Associations between benzene exposure and allergic rhinitis risk and survival in older adults: the mediating role of biological aging and the moderating influence of genetic susceptibility

Allergic rhinitis (AR) is an immune-mediated airway disorder increasingly linked to environmental pollution. This study examined the long-term association of benzene exposure with AR and all-cause mortality in older adults and explored the potential mediating role of biological aging and modification by genetic susceptibility. Data from 76,183 UK Biobank participants aged ≥ 65 years at baseline were linked with annual residential benzene estimates (2006–2020) from the DEFRA 1 km × 1 km model. Cox proportional hazards models evaluated associations with AR incidence and mortality, and restricted cubic splines assessed nonlinearity, and multistate models characterized transitions between AR and death. Four biological aging markers-PhenoAge, Klemera-Doubal biological age (KDM), Homeostatic Dysregulation (HD), and Accelerated Biological Aging (ABA)-were incorporated into bootstrap mediation models. Genetic risk was quantified using a polygenic risk score (PRS) derived from 35 genome-wide significant SNPs. Over median follow-ups of 13.3 years for AR and 14.8 years for mortality, 756 AR cases and 17,963 deaths were recorded. Each interquartile range (IQR, 0.151 μg/m 3 ) increase in benzene concentration was associated with higher risks of AR (HR = 1.44, 95% CI 1.31–1.57) and mortality (HR = 1.21, 95% CI 1.19–1.23). Multistate analyses associated higher benzene exposure with transitions from an AR-free state to incident AR or death, but not from incident AR to death. Thresholds were identified at 0.255 μg/m 3 for AR and 0.277 μg/m 3 for mortality. Biological aging partially mediated these associations (mediation proportion up to 15.2%), and participants in the highest PRS tertile had a higher AR risk than those in the lowest tertile (HR = 1.54, 95% CI 1.29–1.85). Sensitivity analyses supported the robustness of the findings. Chronic low-level benzene exposure was associated with higher risks of AR and all-cause mortality in older adults. Biological aging may partly mediate these associations, with genetic susceptibility further modifying AR risk through positive additive interaction.

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Journal
BMC Geriatrics
Published
2026-09-18
DOI
https://doi.org/10.1186/s12877-026-08302-z
Primary Topic
Occupational exposure and asthma
Type
article
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article

Associations between benzene exposure and allergic rhinitis risk and survival in older adults: the mediating role of biological aging and the moderating influence of genetic susceptibility

Hong Cao, Chi Chen, Bo Gou, Jingyuan Zhang et al.
BMC Geriatrics
Occupational exposure and asthma
article

Associations between benzene exposure and allergic rhinitis risk and survival in older adults: the mediating role of biological aging and the moderating influence of genetic susceptibility

Hong Cao, Chi Chen, Bo Gou, Jingyuan Zhang, Jing Zhang, Yuxi Wei, Jia Li
article en

Abstract

Allergic rhinitis (AR) is an immune-mediated airway disorder increasingly linked to environmental pollution. This study examined the long-term association of benzene exposure with AR and all-cause mortality in older adults and explored the potential mediating role of biological aging and modification by genetic susceptibility. Data from 76,183 UK Biobank participants aged ≥ 65 years at baseline were linked with annual residential benzene estimates (2006–2020) from the DEFRA 1 km × 1 km model. Cox proportional hazards models evaluated associations with AR incidence and mortality, and restricted cubic splines assessed nonlinearity, and multistate models characterized transitions between AR and death. Four biological aging markers-PhenoAge, Klemera-Doubal biological age (KDM), Homeostatic Dysregulation (HD), and Accelerated Biological Aging (ABA)-were incorporated into bootstrap mediation models. Genetic risk was quantified using a polygenic risk score (PRS) derived from 35 genome-wide significant SNPs. Over median follow-ups of 13.3 years for AR and 14.8 years for mortality, 756 AR cases and 17,963 deaths were recorded. Each interquartile range (IQR, 0.151 μg/m 3 ) increase in benzene concentration was associated with higher risks of AR (HR = 1.44, 95% CI 1.31–1.57) and mortality (HR = 1.21, 95% CI 1.19–1.23). Multistate analyses associated higher benzene exposure with transitions from an AR-free state to incident AR or death, but not from incident AR to death. Thresholds were identified at 0.255 μg/m 3 for AR and 0.277 μg/m 3 for mortality. Biological aging partially mediated these associations (mediation proportion up to 15.2%), and participants in the highest PRS tertile had a higher AR risk than those in the lowest tertile (HR = 1.54, 95% CI 1.29–1.85). Sensitivity analyses supported the robustness of the findings. Chronic low-level benzene exposure was associated with higher risks of AR and all-cause mortality in older adults. Biological aging may partly mediate these associations, with genetic susceptibility further modifying AR risk through positive additive interaction.

BMC Geriatrics
Hubei University of Medicine (CN), Fudan University (CN), Shanghai Second People's Hospital (CN), Obstetrics and Gynecology Hospital of Fudan University (CN)
Openalex Percentile: Top 8%
Occupational exposure and asthma
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