Arable soils are a significant source of nitric oxide (NO), a precursor of tropospheric ozone, and thereby contribute to ozone pollution. However, their actual impact on ozone formation is strongly related to their spatial and temporal emission patterns, which warrant high-resolution estimates. Here, we combined an agro-ecosystem model and geo-referenced databases to map these sources over the 12 000 km2 administrative region surrounding Paris, France, with a kilometric level resolution. The six most frequent arable crop species were simulated, with emission rates ranging from 1.4 kg N–NO ha-1 yr-1 to 11.1 kg N–NO ha-1 yr-1. The overall emission factor for fertilizer-derived NO emissions was 1.7%, while background emissions contributed half of the total NO efflux. Emissions were strongly seasonal, being highest in spring due to fertilizer inputs. They were mostly sensitive to soil type, crops' growing season and fertilizer N rates. The use of an agro-ecosystem model at regional scale makes it possible to map the emissions of nitric oxide from arable soils at a resolution compatible with tropospheric ozone models.

Arable soils are a significant source of nitric oxide (NO), a precursor of tropospheric ozone, and thereby contribute to ozone pollution. However, their actual impact on ozone formation is strongly related to their spatial and temporal emission patterns, which warrant high-resolution estimates. Here, we combined an agro-ecosystem model and geo-referenced databases to map these sources over the 12 000 km2 administrative region surrounding Paris, France, with a kilometric level resolution. The six most frequent arable crop species were simulated, with emission rates ranging from 1.4 kg N–NO ha-1 yr-1 to 11.1 kg N–NO ha-1 yr-1. The overall emission factor for fertilizer-derived NO emissions was 1.7%, while background emissions contributed half of the total NO efflux. Emissions were strongly seasonal, being highest in spring due to fertilizer inputs. They were mostly sensitive to soil type, crops' growing season and fertilizer N rates. The use of an agro-ecosystem model at regional scale makes it possible to map the emissions of nitric oxide from arable soils at a resolution compatible with tropospheric ozone models.

Nitric oxide (NO) and ethylene are both important signaling molecules which participate in numerous plant development processes and environmental stress resistance. Here, we investigate whether and how NO interacts with ethylene during the development of endodermal barriers that have major consequences for the apoplastic uptake of cadmium (Cd) in the hyperaccumulator Sedum alfredii. In response to Cd, an increased NO accumulation, while a decrease in ethylene production was observed in the roots of S. alfredii. Exogenous supplementation of NO donor SNP (sodium nitroprusside) decreased the ethylene production in roots, while NO scavenger cPTIO (2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide) had the opposite effect. The exogenous addition of NO affected the ethylene production through regulating the expression of genes related to ethylene synthesis. However, upon exogenous ethylene addition, roots retained their NO accumulation. The abovementioned results suggest that ethylene is downstream of the NO signaling pathway in S. alfredii. Regardless of Cd, addition of SNP promoted the deposition of endodermal barriers via regulating the genes related to Casparian strips deposition and suberization. Correlation analyses indicate that NO positively modifies the formation of endodermal barriers via the NO-ethylene signaling pathway, Cd-induced NO accumulation interferes with the synthesis of ethylene, leading to a deposition of endodermal barriers in S. alfredii.

Fine particulate matter (PM₂.₅) has been associated with risk of oral and respiratory diseases. However, the biological mechanisms of adverse oral and respiratory health response to PM₂.₅ fluctuation have not been well characterized. This study aims to explore the relationships of PM₂.₅ with airway inflammation, salivary biomarkers and buccal mucosa microbiota. We performed a panel study among 40 college students involving 4 follow-ups from August to October 2021 in Hefei, Anhui Province, China. Health outcomes included fractional exhaled nitric oxide (FeNO), salivary biomarkers [C-reactive protein (CRP), cortisol, lysozyme and alpha-amylase] and buccal mucosa microbial diversity. Linear mixed-effect models were applied to explore the cumulative impacts of PM₂.₅ on health indicators. PM₂.₅ was positively correlated with FeNO, CRP, cortisol and alpha-amylase, while negatively with lysozyme. Per 10-μg/m³ increase in PM₂.₅ was linked to maximum increments in FeNO of 10.71% (95%CI: 2.01%, 19.41%) at lag 0–24 h, in CRP of 7.10% (95%CI: 5.39%, 8.81%) at lag 0–24 h, in cortisol of 1.25% (95%CI: 0.44%, 2.07%) at lag 0–48 h, and in alpha-amylase of 2.12% (95%CI: 0.53%, 3.71%) at lag 0–24 h, while associated with maximum decrement in lysozyme of 0.53% (95%CI: 0.12%, 0.95%) at lag 0–72 h. Increased PM₂.₅ was linked to reduction in the richness and evenness of buccal microbe and o_Bacillales and o_Bacteroidales were identified as differential microbes after PM₂.₅ inhalation. Bio-information analysis indicated that immunity system pathway was the most important enriched abundant process altered by PM₂.₅ exposure. In summary, short-term PM₂.₅ exposure may impair oral and respiratory health by inducing inflammatory and stress responses, weakening immune function and altering buccal mucosa microbial diversity.

Vegetable soils with high nitrogen input are hotspots of nitrous oxide (N₂O) and nitric oxide (NO), and biochar amended to soil has been documented to effectively decrease N₂O and NO emissions. However, the aging effects of biochar on soil N₂O and NO production and the relevant mechanisms are not thoroughly understood. A¹⁵N tracing microcosm study was conducted to clarify the responses of N₂O and NO production pathways to the biochar aging process in vegetable soil. The results showed that autotrophic nitrification was the predominant source of N₂O production. Biochar aging increased the O-containing functional groups while lowering the aromaticity and pore size. Fresh biochar enhanced the AOB-amoA gene abundance and obviously stimulated N₂O production by 15.5% via autotrophic nitrification and denitrification. In contrast, field-aged biochar markedly weakened autotrophic nitrification and denitrification and thus decreased N₂O production by 17.0%, as evidenced by the change in AOB-amoA and nosZI gene abundances. However, the amendment with artificially lab-aged biochar had no effect on N₂O production. With the extension of aging time, biochar application reduced the soil NO production dominated by nitrification. Changes in the N₂O and NO fluxes were closely associated with soil NH₄⁺-N and NO₂⁻-N contents, indicating that autotrophic nitrification played a critical role in NO production. Overall, our study demonstrated that field-aged biochar suppressed N₂O production via autotrophic nitrification and denitrification by regulating associated functional genes, but not for lab-aged biochar or fresh biochar. These findings improved our insights regarding the implications of biochar aging on N₂O and NO mitigation in vegetable soils.

Nitric oxide (NO) is an important phytohormone for plant adaptation to mercury (Hg) stress. The effect of Hg on lignin synthesis, NO production in leaf, sheath and root and their relationship were investigated in two members of the grass family - wheat and maize. Hg stress decreased growth and lignin contents, significantly affected phenylpropanoid and monolignol pathways (PAL, phenylalanine ammonia-lyase; 4-coumarate: CoA ligase, 4CL; cinnamyl alcohol dehydrogenase, CAD), with maize identified to be more sensitive to Hg stress than wheat. Among the tissue types, sheath encountered severe damage compared to leaves and roots. Hg translocation in maize was about twice that in wheat. Interestingly, total NO produced under Hg stress was significantly decreased compared to control, with maximum reduction of 43.4% and 42.9% in wheat and maize sheath, respectively. Regression analysis between lignin and NO contents or the activities of three enzymes including CAD, 4CL and PAL displayed the importance of NO contents, CAD, 4CL and PAL for lignin synthesis. Further, the gene expression profiles encoding CAD, 4CL and PAL provided support for the damaging effect of Hg on wheat sheath, and maize shoot. To validate NO potential to mitigate Hg toxicity in maize and wheat, NO donor and NO synthase inhibitor were supplemented along with Hg. The resulting phenotype, histochemical analysis and lignin contents showed that NO mitigated Hg toxicity by improving growth and lignin synthesis and accumulation. In summary, Hg sensitivity was higher in maize seedlings compared to wheat, which was associated with the lower lignin contents and reduced NO contents. External supplementation of NO is proposed as a sustainable approach to mitigate Hg toxicity in maize and wheat.

Potentially toxic metals have become a viable threat to the ecosystem due to their carcinogenic nature. Biochar has gained substantial interest due to its redox-mediated processes and redox-active metals. Biochar has the capacity to directly adsorb the pollutants from contaminated environments through several mechanisms such as coprecipitation, complexation, ion exchange, and electrostatic interaction. Biochar's electron-mediating potential may be influenced by the cyclic transition of surface moieties and conjugated carbon structures. Thus, pyrolysis configuration, biomass material, retention time, oxygen flow, and heating time also affect biochar's redox properties. Generally, reactive oxygen species (ROS) exist as free radicals (FRs) in radical and non-radical forms, i.e., hydroxyl radical, superoxide, nitric oxide, hydrogen peroxide, and singlet oxygen. Heavy metals are involved in the production of FRs during redox-mediated reactions, which may contribute to ROS formation. This review aims to critically evaluate the redox-mediated characteristics of biochar produced from various biomass feedstocks under different pyrolysis conditions. In addition, we assessed the impact of biochar-assisted FRs redox-mediated processes on heavy metal immobilization and mobility. We also revealed new insights into the function of FRs in biochar and its potential uses for environment-friendly remediation and reducing the dependency on fossil-based materials, utilizing local residual biomass as a raw material in terms of sustainability.

Atrazine is an herbicide commonly used in several countries. Due to its long half-life, associated with its use in large scales, atrazine residues remain as environmental pollutants in water bodies. Phytoremediation is often pointed out as an interesting approach to remove atrazine from the aquatic environment, but its practical application is limited by the high toxicity of this herbicide. Here, we characterize the damages triggered by atrazine in Pistia stratiotes, evaluating the role of nitric oxide (NO), a cell-signaling molecule, in increasing the tolerance to the pollutant and the phytoremediation potential of this species. Pistia stratiotes plants were exposed to four treatments: Control; Sodium nitroprusside (SNP) (0.05 mg L⁻¹); Atrazine (ATZ) (150 μg L⁻¹) and ATZ + SNP. The plants remained under those conditions for 24 h for biochemical and physiological analysis and 3 days for the evaluation of relative growth rate. The presence of atrazine in plant cells triggered a series of biochemical and physiological damages, such as the increase in the generation of reactive oxygen species, damages to cell membranes, photosynthesis impairment, and negative carbon balance. Despite this, the plants maintained greater growth rates than other aquatic macrophytes exposed to atrazine and showed high bioconcentration and translocation factors. The addition of SNP, a NO donor, decreased the herbicide toxicity, with an increase of over 60% in the IC₅₀ value (Inhibitor Concentration). Indeed, the NO signaling action was able to increase the tolerance of plants to atrazine, which resulted in increments in pollutant uptake and translocation, with the maintenance of overall cell (e.g. membranes) and organs (root system) structure, and the functioning of central physiological processes (e.g. photosynthesis). These factors allowed for more quickly and efficient removal of the pollutant from the environment, reducing costs, and increasing the viability of the phytoremediation process.

Cigarette smoke (CS) affects immune functions, leading to severe outcomes in smokers. Robust evidence addresses the immunotoxic effects of combustible tobacco products. As heat-not-burn tobacco products (HNBT) vaporize lower levels of combustible products, we here compared the effects of cigarette smoke (CS) and HNBT vapor on Jurkat T cells. Cells were exposed to air, conventional cigarettes or heatsticks of HNBT for 30 min and were stimulated or not with phorbol myristate acetate (PMA). Cell viability, proliferation, reactive oxygen species (ROS) production, 8-OHdG, MAP-kinases and nuclear factor κB (NFκB) activation and metallothionein expression (MTs) were assessed by flow cytometry; nitric oxide (NO) and cytokine levels were measured by Griess reaction and ELISA, respectively. Levels of metals in the exposure chambers were quantified by inductively coupled plasma mass spectrometry. MT expressions were quantified by immunohistochemistry in the lungs and liver of C57Bl/6 mice exposed to CS, HNBT or air (1 h, twice a day for five days: via inhalation). While both CS and HBNT exposures increased cell death, CS led to a higher number of necrotic cells, increased the production of ROS, NO, inflammatory cytokines and MTs when compared to HNBT-exposed cells, and led to a higher expression of MTs in mice. CS released higher amounts of metals. CS and HNBT exposures decreased PMA-induced interleukin-2 (IL-2) secretion and impaired Jurkat proliferation, effects also seen in cells exposed to nicotine. Although HNBT vapor does not activate T cells as CS does, exposure to both HNBT and CS suppressed proliferation and IL-2 release, a pivotal cytokine involved with T cell proliferation and tolerance, and this effect may be related to nicotine content in both products.

Several epidemiological studies have evaluated the fractional exhaled nitric oxide (FeNO) of ambient air pollution but the results were controversial. We therefore conducted a systematic review and meta-analysis to investigate the associations between short-term exposure to air pollutants and FeNO level. We searched PubMed and Web of Science and included a total of 27 articles which focused on associations between ambient air pollutants (PM₁₀, PM₂.₅, black carbon (BC), nitrogen dioxide (NO₂), sulfur dioxide (SO₂), ozone (O₃)) exposure and the change of FeNO. Random effect model was used to calculate the percent change of FeNO in association with a 10 or 1 μg/m³ increase in air pollutants exposure concentrations. A 10 μg/m³ increase in short-term PM₁₀, PM₂.₅, NO₂, and SO₂ exposure was associated with a 3.20% (95% confidence interval (95%CI): 1.11%, 5.29%), 2.25% (95%CI: 1.51%, 2.99%),4.90% (95%CI: 1.98%, 7.81%), and 8.28% (95%CI: 3.61%, 12.59%) change in FeNO, respectively. A 1 μg/m³ increase in short-term exposure to BC was associated with 3.42% (95%CI: 1.34%, 5.50%) change in FeNO. The association between short-term exposure to O₃ and FeNO level was insignificant (P＞0.05). Future studies are warranted to investigate the effect of multiple pollutants, different sources and composition of air pollutants on airway inflammation.