Explore the vast range of titles available.

Background Although major concerns exist regarding the potential consequences of human exposures to nanoscale carbon black (CB) particles, limited human toxicological data is currently available. The purpose of this study was to evaluate if nanoscale CB particles could be responsible, at least partially, for the altered lung function and inflammation observed in CB workers exposed to nanoscale CB particles. Methods Scanning Electron Microscopy (SEM), Transmission Electron Microscopy (TEM), and Brunauer-Emmett-Teller were used to characterize CB. Eighty-one CB-exposed male workers and 104 non-exposed male workers were recruited. The pulmonary function test was performed and pro-inflammatory cytokines were evaluated. To further assess the deposition and pulmonary damage induced by CB nanoparticles, male BALB/c mice were exposed to CB for 6 hours per day for 7 or 14 days. The deposition of CB and the pathological changes of the lung tissue in mice were evaluated by paraffin sections and TEM. The cytokines levels in serum and lung tissue of mice were evaluated by ELISA and immunohistochemical staining (IHC). Results SEM and TEM images showed that the CB particles were 30 to 50 nm in size. In the CB workplace, the concentration of CB was 14.90 mg/m 3 . Among these CB particles, 50.77% were less than 0.523 micrometer, and 99.55% were less than 2.5 micrometer in aerodynamic diameter. The reduction of lung function parameters including FEV1%, FEV/FVC, MMF%, and PEF% in CB workers was observed, and the IL-1β, IL-6, IL-8, MIP-1beta, and TNF- alpha had 2.86-, 6.85-, 1.49-, 3.35-, and 4.87-folds increase in serum of CB workers, respectively. In mice exposed to the aerosol CB, particles were deposited in the lung. The alveolar wall thickened and a large amount of inflammatory cells were observed in lung tissues after CB exposure. IL-6 and IL-8 levels were increased in both serum and lung homogenate. Conclusions The data strongly suggests that nanoscale CB particles could be responsible for the lung function reduction and pro-inflammatory cytokines secretion in CB workers. These results, therefore, provide the first evidence of a link between human exposure to CB and long-term pulmonary effects.

Background Ischemic heart disease (IHD) is a major cardiovascular health concern. In addition to metabolic and behavioral risks, diesel particulate matter (DPM), with a widely exposed population, is an important external environmental risk factor for IHD. However, the effect biomarkers used to diagnose DPM-caused IHD and underlying mechanisms remain unknown. We investigated the biomarkers and underlying mechanisms of DPM in relation to myocardial hypoxia injury. Methods This study applied a unique population of diesel engine testers with stable DPM exposure. Electrocardiogram examination, echocardiogram examination, serum levels of myocardial enzymes, and 6-min walking test were used for the myocardial risks assessment. A mouse model exposed to occupational environmental DPM dose and in vitro models of DPM-induced myocardial hypoxia injury were used for assessment of mitochondrial aerobic metabolism via the oxygraph-2k system, western blotting, and kits. Ion fluorescence probes, ion supplements, and mitochondrial RNA splicing protein 2 (Mrs2) overexpression transfection were used in further investigations and verifications of the mechanism of mitochondrial Mg 2+ deficiency. Results We identified compromised myocardial mitochondrial aerobic metabolism as a precursor biomarker for the cardiac risk of myocardial hypertrophy and hypoxia injury in DPM exposure. DPM induce mitochondrial Mg 2+ deficiency of cardiomyocytes, which in turn disrupt the mitochondrial aerobic metabolism processes, including the tricarboxylic acid cycle, oxidative phosphorylation, and ATP synthesis. Mg 2+ deficiency is mediated by the disruption of Mg 2+ transport proteins, such as DPM-enhanced hyperubiquitination and degradation of Mrs2, a protein responsible for mitochondrial Mg 2+ uptake. Conclusions Our findings show that compromised mitochondrial aerobic metabolism, associated with Mg 2+ deficiency, serves as a critical biomarker for DPM-induced IHD and represents a promising investigative avenue for intervention. Graphical Abstract

Objective Iron and steel industry workers are exposed to high levels of inhalable dust particles that contain various elements, including metals, and cause occupational lung diseases. We aim to assess the relationship between occupational dust exposure, systemic inflammation, and spirometric decline in a cohort of Chinese iron and steel workers. Methods We studied 7513 workers who participated in a Health Surveillance program at Wugang Institute for Occupational Health between 2008 and 2017. Time-weighted exposure intensity (TWEI) of dust was quantified based on self-reported dust exposure history, the experience of occupational hygienists, and historical data of dust exposure for workers with certain job titles. A linear mixed-effects model was used for association analyses. Results The average annual change of lung function was − 50.78 ml/year in forced expiratory volume in 1 s (FEV1) and − 34.36 ml/year in forced vital capacity (FVC) in males, and − 39.06 ml/year in FEV1 and − 26.66 ml/year in FVC in females. Higher TWEI prior to baseline was associated with lower longitudinal measurements of FEV1 and FVC but not with their decline rates. Higher WBC and its differential at baseline were associated with lower longitudinal measurements and a more rapid decline of FEV1 and FVC in a dose-dependent monotonically increasing manner. Moreover, the increase of WBC and its differential post-baseline was also associated with a more rapid decline of FEV1 and FVC. Conclusions Our findings support the important role of systemic inflammation in affecting the temporal change of lung function in iron and steel industry workers.

Hexavalent chromium (Cr(VI)) is a hazardous metallic compound commonly used in industrial processes. The liver, responsible for metabolism and detoxification, is the main target organ of Cr(VI). Toxicity experiments were performed to investigate the impacts of low-dose exposure to Cr(VI) on rat livers. It was revealed that exposure of 0.05 mg/kg potassium dichromate (K 2 Cr 2 O 7 ) and 0.25 mg/kg K 2 Cr 2 O 7 notably increased malondialdehyde (MDA) levels and the expressions of P-AMPK, P-ULK, PINK1, P-Parkin, and LC3II/LC3I, and significantly reduced SOD activity and P-mTOR and P62 expression levels in liver. Electron microscopy showed that CR(VI) exposure significantly increased mitophagy and the destruction of mitochondrial structure. This study simulates the respiratory exposure mode of CR(VI) workers through intratracheal instillation of CR(VI) in rats. It confirms that autophagy in hepatocytes is induced by low concentrations of CR(VI) and suggest that the liver damage caused by CR(VI) may be associated with the AMPK-related PINK/Parkin signaling pathway.

Carbon black (CB) particulates as virtually pure elemental carbon can deposit deep in the lungs of humans. International Agency for Research on Cancer classified CB as a Group 2B carcinogen due to inconclusive human evidence. A molecular epidemiological study was conducted in an established cohort of CB packers (CBP) to assess associations between CB exposure and genomic instability in peripheral lymphocytes using cytokinesis-block micronucleus assay (CBMN). Carbon content in airway macrophages (CCAM) was quantified as a bio-effective dosimeter for chronic CB exposure. Dose–response observed in CBPs was compared to that seen in workers exposed to diesel exhaust. The association between CB exposure status and CBMN endpoints was identified in 85 CBPs and 106 non-CBPs from a 2012 visit and replicated in 127 CBPs and 105 non-CBPs from a 2018 visit. The proportion of cytoplasm area occupied by carbon particles in airway macrophages was over fivefold higher in current CBPs compared to non-CBPs and was associated with CBMN endpoints in a dose-dependent manner. CB aerosol and diesel exhaust shared the same potency of inducing genomic instability in workers. Circulatory pro-inflammatory factors especially TNF-α was found to mediate associations between CB exposure and CBMN endpoints. In vitro functional validation supported the role of TNF-α in inducing genomic instability. An estimated range of lower limits of benchmark dose of 4.19–7.28% of CCAM was recommended for risk assessment. Chronic CB exposure increased genomic instability in human circulation and this provided novel evidence supporting its reclassification as a human carcinogen.

Background Diesel exhaust (DE) is a major source of ultrafine particulate matters (PM) in ambient air and contaminates many occupational settings. Airway remodeling assessed using computerized tomography (CT) correlates well with spirometry in patients with obstructive lung diseases. Structural changes of small airways caused by chronic DE exposure is unknown. Wall and lumen areas of 6th and 9th generations of four candidate airways were quantified using end-inhalation CT scans in 78 diesel engine testers (DET) and 76 non-DETs. Carbon content in airway macrophage (CCAM) in sputum was quantified to assess the dose-response relationship. Results Environmental monitoring and CCAM showed a much higher PM exposure in DETs, which was associated with higher wall area and wall area percent for 6th generation of airways. However, no reduction in lumen area was identified. No study subjects met spirometry diagnosis of airway obstruction. This suggested that small airway wall thickening without lumen narrowing may be an early feature of airway remodeling in DETs. The effect of DE exposure status on wall area percent did not differ by lobes or smoking status. Although the trend test was of borderline significance between categorized CCAM and wall area percent, subjects in the highest CCAM category has a 14% increase in wall area percent for the 6th generation of airways compared to subjects in the lowest category. The impact of DE exposure on FEV1 can be partially explained by the wall area percent with mediation effect size equal to 20%, P perm  = 0.028). Conclusions Small airway wall thickening without lumen narrowing may be an early image feature detected by CT and underlie the pathology of lung injury in DETs. The pattern of changes in small airway dimensions, i.e., thicker airway wall without lumen narrowing caused by occupational DE exposure was different to that (i.e., thicker airway wall with lumen narrowing) seen in our previous study of workers exposed to nano-scale carbon black aerosol, suggesting constituents other than carbon cores may contribute to such differences. Our study provides some imaging indications of the understanding of the pulmonary toxicity of combustion derived airborne particulate matters in humans.

The global transition to electric vehicles hinges on lithium‐ion batteries, yet the health risks of their core components, such as nickel‐manganese‐cobalt (NCM) cathodes, remain a critical and misunderstood gap, threatening a truly sustainable energy transition. Herein, we reveal that inhaled NCM particles undergo sustained lysosomal dissolution, transforming into metal mixtures whose composition mirrors the parent material. Crucially, we decipher the unique toxicological interactions within this biologically generated mixture—antagonism from Ni/Co and synergy from Mn. This fundamental discovery of NCM's biological fate unlocks accurate risk assessment. Building on this mechanistic insight, we identified the Integrated Addition and Interaction (IAI) model as the framework capable of capturing complex interactions. Applying this model to real‐world exposure data uncovers moderate yet significant population‐level health risks. Our work establishes a transformative, evidence‐based paradigm that connects in‐body material transformation to real‐world health outcomes, providing the scientific foundation to ensure that the clean energy transition is not only green but fundamentally safe for human well‐being. Inhaled NCM particles undergo lysosomal degradation, releasing complex ion mixtures that induce systemic impact. The impact is determined by a critical balance between antagonistic Ni‐Co interactions and synergistic Mn effects. To capture these complexities in risk assessment, we develop an IAI model, ensuring a more accurate quantitative risk assessment. Application to NCM high‐exposure populations indicates major moderate health risks.

The relationship between CDH23 gene variants and NIHL is unclear. This study investigates the association between ( ) gene variants and noise-induced hearing loss (NIHL). This is a case-control study. Workers who were exposed to noise from a steel factory in North China were recruited and divided into two groups: the case group (both ears' high-frequency threshold average [BHFTA] ≥40dB) and the control group (BHFTA ≤25 dB). This study used the generalised multifactor dimensionality reduction method to analyse the association among 18 single-nucleotide polymorphisms (SNPs) in and NIHL. Logistic regression was performed to investigate the main effects of SNPs and the interactions between cumulative noise exposure (CNE) and SNPs. Furthermore, CNE was adjusted for age, gender, smoking, drinking, physical exercise and hypertension. This study recruited 1,117 participants. The results showed that for rs11592462, participants who carried the GG genotype showed an association with NIHL greater than that of those who carried the CC genotype. Accordingly, genetic variation in the gene could play an essential role in determining individual susceptibility to NIHL. Genetic variations in the gene may play an important role in determining individual susceptibility to NIHL. These results provide new insight into the pathogenesis and early prevention of NIHL.

Noise-induced hearing loss (NIHL) is the second-most frequent form of sensorineural hearing loss. When exposed to the same noise, some workers develop NIHL while others do not, suggesting that NIHL may be associated with genetic factors. To explore the relationship between single nucleotide polymorphisms (SNPs) in heat shock protein 70 (HSP70) genes (HSPA1A, HSPA1B and HSPA1L) and susceptibility to NIHL in Han Chinese workers exposed to noise, a case-control association study was carried out with 286 hearing loss cases and 286 matched with gender, age, type of work, and exposure time, drawn from a population of 3790 noise-exposed workers. Four SNPs were selected and genotyped. Subsequently, the effects of the alleles and genotypes of the three HSP70 genes (HSPA1A, HSPA1B and HSPA1L) on NIHL were analyzed by using a conditional logistic regression. A generalized multiple dimensionality reduction (GMDR) was applied to further detect an interaction between the four SNPs. Compared with the combined genotypes CC/TC, carriers of the TT genotype of rs2763979 appeared to show greater susceptibility to NIHL (P = 0.042, adjusted OR = 1.731, 95% CI 1.021-2.935). A significant interaction between rs2763979 and CNE was found (P = 0.029), and a significant association was found between TT of s2763979 and NIHL (P = 0.024, adjusted OR = 5.694, 95%CI 1.256-25.817) in the 96 dB (A)≤CNE<101 dB (A) group. The results suggest that the rs2763979 locus of the HSP70 genes may be associated with susceptibility to NIHL in Chinese individuals, and other HSP70 genes may also be susceptibility genes for NIHL, but the results must be further replicated in additional independent sample sets.

Background Noise-induced hearing loss (NIHL) is a complex, irreversible disease caused by the interaction of genetic and environmental factors. In recent years, a great many studies have been done to explore the NIHL susceptibility genes among humans. So far, high powerful detections have been founded that genes of potassium ion channel genes ( KCNQ4 and KCNE1 ), catalase ( CAT ), protocadherin 15 ( PCDH15 ), myosin 14 ( MYH14 ) and heart shock protein ( HSP70 ) which have been identified in more than one population may be associated with the susceptibility to NIHL. As for metabolic glutamate receptor7 gene ( GRM7 ), a lot of researches mainly focus on age-related hearing loss (ARHL) and the results have shown that the polymorphisms of GRM7 are linked to the development of ARHL. However, little is known about the association of GRM7 and the susceptibility to NIHL. Therefore, the aim of this study was to explore the effect of GRM7 polymorphisms on the susceptibility to NIHL. Methods A nested case-control study based on the cohort in a Chinese steel factory was implemented in 292 cases and 584 controls matched with the same sex, the age difference ≤ 5 years old, the same type of work, duration of occupational noise exposure ≤2 years. Five single nucleotide polymorphisms (SNPs) of GRM7 were gained through selecting and genotyping SNPs. Conditional logistic regression analysis was used to assess the main effect of GRM7 polymorphisms on the susceptibility to NIHL and the gene-by-environment interaction. Furthermore, the gene-by-gene interactions were analyzed by generalized multiple dimensionality reduction (GMDR). Results This research discovered for the first time that the mutant allele C in rs1485175 of the GMR7 may decrease individuals’ susceptibility to NIHL. The interaction between rs1485175 and cumulative noise exposure (CNE) at high level was found after the stratification according to CNE ( p / p bon  = 0.014/0.007, OR = 0.550, 95% CI: 0.340–0.891). Permutation test of GMDR suggested that rs1920109, rs1485175 and rs9826579 in GRM7 might interact with each other in the process of developing NIHL ( p  = 0.037). Conclusions The results suggest that the mutant allele C of rs1485175 in GRM7 may reduce the susceptibility to NIHL in Chinese Han population.