What this means
Chronic benzene (BZ) exposure is a well-established cause of hematological malignancies, but its potential association with immunosenescence-related alterations at occupational exposure levels below current regulatory limits remains unclear. This cross-sectional study investigated the associations of cumulative BZ exposure with genotoxicity, immunosenescence-related, and hematological biomarkers.
A plain-English summary is on its way. Until then, this is the start of the authors' own summary.
- Who it was tested in
- People
- Kind of research
- A study
The science
- Original title
- Associations of cumulative occupational benzene exposure with genotoxic and immunosenescence-related biomarkers: a cross-sectional study.
- Authors
- Xu W, Ruan X, He L et al.
- Journal
- Frontiers in public health
- Published
- Oct 29, 2026
- Study type
- Study · in humans
- PMID
- 42952844 ↗
Abstract
Background
Chronic benzene (BZ) exposure is a well-established cause of hematological malignancies, but its potential association with immunosenescence-related alterations at occupational exposure levels below current regulatory limits remains unclear. This cross-sectional study investigated the associations of cumulative BZ exposure with genotoxicity, immunosenescence-related, and hematological biomarkers.
What they did
The study included 228 participants: 115 workers directly involved in BZ production, 75 administrative workers from the same factories without direct involvement in BZ production, and 38 external controls without occupational exposure to industrial solvents. BZ exposure was assessed using personal air monitoring, and cumulative exposure dose (CED) was calculated from airborne BZ concentrations and exposure duration. Genomic damage was evaluated using the cytokinesis-block micronucleus (CBMN) and comet assays. Immunosenescence-related and cellular-stress markers included the CD4/CD8 ratio, CD28- frequency, p53 expression, γ-H2AX expression, and mitochondrial DNA copy number. Hematological parameters were assessed using peripheral blood cell counts. Spearman correlation analysis and outcome-appropriate generalized linear models were used to evaluate the associations between CED and the investigated biomarkers.
What they found
After full multivariable adjustment, higher CED was associated with greater comet tail intensity (MR = 1.0827, p < 0.001) and tail moment (MR = 1.0922, p < 0.001) and with lower CD4/CD8 ratio (MR = 0.9743, p < 0.001) and p53 expression (MR = 0.9739, p < 0.001). CED was associated with higher micronucleus frequency (MNF) in the age- and sex-adjusted model (RR = 1.0137, p = 0.033). After further adjustment for BMI, hypertension, smoking status, and alcohol use, the effect estimate remained positive, but the association did not reach conventional statistical significance (RR = 1.0123, p = 0.053). No statistically significant associations were observed between CED and comet tail length, CD28- frequency, γ-H2AX expression, mitochondrial DNA copy number, WBC, RBC, platelet count, or neutrophil count in the fully adjusted models. Cumulative occupational BZ exposure below the applicable regulatory limits was associated with increased comet-assessed DNA damage and selected immune-related alterations, particularly lower CD4/CD8 ratio and p53 expression. The association between CED and MNF remained positive but was not statistically significant after full adjustment. These findings suggest a selective pattern of BZ-associated genotoxic and immune-related alterations rather than generalized hematological toxicity or a uniform immunosenescence phenotype. Prospective studies are needed to determine their long-term clinical and occupational health significance.
The authors' abstract, grouped under plain headings from its own section labels.
Xu W, Ruan X, He L et al. Associations of cumulative occupational benzene exposure with genotoxic and immunosenescence-related biomarkers: a cross-sectional study. Frontiers in public health. 2026. doi:10.3389/fpubh.2026.1972556. PMID: 42952844. https://pubmed.ncbi.nlm.nih.gov/42952844/