Cumulative occupational benzene exposure below applicable regulatory limits was associated with increased comet-assessed DNA damage and selected immune-related alterations, particularly lower CD4/CD8 ratio and p53 expression, suggesting a selective pattern rather than generalized hematological toxicity or a uniform immunosenescence phenotype.
Key Findings
Results
Higher cumulative benzene exposure dose (CED) was associated with greater comet-assay DNA damage, specifically tail intensity and tail moment, after full multivariable adjustment.
Comet tail intensity: MR = 1.0827, p < 0.001.
Tail moment: MR = 1.0922, p < 0.001.
Models were outcome-appropriate generalized linear models adjusted for age, sex, BMI, hypertension, smoking status, and alcohol use.
Comet tail length showed no statistically significant association with CED in fully adjusted models.
Results
Higher CED was associated with a lower CD4/CD8 ratio after full adjustment.
MR = 0.9743, p < 0.001.
CD4/CD8 ratio was one of the immunosenescence-related markers assessed.
The study included 228 participants: 115 benzene production workers, 75 administrative workers from the same factories, and 38 external controls.
Results
Higher CED was associated with lower p53 expression after full adjustment.
MR = 0.9739, p < 0.001.
p53 was assessed as an immunosenescence-related and cellular-stress marker.
The direction of the association was inverse, with higher exposure linked to lower expression.
Results
The association between CED and micronucleus frequency (MNF) was significant in the age- and sex-adjusted model but not after full adjustment.
Age- and sex-adjusted: RR = 1.0137, p = 0.033.
After further adjustment for BMI, hypertension, smoking, and alcohol use: RR = 1.0123, p = 0.053.
The estimate remained positive but did not reach conventional statistical significance.
MNF was measured by the cytokinesis-block micronucleus (CBMN) assay.
Results
No statistically significant associations were found between CED and several other immune, cellular-stress, and hematological markers in fully adjusted models.
Non-significant outcomes: CD28- frequency, γ-H2AX expression, mitochondrial DNA copy number.
Also non-significant: WBC, RBC, platelet count, and neutrophil count.
This indicates no generalized hematological toxicity at the exposure levels studied.
Conclusions
The study found benzene-associated alterations at exposure levels below applicable regulatory limits, in a selective pattern.
Benzene exposure was assessed by personal air monitoring; CED was computed from airborne concentrations and exposure duration.
Analyses used Spearman correlation and outcome-appropriate generalized linear models.
The authors interpret the findings as a selective pattern of genotoxic and immune-related alterations rather than a uniform immunosenescence phenotype.
The cross-sectional design limits inference; prospective studies are needed to determine long-term clinical and occupational health significance.
What This Means
This study looked at 228 people in Chinese factory settings: 115 who worked directly in benzene production, 75 administrative workers at the same factories, and 38 people with no solvent exposure. Researchers measured each worker's benzene exposure with personal air monitors and combined it with years on the job to estimate lifetime workplace dose. They then compared this with blood-based markers of DNA damage, immune aging, and blood cell counts.
Even though exposures were below applicable regulatory limits, higher cumulative benzene exposure was linked to more DNA damage as measured by the comet assay, a lower CD4/CD8 immune cell ratio, and lower p53 levels (a protein involved in responding to DNA damage). A link with micronuclei (another sign of chromosome damage) was seen in a simpler analysis but was borderline once lifestyle and health factors such as smoking, alcohol, BMI, and hypertension were accounted for. Other markers, including routine blood counts, showed no clear association.
This research suggests that benzene may have subtle effects on DNA and the immune system at exposure levels considered permissible, but the pattern was selective rather than widespread. Because the study captured a single point in time, it cannot show that benzene caused these changes or whether they lead to disease. Longer-term follow-up studies are needed to understand their health significance.
Xu W, Ruan X, He L, Zhang Y, Sun Y. (2026). Associations of cumulative occupational benzene exposure with genotoxic and immunosenescence-related biomarkers: a cross-sectional study.. Frontiers in public health. https://doi.org/10.3389/fpubh.2026.1972556