The emission and deposition of global atmospheric phosphorus (P) have long been considered unbalanced, and primary biogenic aerosol particles (PBAP) and phosphine (PH₃) are considered to be the only atmospheric P sources from the ecosystem. In this work, we found and quantified volatile organic phosphorus (VOP) emissions from plants unaccounted for in previous studies. In a greenhouse in which lemons were cultivated, the atmospheric total phosphorus (TP) concentration of particulate matter (PM) was 41.8% higher than that in a greenhouse containing only soil, and the proportion of organic phosphorus (OP) in TP was doubled. ³¹P nuclear magnetic resonance tests (³¹P-NMR) of PM showed that phosphate monoesters were the main components contributed by plants in both the greenhouse and at an outside observation site. Atmospheric gaseous P was directly measured to be 1–2 orders of magnitude lower than P in PM but appeared to double during plant growing seasons relative to other months. Bag-sampling and gas chromatography mass spectrometry (GCMS) tests showed that the gaseous P emitted by plants in the greenhouse was triethyl phosphate. VOP might be an important component of atmospheric P that has been underestimated in previous studies.

Continuous exposure to low levels of toxic substances can be associated with delayed physical disturbances, which can be preceded by changes in enzyme activities and gene expression. Thus, understanding changes in the transcriptional profile could help in recognition of early molecular events involved in the toxicity mechanism of toxicants. Vinylcyclohexene (VCH) and methylmercury (MeHg⁺) are xenobiotics, which do not present a completely elucidated mechanism of toxicity. Metabolites of both compounds have some overlapping chemical properties that involve moderate to high affinity for thiol and selenol groups. In this work, we characterized by deep-sequencing transcriptomic approach the effects of VCH and MeHg⁺ on the mRNA transcriptional profile of adults fruit flies (Drosophila melanogaster) after individual and concomitant exposure to VCH and MeHg⁺. The flies were separated into four groups: control, VCH, MeHg⁺, and VCH + MeHg⁺. After individual exposure, VCH deregulated 38 genes (of which the majority was up-regulated), whereas MeHg⁺ altered 26 genes (i.e., 14 down-regulated). VCH and MeHg⁺ co-exposure changed 72 genes with a high number of genes down-regulated. Together, the results suggest that although the compounds could have some similar protein targets (e.g., sulfhydryl-containing proteins), the transcriptional profile after individual exposures and co-exposure were completely different.

The environmental forensics approach is most often applied in petroleum and fuel spill incidents, for which sophisticated chemical fingerprinting procedures have evolved. In cases in which pollutant discharges occur in settings with prior contamination, more care must be taken in source discrimination, requiring further advances in methodology. Additional obstacles can arise if the spill is an atypical industrial discharge. This would necessitate painstaking characterization of unfamiliar substances lying outside of existing regulatory regimes and thus overlooked by mandated analytical protocols (i.e., contaminants of emerging concern). Towards these ends, this paper presents a systematic, multi-faceted GC-MS approach using the saturated, aromatic, and resin fractions of contaminated soil extracts, alongside soil thermal desorption and analytical pyrolysis of the soil and its asphaltene fraction. This complimentary “extract + thermal” approach is applied to a typical fuel oil spill, sediments of a severely-impacted urban river, and brownfield soils from coke, petrochemical, and Hg-As pyrometallurgical plants. The insights thus attained can serve to better inform brownfield remediation planning in the public interest.

Pesticide exposure is regarded as a contributing factor to the high gross loss rates of managed colonies of Apis mellifera. Pesticides enter the hive through contaminated nectar and pollen carried by returning forager honey bees or placed in the hive by beekeepers when managing hive pests. We used an in vitro rearing method to characterize the effects of seven pesticides on developing brood subjected dietary exposure at worse-case environmental concentrations detected in wax and pollen. The pesticides tested included acaricides (amitraz, coumaphos, fluvalinate), insecticides (chlorpyrifos, imidacloprid), one fungicide (chlorothalonil), and one herbicide (glyphosate). The larvae were exposed chronically for six days of mimicking exposure during the entire larval feeding period, which is the worst possible scenario of larval exposure. Survival, duration of immature development, the weight of newly emerged adult, morphologies of the antenna and the hypopharyngeal gland, and gene expression were recorded. Survival of bees exposed to amitraz, coumaphos, fluvalinate, chlorpyrifos, and chlorothalonil was the most sensitive endpoint despite observed changes in many developmental and physiological parameters across the seven pesticides. Our findings suggest that pesticide exposure during larvae development may affect the survival and health of immature honey bees, thus contributing to overall colony stress or loss. Additionally, pesticide exposure altered gene expression of detoxification enzymes. However, the tested exposure scenario is unlikely to be representative of real-world conditions but emphasizes the importance of proper hive management to minimize pesticide contamination of the hive environment or simulates a future scenario of increased contamination.

As previous studies found that the direct associations between urinary polycyclic aromatic hydrocarbon (PAH), benzene and toluene (BT) metabolites and the decreased lung function were not conclusive, we further investigated relationship of oxidative damage and airway inflammation induced by PAHs and BTs exposure with lung function. A total of 262 children diagnosed with asthma and 72 heathy children were recruited. Results showed that asthmatic children had higher levels of PAHs and BTs exposure, as well as Malonaldehyde (MDA) and 8-hydroxy-2′-deoxyguanosine (8-OHdG) compared with healthy children. Furthermore, binary logistic regression showed that each unit increases in level of urinary 2-&3-hydroxyfluorene (2-&3-OHF), 2-hydroxyphenanthrene (2-OHPhe), 1-hydroxyphenanthrene (1-OHP) and S-phenylmercapturic acid (S-PMA) were significantly associated with an elevated risk of asthma in children with odds ratios of 1.5, 2.3, 1.7 and 1.4, respectively, suggesting that PAHs and BTs exposure could increase the risk of asthma for children. Neither PAH nor BT metabolite could comprehensively indicate the decreased lung function as only 2-&3-OHF and 1-OHP were significantly and negatively correlated with forced vital capacity (FVC). Moreover, levels of most individual PAH and BT metabolite were significantly correlated to MDA and 8-OHdG. Further hierarchical regression analysis indicated that MDA and 8-OHdG levels did not show significant effects on the decreased lung function, suggesting that they are not the suitable biomarkers to indirectly indicate the altered lung function induced by PAHs and BTs. Urinary 2-OHPhe and 1-&9-hydroxyphenanthrene (1-&9-OHPhe) were significantly correlated with fractional exhaled nitric oxide (FeNO). Moreover, FeNO significantly contributed to decreased lung function and explained 7.7% of variance in ratio of forced expiratory volume in 1 s (FEV₁) and FVC (FEV₁/FVC%). Hence, FeNO, rather than oxidative damage indicators or any urinary PAH and BT metabolite, is more sensitive to indirectly reflect the decreased lung function induced by PAHs and BTs exposure for asthmatic children.

Sulfate radical (SO₄⁻)-based advanced oxidation processes (SR-AOPs) are promising in-situ chemical oxidation technologies widely applied for soil/groundwater remediation. The presence of non-target water constituents may interfere the abatement of contaminants by SR-AOPs as well as result in the formation of unintended byproducts. Herein, we reported the formation of toxic chloronitrophenols during thermally activated persulfate oxidation of 2-chlorophenol (2CP) in the presence of nitrite (NO₂⁻). 2-Chloro-4-nitrophenol (2C4NP) and 2-chloro-6-nitrophenol (2C6NP) were identified as nitrated byproducts of 2CP with total yield up to 90%. The formation of nitrated byproducts is a result of coupling reaction between 2CP phenoxyl radical (ClPhO) and nitrogen dioxide radical (NO₂). As a critical step, the formation of ClPhO was supported by density functional theory (DFT) computation. Both 2C4NP and 2C6NP could convert to 2-chloro-4,6-dinitrophenol (2C46DNP) upon further treatment via a denitration-renitration process. The formation rate of 2C4NP and 2C6NP was closely dependent on the concentration of NO₂⁻, solution pH, and natural water constituents. ECOSAR calculation suggests that chloronitrophenols are generally more hydrophobic and ecotoxic than 2CP. Our result therefore reveals the potential risks in the abatement of chlorophenols by SR-AOP, particularly when high level of NO₂⁻ is present in water matrix.

Although the coexistence of heavy metals and environmental hormones always occur in aquatic environment, the information of the combined impacts remains unclear. To explore the multi-generational toxicity of cadmium (Cd) and tributyltin (TBT), adult zebrafish (Danio rerio) (F0) were exposed to different treated groups (100 ng/l Cd, 100 ng/l TBT and their mixture) for 90 d, with their offspring (F1 and F2) subsequently reared in the same exposure solutions corresponding to their parents. Both developmental neurotoxicity and thyroid disturbances were examined in the three (F0, F1, and F2) generations. Our results showed that co-exposure to Cd and TBT induced the developmental neurotoxicity in F1 and F2 generations, reflected by the significant lower levels of neurotransmitters (dopamine and serotonin) and the inhibited acetylcholinesterase (AChE) activities. And the thyroid endocrine disruption were observed in the two-generations larval offspring by parental exposure to Cd and/or TBT, including the significantly decreasing levels of thyroid hormones and the down-regulated the expression of genes involved in the hypothalamus-pituitary-thyroid axis, compared to the control. Additional, the embryonic toxicity and growth inhibition were also determined in the fish larvae. Overall, this study examined the impacts of parental co-exposure to Cd and TBT, with regard to developmental inhibition, nervous system damage and endocrine disruption, which highlighted that co-exposure influences are complicated and need to be considered for accurate environmental risk assessment.

Tris (2-ethylhexyl) phosphate (TEHP) is one of the most commonly used organophosphorus flame retardant (OPFR) analogues and is commonly detected in surface water and sediments. Limited information is available about the metabolic pathway or metabolite formation related to TEHP in fish. In this study, rare minnows (Gobiocyprisrarus) were exposed to TEHP in static water for 30 d to investigate the bioaccumulation and metabolite distribution in the fish muscle, liver, kidney, gill, GI-tract, ovary and testis. Based on the estimated kᵤₚ,ₚₐᵣₑₙₜ and kd,ₚₐᵣₑₙₜ values, the bioconcentration factors (BCFₚₐᵣₑₙₜ) of TEHP in fish tissues were calculated in the order of kidney > ovary ≈ liver ≈ testis > gill ≈ GI-tract > muscle; this finding was consistent with the results of our previous study on other alkyl-substituted OPFRs. In addition, this study identified the metabolic profiles of TEHP in the liver. TEHP was oxidatively metabolized by the fish to a dealkylated metabolite (di 2-ethylhexyl phosphate; DEHP) and hydroxylated TEHP (OH-TEHP). OH-TEHP further underwent extensive phase II metabolism to yield glucuronic acid conjugates. DEHP was mainly distributed in rare minnow in the following order: liver > GI-tract > kidney ≫ other tissues. However, the metabolite showed lower accumulation potential in fish tissues than TEHP, with metabolite parent concentration factors (MPCFs) for DEHP of less than 0.1 in all the investigated tissues. The BCFₚₐᵣₑₙₜ values of TEHP in various fish tissues were only 9.0 × 10⁻³-7.2 × 10⁻⁴ times its estimated tissue-water partition coefficient (Kₜᵢₛₛᵤₑ₋wₐₜₑᵣ) values based on tissue lipid, protein and water contents, which indicated the significance of biotransformation in reducing the bioaccumulation potential of TEHP in fish. The toxicokinetic data in the present study help in understanding the tissue-specific bioaccumulation and metabolism pathways of TEHP in fish and highlight the importance of toxicology research on TEHP metabolites in aquatic organisms.

Evidence is emerging that environmental exposure to bisphenol S (BPS), a substitute for bisphenol A (BPA), to humans and wildlife is on the rise. However, research on the neurobehavioral effects of this endocrine disruptive chemical is still in its infancy. In this study, we aimed to investigate the effects of long-term exposure to environmentally relevant concentrations of BPS on recognition memory and its mechanism(s) of action, especially focusing on the glutamatergic/ERK/CREB pathway in the brain. Adult female zebrafish were exposed to the vehicle, 17β-estradiol (E2, 1 μg/L), or BPS (1, 10 and 30 μg/L) for 120 days. Fish were then tested in the object recognition (OR), object placement (OP), and social recognition tasks (SR). Chronic exposure to E2 and 1 μg/L of BPS improved fish performance in OP task. This was associated with an up-regulation in the mRNA expression of several subtypes of metabotropic and ionotropic glutamate receptors, an increase in the phosphorylation levels of ERK1/2 and CREB, and an elevated transcript abundance of several immediate early genes involved in synaptic plasticity and memory formation. In contrast, the exposure to 10 and 30 μg/L of BPS attenuated fish performance in all recognition memory tasks. The impairment of these memory functions was associated with a marked down-regulation in the expression and activity of genes and proteins involved in glutamatergic/ERK/CREB signaling cascade. Collectively, our study demonstrated that the long-term exposure to BPS elicits hermetic effects on the recognition memory in zebrafish. Furthermore, the effect of BPS on the recognition memory seems to be mediated by the glutamatergic/ERK/CREB signaling pathway.

Achieving large pore size, high catalytic performance with stable structure is critical for metal–organic frameworks (MOFs) to have more hopeful prospects in catalytic applications. Herein, we had reported a method to synthesize highly reactive yet stable defective iron-based Metal organic frameworks by using different monocarboxylic acids with varying lengths as a modulator. The physical−chemical characterization illustrating that modulators could improve the crystallinity, enlarge pore size and enhance catalytic performance and octanoic acid (OA) was screened to be the suitable choice. The catalytic performance of catalysts was detected through persulfate (PS) activation for degrading Tetrabromobisphenol A (TBBPA). The study demonstrated that the highest degradation efficiency for 0.018 mmol L−1 TBBPA was that 97.79% in the conditions of the 1.0 g L−1 Fe(BDC)(DMF,F)-OA-30 dosage and TBBPA:PS = 200:1. In addition, there was observed that no obvious change of the crystal structure, little the leachable iron concentration in the solutions and no significant loss of catalytic activities of Fe(BDC)(DMF,F)-OA-30 after 5th cycles. The iron valence state of Fe(BDC)(DMF,F)-OA-30 before and after degradation and electrochemical properties reveal that the partial substitution of organic ligands by octanoic acid, when removing OA and forming defects by heat and vacuum treatment to generate coordinatively unsaturated metal sites and accelerate the original transmission of electronic, leading to enhance the activity of persulfate activation for efficient removal TBBPA.