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<p>Cadmium (Cd) and benzo[a]pyrene (BaP) are widely present in indoor dust. However, research on their combined health impacts on humans remains insufficient. To this end, this study employs human bronchial epithelial cells (16HBE) as an exposure model to elucidate the combined toxic effects of Cd and BaP in indoor dust. Cellular studies have demonstrated that Cd and BaP in dust exhibit synergistic toxicity in inducing apoptosis. Compared to the control group, as the combined concentration of Cd and BaP increased (from 5 + 5 to 40 + 100 μM, Cd + BaP), the synergistic toxicity significantly exacerbated cellular damage: Cell viability decreased to as low as 34.1%, lactate dehydrogenase (LDH) release rates rose to 140.2%, and oxidative stress (with catalase (CAT) activity dropping to 73.4%) drove a sharp increase in apoptosis (early apoptosis increased from 6.76% to 15.4%, while late apoptosis rose from 1.90% to 10.9%). Additionally, the expression levels of the pro-apoptotic gene Bcl-2-associated X protein (Bax) and executioner caspase gene Caspase-3 were upregulated by 1.8-fold and 3.7-fold, respectively. Cadmium and BaP promote late apoptosis and early apoptosis, respectively. However, their co-exposure synergistically exacerbates the apoptotic process by complementarily enhancing these pathways in cellular mechanisms. The fitting of the linear equation for Cd-BaP composite pollution lays the foundation for predicting the potential impacts of composite concentrations on the respiratory system. The research findings provide a scientific basis for determining the safety threshold values of Cd and BaP in indoor dust pollutants and for implementing environmental remediation strategies in residential settings.</p>

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Cadmium and Benzo[a]pyrene Co-exposure Synergistically Induces Apoptosis in Bronchial Epithelium: Mechanistic Insights and Predictive Risk Modeling for Indoor Dust

  • 期刊论文

  • 发表日期：

    2025年9月19日

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  • Junbo Liu,
  • Linxi Yang,
  • Jixiang Chen,
  • Yu Bon Man,
  • Ming Hung Wong,
  • Zhang Cheng

摘要

Cadmium (Cd) and benzo[a]pyrene (BaP) are widely present in indoor dust. However, research on their combined health impacts on humans remains insufficient. To this end, this study employs human bronchial epithelial cells (16HBE) as an exposure model to elucidate the combined toxic effects of Cd and BaP in indoor dust. Cellular studies have demonstrated that Cd and BaP in dust exhibit synergistic toxicity in inducing apoptosis. Compared to the control group, as the combined concentration of Cd and BaP increased (from 5 + 5 to 40 + 100 μM, Cd + BaP), the synergistic toxicity significantly exacerbated cellular damage: Cell viability decreased to as low as 34.1%, lactate dehydrogenase (LDH) release rates rose to 140.2%, and oxidative stress (with catalase (CAT) activity dropping to 73.4%) drove a sharp increase in apoptosis (early apoptosis increased from 6.76% to 15.4%, while late apoptosis rose from 1.90% to 10.9%). Additionally, the expression levels of the pro-apoptotic gene Bcl-2-associated X protein (Bax) and executioner caspase gene Caspase-3 were upregulated by 1.8-fold and 3.7-fold, respectively. Cadmium and BaP promote late apoptosis and early apoptosis, respectively. However, their co-exposure synergistically exacerbates the apoptotic process by complementarily enhancing these pathways in cellular mechanisms. The fitting of the linear equation for Cd-BaP composite pollution lays the foundation for predicting the potential impacts of composite concentrations on the respiratory system. The research findings provide a scientific basis for determining the safety threshold values of Cd and BaP in indoor dust pollutants and for implementing environmental remediation strategies in residential settings.