adversely affects female reproductive health.

Distinct biomagnification of chlorinated persistent organic pollutants in adjacent aquatic and terrestrial food webs.

Biomagnification of persistent organic pollutants (POPs) in food webs has been studied for many years. However, the different processes and influencing factors in biomagnification of POPs in aquatic and terrestrial food webs still need clarification. Polychlorinated biphenyls (PCBs) and short-chain chlorinated paraffins (SCCPs) were measured in organisms from adjacent terrestrial and aquatic environment in this study. The median levels of PCBs in terrestrial and aquatic organisms were 21.7-138 ng/g lw and 37.1-149 ng/g lw, respectively. SCCP concentrations were 18.6-87.3 µg/g lw and 21.4-93.9 µg/g lw in terrestrial and aquatic organisms, respectively. Biomagnification factors (BMFs) of PCBs increased with higher log KOW in all food chains. BMFs of SCCPs were negatively correlated with log KOW in aquatic food chains, but positively correlated with log KOW in terrestrial food chains. The terrestrial food web had similar trophic magnification factors (TMFs) of PCBs, and higher TMFs of SCCPs than the aquatic food web. Biomagnification of PCBs was consistent in aquatic and terrestrial food webs, while SCCPs had higher biomagnification potential in terrestrial than aquatic organisms. The distinct biomagnification of SCCPs was affected by the respiratory elimination for terrestrial organisms, the different metabolism rates in various species, and more homotherms in terrestrial food webs. Fugacity model can well predict levels of less hydrophobic chemicals, and warrants more precise toxicokinetic data of SCCPs.

Amyotrophic Lateral Sclerosis-Associated Persistent Organic Pollutant cis-Chlordane Causes GABAA-Independent Toxicity to Motor Neurons, Providing Evidence toward an Environmental Component of Sporadic Amyotrophic Lateral Sclerosis.

Amyotrophic lateral sclerosis (ALS) is an incurable neurodegenerative disease characterized by the death of upper and lower motor neurons. While causative genes have been identified, 90% of ALS cases are not inherited and are hypothesized to result from the accumulation of genetic and environmental risk factors. While no specific causative environmental toxin has been identified, previous work has indicated that the presence of the organochlorine pesticide cis-chlordane in the blood is highly correlated with ALS incidence. Never before tested on the motor system, here, we show that cis-chlordane is especially toxic to motor neurons in vitro- and in vivo-independent of its known antagonism of the GABAA receptor. We find that human stem-cell-derived motor neurons are more sensitive to cis-chlordane than other cell types and their action potential dynamics are altered. Utilizing zebrafish larvae, we show that cis-chlordane induces motor neuron and neuromuscular junction degeneration and subsequent motor deficits in a touch-evoked escape response. Together, our work points to cis-chlordane as a potential sporadic ALS exacerbating environmental pollutant.

Persistent organic pollutant exposure and associations with gene expression in northern fur seals (Callorhinus ursinus) from St. Paul Island, Alaska.

Persistent organic pollutants (POPs) are highly lipophilic compounds that accumulate at increased concentrations in high tropic level organisms like marine mammals. Marine mammals' reliance on blubber makes them susceptible to accumulating POPs at potentially toxic concentrations. In this study, we analyzed POP concentrations, (polychlorinated biphenyls (PCBs), organochlorine pesticides (OCPs), polybrominated diphenyl ethers (PBDEs), and methoxylated-BDE (MeOBDE), in the blubber of 16 subsistence harvested sub-adult, male northern fur seals as well as assessed changes in mRNA gene expression of nine relevant biomarkers including the aryl hydrocarbon receptor, thyroid receptor-α, and adiponectin. PBDE and MeOBDE concentrations were significantly lower than PCB and OCP concentrations. A negative relationship was observed between percent lipid in the blubber and contaminant concentrations, both individual and sum. Expression changes in eight biomarkers were correlated with individual and sum contaminant concentrations. This study shows that contaminant concentrations measured are correlated to changes in expression of genes from different physiological systems, metabolism and endocrine, that are important for the regulation of blubber metabolism. Northern fur seals are reliant on blubber as an energy source during times of low food intake. Potential contaminant induced changes in blubber metabolism pathways could have significant impacts on the health of individuals during critical periods.

Plants to mine metals and remediate land.

Engineered plants can clean up pollution and recover technology-critical metals.

Utilizing ion mobility spectrometry-mass spectrometry for the characterization and detection of persistent organic pollutants and their metabolites.

Persistent organic pollutants (POPs) are xenobiotic chemicals of global concern due to their long-range transport capabilities, persistence, ability to bioaccumulate, and potential to have negative effects on human health and the environment. Identifying POPs in both the environment and human body is therefore essential for assessing potential health risks, but their diverse range of chemical classes challenge analytical techniques. Currently, platforms coupling chromatography approaches with mass spectrometry (MS) are the most common analytical methods employed to evaluate both parent POPs and their respective metabolites and/or degradants in samples ranging from d rinking water to biofluids. Unfortunately, different types of analyses are commonly needed to assess both the parent and metabolite/degradant POPs from the various chemical classes. The multiple time-consuming analyses necessary thus present a number of technical and logistical challenges when rapid evaluations are needed and sample volumes are limited. To address these challenges, we characterized 64 compounds including parent per- and polyfluoroalkyl substances (PFAS), pesticides, polychlorinated biphenyls (PCBs), industrial chemicals, and pharmaceuticals and personal care products (PPCPs), in addition to their metabolites and/or degradants, using ion mobility spectrometry coupled with MS (IMS-MS) as a potential rapid screening technique. Different ionization sources including electrospray ionization (ESI) and atmospheric pressure photoionization (APPI) were employed to determine optimal ionization for each chemical. Collectively, this study advances the field of exposure assessment by structurally characterizing the 64 important environmental pollutants, assessing their best ionization sources, and evaluating their rapid screening potential with IMS-MS.

Comprehensive insights into the interactions of dicyclohexyl phthalate and its metabolite to human serum albumin.

Phthalate esters (PAEs) are a type of persistent organic pollutants and have received widespread concerns due to their adverse effects on human health. Dicyclohexyl phthalate (DCHP) and its metabolite monocyclohexyl phthalate (MCHP) were selected to explore the mechanism for interaction of PAEs with human serum albumin (HSA) through molecular docking and several spectroscopic techniques. The results showed that DCHP/MCHP can spontaneously occupy site I to form a binary complex with HSA, and DCHP exhibited higher binding affinity to HSA than MCHP. At 298 K, the binding constants (Kb) of DCHP and MCHP to HSA were 24.82 × 104 and 1.04 × 104 M-1, respectively. Hydrogen bonds and van der Waals forces were the major driving forces in DCHP/MCHP-HSA complex. The presence of DCHP/MCHP induced the secondary structure changes in HSA, and the pi electrons of the benzene ring skeleton of DCHP/MCHP played a key role in this binding processes. Exposure of DCHP/MCHP to TM4 cells revealed that interactions between PAEs and serum albumin can affect their cytotoxicity; DCHP showed higher toxicity than MCHP. The binding affinity of PAEs with HSA may be a valuable parameter for rapid assessment of their toxicity to organisms.

A mixture of persistent organic pollutants detected in human follicular fluid increases progesterone secretion and mitochondrial activity in human granulosa HGrC1 cells.

Disruption of granulosa cells (GCs), the main functional cells in the ovary, is associated with impaired female fertility. Epidemiological studies demonstrated that women have detectable levels of organic pollutants (e.g., perfluorooctanoate, perfluorooctane sulfonate, 2,2-dichlorodiphenyldichloroethylene, polychlorinated biphenyl 153, and hexachlorobenzene) in their follicular fluid (FF), and thus these compounds may directly affect the function of GCs in the ovary. Considering that humans are exposed to multiple pollutants simultaneously, we elucidated the effects of a mixture of endocrine-disrupting chemicals (EDCs) on human granulosa HGrC1 cells. The EDC mixture directly increased progesterone secretion by upregulating 3ß-hydroxysteroid dehydrogenase (3ßHSD) expression. Furthermore, the EDC mixture increased activity of mitochondria, which are the central sites for steroid hormone biosynthesis, and the ATP content. Unexpectedly, the EDC mixture reduced glucose transporter 4 (GLUT4) expression and perturbed glucose uptake; however, this did not affect the glycolytic rate. Moreover, inhibition of GLUT1 by STF-31 did not alter the effects of the EDC mixture on steroid secretion but decreased basal estradiol secretion. Taken together, our results demonstrate that the mixture of EDCs present in FF can alter the functions of human GCs by disrupting steroidogenesis and may thus adversely affect female reproductive health. This study highlights that the EDC mixture elicits its effects by targeting mitochondria and increases mitochondrial network formation, mitochondrial activity, and expression of 3ßHSD, which is associated with the inner mitochondrial membrane.