The present study investigated the association between blood benzene levels and severe periodontitis in a large, nationally representative sample of U.S. adults. Our main findings suggest that individuals with higher blood benzene levels are more likely to have severe periodontitis, a progressive inflammatory oral condition.
Benzene, a ubiquitous environmental pollutant, has been linked to various adverse health outcomes, including hematological disorders, cancer, and immune system dysfunction [20]. However, its potential impact on periodontal health has not been thoroughly investigated. Our study provided new evidence supporting the association between benzene exposure and severe periodontitis.
Benzene and its metabolites have been shown to induce oxidative stress, which plays a crucial role in the pathogenesis of periodontal disease [21, 22]. Oxidative stress can lead to the activation of redox-sensitive transcription factors, such as nuclear factor-kappa B (NF-κB), which regulate the expression of proinflammatory cytokines and matrix metalloproteinases involved in periodontal tissue destruction [23]. Additionally, benzene exposure has been associated with alterations in immune function, including decreased lymphocyte counts and impaired T-cell function, which may compromise the host's ability to mount an effective defense against periodontal pathogens [24].
The relationship between benzene exposure and periodontal disease may be mediated by several mechanisms [25]. Our study demonstrated that the level of cotinine, a biomarker of tobacco smoke exposure, mediates the association between benzene exposure and severe periodontitis. This finding suggested that smoking may be a critical factor in the pathway leading to periodontal disease among individuals exposed to benzene. Cigarette smoke contains benzene, and exposure to this toxin through smoking can lead to increased oxidative stress and inflammation in the oral cavity [26]. Oxidative stress has been implicated in the destruction of periodontal tissues, while inflammation can accelerate the progression of periodontal disease [27]. Furthermore, smoking has been associated with alterations in the oral microbiome, promoting the growth of periodontal pathogens such as Porphyromonas gingivalis and Tannerella forsythia [28]. These changes in the oral microbiome, coupled with the suppression of the host immune response due to smoking, can create a favorable environment for the development and progression of periodontal disease [29]. Impaired immune function may hinder the body's ability to combat pathogenic bacteria and maintain periodontal health [30]. Consequently, our study emphasizes the importance of considering smoking as a potential mediator in the relationship between benzene exposure and periodontal disease, as smoking can influence various pathways involved in the pathogenesis of this oral health condition.
Our findings are consistent with previous studies reporting associations between benzene and periodontal disease. For example, a systematic review published by Rahimpoor et al. provides detailed insights into the biological, chemical, and environmental mechanisms of benzene exposure, particularly in occupational settings [31]. Several key biomarkers have been identified for use in monitoring benzene exposure, notably urinary benzene, which is effective at low exposure levels. These biomarkers include recent exposure and trans-trans muconic acid (TTMA) and S-phenyl mercapturic acid (SPMA), which are more relevant at higher exposure levels and reflect the body’s metabolic response to benzene [31]. Metabolites such as TTMA and SPMA can modulate immune responses, potentially disrupting them and leading to heightened inflammatory responses [31].
The strengths of our study include the use of a large, nationally representative sample, the objective assessment of periodontal status using standardized clinical measures, and the measurement of blood benzene levels as a biomarker of exposure. However, some limitations should be acknowledged. The cross-sectional design precludes causal inferences, and the possibility of residual confounding cannot be eliminated. Additionally, blood benzene levels reflect recent exposure and may not capture long-term or cumulative exposure, which could be more relevant for the development of chronic conditions such as periodontal disease.