OBJECTIVE: To examine the mechanistic of organochlorine-associated changes in lung function. METHODS: This study investigated 76 healthy older adults in Jinan, Shandong Province, over a five-month period. Personal exposure to organochlorines was quantified using wearable passive samplers, while inflammatory factors and thyroid hormones were analyzed from blood samples. Participants' lung function was evaluated. After stratifying participants according to their thyroid hormone levels, we analyzed the differential effects of organochlorine exposure on lung function and inflammatory factors across the low and high thyroid hormone groups. Mediation analysis was further conducted to elucidate the relationships among organochlorine exposures, inflammatory factors, and lung function. RESULTS: Bis (2-chloro-1-methylethyl) ether (BCIE), was negatively associated with forced vital capacity (FVC, -2.05%, 95% CI: -3.11% to -0.97%), and associated with changes in inflammatory factors such as interleukin (IL)-2, IL-7, IL-8, and IL-13 in the low thyroid hormone group. The mediation analysis indicated a mediating effect of IL-2 (15.63%, 95% CI: 0.91% to 44.64%) and IL-13 (13.94%, 95% CI: 0.52% to 41.07%) in the association between BCIE exposure and FVC. CONCLUSION Lung function and inflammatory factors exhibited an increased sensitivity to organochlorine exposure at lower thyroid hormone levels, with inflammatory factors potentially mediating the adverse effects of organochlorines on lung function.
Environmental Exposure ; Hydrocarbons, Chlorinated/metabolism* ; China ; Ethyl Ethers/metabolism* ; Environmental Monitoring ; Thyroid Hormones/blood* ; Lung/physiology* ; Inhalation Exposure/statistics & numerical data* ; Air Pollution/statistics & numerical data* ; Air Pollutants/metabolism* ; Humans ; Male ; Female ; Middle Aged ; Aged

Ambient air pollution is increasingly being recognized as a risk factor for heart failure; however, its effects on cardiac biomarkers remain unclear. This scoping review assessed the existing evidence on the association between air pollution and cardiac biomarkers in heart failure, described the key concepts, synthesized data, and identified research gaps. Following the PRISMA-ScR guidelines, PubMed, Embase, Web of Science, and CNKI databases were searched for studies on air pollution, heart failure, and biomarkers. A total of 765 records were screened, and 81 full texts were assessed for eligibility, resulting in 15 studies. The results showed that the exposure to particulate matter was associated with elevated N-terminal pro-B-type natriuretic peptide and troponin levels. Several studies have linked particulate matter exposure to a higher cardiovascular risk and heart failure biomarkers. Inflammatory and oxidative stress markers were consistently elevated across studies, supporting the biological relevance of these associations. However, few studies have focused specifically on populations with heart failure or clinically relevant biomarkers, and the evidence for gaseous pollutants remains inconclusive. These findings highlight the need to integrate environmental risk assessment into heart failure care and inform policy efforts to reduce the pollution-related cardiovascular burden. Further research should address these gaps through improved exposure assessments and the integration of mechanistic evidence.
Heart Failure/epidemiology* ; Biomarkers/metabolism* ; Humans ; Air Pollution/adverse effects* ; Air Pollutants/adverse effects* ; Particulate Matter/adverse effects* ; Environmental Exposure ; Natriuretic Peptide, Brain/blood* ; Oxidative Stress ; Troponin/blood*

Objective: Epidemiological studies reveal that exposure to fine particulate matter (aerodynamic diameter ≤ 2.5 μm, PM Methods: EVs were isolated from the serum of healthy subjects, quantified Results: PM Conclusions EVs treatment promotes cell survival and attenuates PM
A549 Cells ; Air Pollutants/toxicity* ; Apoptosis/drug effects* ; Cell Survival/drug effects* ; Extracellular Vesicles ; Humans ; Male ; Middle Aged ; Particulate Matter/toxicity* ; Protective Agents/pharmacology* ; Proto-Oncogene Proteins c-akt/metabolism* ; Serum

BACKGROUND: Particulate matter (PM) < 2.5 μm (PM METHODS: We obtained DNA methylation and exercise data of 496 participants (aged between 30 and 70 years) from the Taiwan Biobank (TWB) database. We also extracted PM RESULTS: DLEC1 methylation and PM CONCLUSIONS We found significant positive associations between PM
Adult ; Aged ; Air Pollutants/adverse effects* ; DNA Methylation/drug effects* ; Environmental Exposure/adverse effects* ; Exercise ; Female ; Humans ; Male ; Middle Aged ; Particulate Matter/adverse effects* ; Taiwan ; Tumor Suppressor Proteins/metabolism*

Objective: To screen the differentially expressed proteins (DEPs) in human bronchial epithelial cells (HBE) treated with atmospheric fine particulate matter (PM ). Methods: HBE cells were treated with PM samples from Shenzhen and Taiyuan for 24 h. To detect overall protein expression, the Q Exactive mass spectrometer was used. Gene ontology (GO), Kyoto encyclopedia of genes and genomes (KEGG), and Perseus software were used to screen DEPs. Results: Overall, 67 DEPs were screened in the Shenzhen sample-treated group, of which 46 were upregulated and 21 were downregulated. In total, 252 DEPs were screened in the Taiyuan sample-treated group, of which 134 were upregulated and 118 were downregulated. KEGG analysis demonstrated that DEPs were mainly enriched in ubiquitin-mediated proteolysis and HIF-1 signal pathways in Shenzhen PM samples-treated group. The GO analysis demonstrated that Shenzhen sample-induced DEPs were mainly involved in the biological process for absorption of various metal ions and cell components. The Taiyuan PM -induced DEPs were mainly involved in biological processes of protein aggregation regulation and molecular function of oxidase activity. Additionally, three important DEPs, including ANXA2, DIABLO, and AIMP1, were screened. Conclusion Our findings provide a valuable basis for further evaluation of PM -associated carcinogenesis.
Air Pollutants ; analysis ; Bronchi ; drug effects ; metabolism ; Computational Biology ; Epithelial Cells ; drug effects ; metabolism ; Gene Expression ; drug effects ; Humans ; Mass Spectrometry ; Particle Size ; Particulate Matter ; analysis ; Proteomics

Adult ; Aged ; Aged, 80 and over ; Air Pollutants ; adverse effects ; Blood Chemical Analysis ; Coke ; adverse effects ; Environmental Exposure ; Female ; Humans ; Immunoglobulins ; metabolism ; Male ; Middle Aged ; Polycyclic Aromatic Hydrocarbons ; adverse effects ; Young Adult

BACKGROUND: Wood is a valuable material for interiors, and the psychophysiological relaxation effects of volatile organic compounds (VOCs) from wood chips and essential oils have been reported. However, few studies have identified the odors in full-scale wooden environment, and also, differences in gender have not been clarified. In this study, we aimed to confirm the effects of VOCs emitted from interior wood walls in both human male and female participants. METHODS: We used Japanese cedar timber and analyzed VOCs in the experimental rooms with and without Japanese cedar timber by gas chromatography-mass spectrometry (GC-MS). The physiological effects were measured using neuroendocrinological and immunological parameters in saliva. A questionnaire was used to evaluate the subjective responses to each odor in the experimental rooms. RESULTS: The main compound emitted from Japanese cedar timber was δ-cadinene, and the total volume of VOCs in the wood condition (presence of VOCs emitted from Japanese cedar) was 282.4 (μg/m). Significant differences between genders in salivary parameters were shown that there were decreases of α-amylase in wood condition and increases of cortisol in the control (absence of VOCs) condition in female participants compared to male participants. The results demonstrated that VOCs in the experimental room with Japanese cedar timber tend to suppress the activation of the sympathetic nervous activity and non-VOCs of Japanese cedar in the control room increase cortisol in female participants. CONCLUSIONS These results suggest that an indoor environment with wood interior materials has the potential to be useful for health management, especially women's health.
Adult ; Air Pollutants ; analysis ; Air Pollution, Indoor ; adverse effects ; analysis ; Cryptomeria ; chemistry ; Female ; Gas Chromatography-Mass Spectrometry ; Humans ; Hydrocortisone ; metabolism ; Male ; Saliva ; chemistry ; Salivary alpha-Amylases ; metabolism ; Sesquiterpenes ; analysis ; Sex Factors ; Volatile Organic Compounds ; adverse effects ; Wood ; chemistry ; Young Adult

With the increasing occurrence of haze during the summer, the physicochemical characteristics and toxicity differences in PM_2.5 in different seasons are of great concern. Hangzhou is located in an area that has a subtropical monsoon climate where the humidity is very high during both the summer and winter. However, there are limited studies on the seasonal differences in PM_2.5 in these weather conditions. In this test, PM_2.5 samples were collected in the winter and summer, the morphology and chemical composition of PM_2.5 were analyzed, the toxicity of PM_2.5 to human bronchial cells BEAS-2B was compared, and the correlation between PM_2.5 toxicity and the chemical composition was discussed. The results showed that during both the winter and summer, the main compounds in the PM_2.5 samples were water-soluble ions, particularly SO₄^2-, NO₃^-, and NH₄⁺, followed by organic components, while heavy metals were present at lower levels. The higher the mass concentration of PM_2.5, the greater its impact on cell viability and ROS levels. However, when the mass concentration of PM_2.5 was similar, the water extraction from the summer samples showed a greater impact on BEAS-2B than that from the winter samples. The cytotoxicity of PM_2.5 was closely associated with heavy metals and organic pollutants but less related to water-soluble ions.
Air Pollutants/toxicity* ; Bronchi/metabolism* ; Carbon/chemistry* ; Environmental Monitoring ; Humans ; Ions ; Metals, Heavy ; Organic Chemicals ; Particle Size ; Particulate Matter/toxicity* ; Seasons ; Temperature ; Water

OBJECTIVEThe effect of the silica nanoparticles (SNs) on lungs injury in rats was investigated to evaluate the toxicity and possible mechanisms for SNs.

METHODSMale Wistar rats were instilled intratracheally with 1 mL of saline containing 6.25, 12.5, and 25.0 mg of SNs or 25.0 mg of microscale SiO2 particles suspensions for 30 d, were then sacrificed. Histopathological and ultrastructural change in lungs, and chemical components in the urine excretions were investigated by light microscope, TEM and EDS. MDA, NO and hydroxyproline (Hyp) in lung homogenates were quantified by spectrophotometry. Contents of TNF-α, TGF-β1, IL-1β, and MMP-2 in lung tissue were determined by immunohistochemistry staining.

RESULTSThere is massive excretion of Si substance in urine. The SNs lead pulmonary lesions of rise in lung/body coefficients, lung inflammation, damaged alveoli, granuloma nodules formation, and collagen metabolized perturbation, and lung tissue damage is milder than those of microscale SiO2 particles. The SNs also cause increase lipid peroxidation and high expression of cytokines.

CONCLUSIONThe SNs result into pulmonary fibrosis by means of increase lipid peroxidation and high expression of cytokines. Milder effect of the SNs on pulmonary fibrosis comparing to microscale SiO2 particles is contributed to its elimination from urine due to their ultrafine particle size.

Air Pollutants ; toxicity ; Animals ; Dose-Response Relationship, Drug ; Lung ; drug effects ; pathology ; ultrastructure ; Male ; Microscopy, Electron, Transmission ; Nanoparticles ; toxicity ; Pulmonary Fibrosis ; chemically induced ; metabolism ; pathology ; Random Allocation ; Rats ; Rats, Wistar ; Silicon Dioxide ; toxicity ; Specific Pathogen-Free Organisms ; Spectrometry, X-Ray Emission ; Urine ; chemistry

OBJECTIVETo investigate the effect of nickel-smelting fumes on the expression of bcl-2 and bax in mammalian cells.

METHODSLogarithmic growth NIH/3T3 cells were exposed to venom for 24 h, which sample fumes concentration was respectively 0, 6.25, 12.50, 25.00, 50.00, 100.00 µg/ml. Cell viability was assessed by MTT assay and the level of extracellular LDH activity was detected with Lactate Dehydrogenase (LDH) kit. Morphological changes of apoptotic were observed with Hoechst33342, while Western blot was used to measure the expression of bcl-2 and bax.

RESULTSIn addition to 7 days of 6.25 µg/ml nickel-smelting fumes group, each time point and dose group's cell viability reduced with significant differences compared with the control group (P < 0.05). the extracellular LDH activity increased with increasing dose of nickel-smelting fumes, and the extracellular LDH activity of 6.25, 12.50, 25.00, 50.00, 100.00 µg/ml nickel-smelting fumes group increased as compared with the control group (P < 0.05). Simultaneously, the cells, treated with 100.00 µg/ml nickel-smelting fumes for 24 h, appeared obvious morphological changes of apoptosis, such as chromatin condensation and cell shrinkage. the expression of bcl-2 significantly increased in groups of 6.25, 12.50, 25.00 µg/ml nickel-smelting fumes (0.58 ± 0.01, 0.6 3± 0.01 and 0.57 ± 0.01) and decreased in groups of 50.00, 100.00 µg/m nickel-smelting fume (0.35 ± 0.01 and 0.27 ± 0.01) as compared with that of the control group (P < 0.05). And the expression of bax significantly decreased in group of 6.25 µg/ml nickel-smelting fumes (0.58 ± 0.00) and increased in groups of 50.00, 100.00 µg/m nickel-smelting fumes (0.71 ± 0.01 and 0.78 ± 0.02) as compared with that of the control group (P < 0.05).

CONCLUSIONApoptosis was activated in NIH/3T3 cell after 24 h of exposure to Ni-smelting fumes, which may be induced by oxidative stress.

Air Pollutants ; toxicity ; Animals ; Apoptosis ; drug effects ; Cell Survival ; drug effects ; L-Lactate Dehydrogenase ; Mice ; NIH 3T3 Cells ; drug effects ; Nickel ; toxicity ; Oxidative Stress ; Proto-Oncogene Proteins c-bcl-2 ; metabolism ; bcl-2-Associated X Protein ; metabolism