ABSTRACT
Exposure to fine particulate matter (PM2.5) is a significant concern for respiratory health. However, the sources, trigger points, and effect size of specific associations between PM2.5 components, particularly polycyclic aromatic hydrocarbons (PAHs) and the airway inflammatory marker fractional exhaled nitric oxide (FeNO) have not been fully explored. In this study, 69 healthy college students were enrolled and followed up 16 times from 2014 to 2018. Individual FeNO was measured and ambient air PM2.5 samples were collected for 7 consecutive days before each follow-up. PAHs were quantified using Gas Chromatography-Mass Spectrometry. Linear mixed-effect regression models were employed to evaluate the associations between PM2.5-bound PAHs and FeNO. Additionally, PMF (Positive Matrix Factorization) was utilized to identify sources of PM2.5-bound PAHs and assess their impact on FeNO. Throughout the study, the average (SD) of ΣPAHs concentrations was 78.50 (128.9) ng/m3. PM2.5 and PM2.5-bound PAHs were significantly associated with FeNO at various lag days. Single-day lag analyses revealed maximum effects of PM2.5 on FeNO, with an increase of 7.71% (95% CI: 4.67%, 10.83%) per interquartile range (IQR) (48.10 µg/m3) increase of PM2.5 at lag2, and ΣPAHs showed a maximum elevation in FeNO of 6.40% (95% CI: 2.33%, 10.63%) at lag4 per IQR (57.39 ng/m3) increase. Individual PAHs exhibited diversity peak effects on FeNO at lag3 (6 of 17), lag4 (9 of 17) in the single-day model, and lag0-5 (8 of 17) (from lag0-1 to lag0-6) in the cumulative model. Source apportionment indicated coal combustion as the primary contributor (accounting for 30.7%). However, a maximum effect on FeNO (an increase of 21.57% (95% CI: 13.58%, 30.13%) per IQR increase) was observed with traffic emissions at lag4. The findings imply that strategic regulation of particular sources of PAHs, like traffic emissions, during specific periods could significantly contribute to safeguarding public health.
Subject(s)
Air Pollutants , Nitric Oxide , Particulate Matter , Polycyclic Aromatic Hydrocarbons , Polycyclic Aromatic Hydrocarbons/analysis , Humans , Particulate Matter/analysis , Air Pollutants/analysis , Nitric Oxide/metabolism , Nitric Oxide/analysis , Male , Female , Young Adult , Adult , Follow-Up Studies , Environmental Monitoring , Exhalation , Environmental Exposure/statistics & numerical data , Environmental Exposure/analysisABSTRACT
Magnesium (Mg) and zinc (Zn) are essential nutrients for plants. Mg deficiency often occurs in rice plants grown in Zn-polluted soil. However, the mechanism for this correlation is unclear. Here, we performed culture experiments on rice plants (Oryza sativa L.) and used Mg isotopes to investigate mechanisms of Zn stress on plant Mg deficiency. Our results show that excess Zn can significantly reduce the uptake of Mg in rice tissues. The root displays positive Δ26Mgplant-nutrient values (δ26Mgplant-δ26Mgnutrient; 1.90 to 2.06 ), which suggests that Mg enters the root cells mainly via Mg-specific transporters rather than non-selective diffusion. The decreased Δ26Mgplant-nutrient values with increasing Zn supply can be explained by the competition between Zn and Mg, both of which combine with same transporters in roots. In contrast, the shoots (stem and leaf) display much lower δ26Mg values than roots, which suggests that the transport of Mg from roots to aerial biomass is mainly via free Mg ions, during which Zn cannot competitively inhibit the movement of Mg. Our study suggests that the Mg deficiency in rice plants can be caused by high Zn-levels in soils and highlights the necessity of soil Zn-remediation in solving Mg deficiency problems in rice plants.
Subject(s)
Magnesium Deficiency , Oryza , Zinc/toxicity , Zinc/analysis , Magnesium , Isotopes , Soil , Plant Roots/chemistry , Zinc IsotopesABSTRACT
Carboxylesterase (CXE) is a class of hydrolases that contain an α/ß folding domain, which plays critical roles in plant growth, development, and stress responses. Based on the genomic and transcriptomic data of Salvia miltiorrhiza, the SmCXE family was systematically analyzed using bioinformatics. The results revealed 34 SmCXE family members in S. miltiorrhiza, and the SmCXE family could be divided into five groups (Group I, Group II, Group III, Group IV, and Group V). Cis-regulatory elements indicated that the SmCXE promoter region contained tissue-specific and development-related, hormone-related, stress-related, and photoresponsive elements. Transcriptome analysis revealed that the expression levels of SmCXE2 were highest in roots and flowers (SmCXE8 was highest in stems and SmCXE19 was highest in leaves). Further, two GA receptors SmCXE1 (SmGID1A) and SmCXE2 (SmGID1B) were isolated from the SmCXE family, which are homologous to other plants. SmGID1A and SmGID1B have conserved HGGSF motifs and active amino acid sites (Ser-Asp-Val/IIe), which are required to maintain their GA-binding activities. SmGID1A and SmGID1B were significantly responsive to gibberellic acid (GA3) and methyl jasmonate (MeJA) treatment. A subcellular assay revealed that SmCXE1 and SmCXE2 resided within the nucleus. SmGID1B can interact with SmDELLAs regardless of whether GA3 exists, whereas SmGID1A can only interact with SmDELLAs in the presence of GA3. A Further assay showed that the GRAS domain mediated the interactions between SmGID1s and SmDELLAs. This study lays a foundation for further elucidating the role of SmCXE in the growth and development of S. miltiorrhiza.
Subject(s)
Salvia miltiorrhiza , Salvia miltiorrhiza/genetics , Salvia miltiorrhiza/metabolism , Carboxylesterase/genetics , Carboxylesterase/metabolism , Plant Proteins/metabolism , Cloning, Molecular , Gene Expression Profiling , Gene Expression Regulation, PlantABSTRACT
Studies have shown that the cardio/cerebrovascular toxicity of ambient PM2.5 is related to its bound polycyclic aromatic hydrocarbons (PAHs). Currently, only a few studies have reported the relationship between PM2.5-bound PAHs and promoted blood coagulation and thrombosis, but there isn't a consistent conclusion. Therefore, we conducted a prospective panel study to investigate the association. Thirty-three young healthy adults participated in sixteen repeated visits from 2014 to 2018 in Tianjin, China. During each visit, three pro-thrombotic biomarkers: ADAMTS13 (a disintegrin and metalloproteinase with thrombospondin motif 13), D-dimer and Myeloperoxidase (MPO) were measured. Before each visit, ambient PM2.5 samples were daily collected for one week. Sixteen PAHs were determined using Gas Chromatography-Mass Spectrometer, and the positive matrix factorization (PMF) model was applied to identify the sources. Linear mixed-effects models were fitted to investigate the associations between PM2.5-bound PAHs exposure and the biomarkers. Thirteen time-metrics were defined to identify significant time points of PM2.5-bound PAHs' effects. We observed that the increase of PM2.5-bound PAHs exposure was significantly associated with reduced ADAMTS13, elevated D-dimer and MPO. At lag0, each 5.7 ng/m3 increase in Benzo[j]fluoranthene and per 3.4 ng/m3 increase Dibenz[a,h]anthracene could make a maximum change of -19.08 % in ADAMTS13 and 132.60 % in D-dimer. Additionally, per 16.43 ng/m3 increase in Chrysene could lead to a maximum elevation of 32.14 % in MPO at lag4. The PM2.5-bound PAHs often triggered more significant changes at lag 3,4 and 6. The ambient PM2.5-bound PAHs originated from six sources: coal combustion (43.10 %), biomass combustion (20.77 %), diesel emission (14.78 %), gasoline emission (10.95 %), industrial emission (7.58 %), and cooking emission (2.83 %). The greatest contributors to alterations in ADAMTS13, D-dimer and MPO are industrial emission (-48.43 %), biomass combustion (470.32 %) and diesel emission (13.14 %) at lag4. Our findings indicated that short-term exposure to ambient PM2.5-bound PAHs can induce alterations of pro-thrombotic biomarkers among healthy adults.
Subject(s)
Air Pollutants , Polycyclic Aromatic Hydrocarbons , Thrombosis , Adult , Humans , Particulate Matter/analysis , Air Pollutants/analysis , Environmental Monitoring , Polycyclic Aromatic Hydrocarbons/analysis , Prospective Studies , China , SeasonsABSTRACT
Atmospheric particulate matter (PM) enriched with lead (Pb) has severe irreversible effects on human health. Therefore, identifying the contribution of Pb emission sources is essential for protecting the health of residents. Using the Pb isotopic tracer method, this study explored the seasonal characteristics and primary anthropogenic Pb sources for atmospheric PM in Tianjin in 2019. We calculated the contribution of Pb sources using the end-member and MixSIAR models. The results showed that Pb loaded in PM10 was more abundant in January than in July, and was strongly influenced by meteorological conditions and anthropogenic emissions. The primary Pb sources of the aerosol samples originated from coal combustion and vehicle and steel plant emissions, mainly originating from local Pb emission sources in Tianjin. The PM10-bond Pb in January was influenced by regional transportation and local sources. The MixSIAS model calculated the contribution of coal combustion as approximately 50 %. Compared with that in January, the contribution of coal combustion decreased by 9.6 % in July. Our results indicate that some of the benefits of phased-out leaded gasoline have been short-lived, whereas other industrial activities releasing Pb have increased. Furthermore, the results emphasise the practicability of the Pb isotope tracer source approach for identifying and distinguishing between different anthropogenic Pb inputs. Based on this study, scientific and effective air pollution prevention and control programs can be formulated to provide decision support for the guidance and control of air pollutant emissions.