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<p>Cigarette smoking is a major global health hazard, responsible for millions of deaths annually. This study aimed to evaluate the effects of cigarette smoke and its heavy metal constituents on the respiratory system of Sprague–Dawley (SD) rats following prolonged exposure. It further sought to elucidate the underlying mechanisms and identify key biomarkers and microbial taxa associated with respiratory pathology, thereby providing a scientific basis for future investigations into the impact of cigarette smoke on human respiratory health. This study aimed to evaluate the effects of cigarette smoke and its heavy metal constituents on the respiratory system of SD rats following prolonged exposure. It further sought to elucidate the underlying mechanisms and identify key microbial taxa associated with respiratory pathology. SD rats were randomly allocated to a cigarette smoke exposure group (CS) or a control group (C). The CS group received continuous cigarette smoke exposure, while the control group received no special treatment. Heavy metal concentrations in tobacco and ash were measured to estimate external exposure. After the exposure period, pulmonary function tests were performed, heavy metal levels in lung tissue were quantified, lung tissues were subjected to hematoxylin and eosin (HE) staining for histopathological analysis, and bronchoalveolar lavage fluid (BALF) was analyzed for microbial community structure. Data analysis was conducted using SPSS and R software. Seven heavy metals—mercury, lead, nickel, copper, zinc, cadmium, and arsenic—were found to transfer from tobacco to cigarette smoke, with Cd cadmium exhibiting the highest estimated transfer efficiency from tobacco to smoke when approximated by the tobacco and ash differences. The CS group showed elevated lung concentrations of all metals compared to controls, with significant differences in Cd, Cu, and Zn levels. Cigarette smoke exposure significantly altered respiratory parameters, including respiratory rate (f), functional residual capacity (Frc), specific airway resistance (sRaw), airway resistance (Raw), and peak inspiratory flow (PIF). Ni was positively correlated with sRaw; Cu was positively correlated with f and sRaw and negatively with PIF; Cd was positively correlated with sRaw and negatively with PIF. Histopathological examination confirmed severe lung injury in the CS group. Significant differences in microbial composition were observed, particularly in <i>Blastomonas</i>, <i>Rothia</i>, and other microbiome (<i>p</i> &lt; 0.05). Prolonged exposure to cigarette smoke and its heavy metals induces significant pulmonary dysfunction and alters the bronchoalveolar microbiota, resulting in pronounced lung injury in rats.</p>

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Heavy Metal Transfer from Cigarette Smoke to Lung Tissue: Inducing on Pulmonary Function and Bronchoalveolar Microbiome Dysregulation in Rats

  • 期刊论文

  • 发表日期：

    2025年10月28日

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  • Rongjie Wu,
  • Xiong Yue,
  • Shuxia Yu,
  • Yiwen Zhang,
  • Junpu Yu,
  • Fanhui Luo,
  • Rentong Chen,
  • Tian Tian,
  • Bin Luo,
  • Li Ma

摘要

Cigarette smoking is a major global health hazard, responsible for millions of deaths annually. This study aimed to evaluate the effects of cigarette smoke and its heavy metal constituents on the respiratory system of Sprague–Dawley (SD) rats following prolonged exposure. It further sought to elucidate the underlying mechanisms and identify key biomarkers and microbial taxa associated with respiratory pathology, thereby providing a scientific basis for future investigations into the impact of cigarette smoke on human respiratory health. This study aimed to evaluate the effects of cigarette smoke and its heavy metal constituents on the respiratory system of SD rats following prolonged exposure. It further sought to elucidate the underlying mechanisms and identify key microbial taxa associated with respiratory pathology. SD rats were randomly allocated to a cigarette smoke exposure group (CS) or a control group (C). The CS group received continuous cigarette smoke exposure, while the control group received no special treatment. Heavy metal concentrations in tobacco and ash were measured to estimate external exposure. After the exposure period, pulmonary function tests were performed, heavy metal levels in lung tissue were quantified, lung tissues were subjected to hematoxylin and eosin (HE) staining for histopathological analysis, and bronchoalveolar lavage fluid (BALF) was analyzed for microbial community structure. Data analysis was conducted using SPSS and R software. Seven heavy metals—mercury, lead, nickel, copper, zinc, cadmium, and arsenic—were found to transfer from tobacco to cigarette smoke, with Cd cadmium exhibiting the highest estimated transfer efficiency from tobacco to smoke when approximated by the tobacco and ash differences. The CS group showed elevated lung concentrations of all metals compared to controls, with significant differences in Cd, Cu, and Zn levels. Cigarette smoke exposure significantly altered respiratory parameters, including respiratory rate (f), functional residual capacity (Frc), specific airway resistance (sRaw), airway resistance (Raw), and peak inspiratory flow (PIF). Ni was positively correlated with sRaw; Cu was positively correlated with f and sRaw and negatively with PIF; Cd was positively correlated with sRaw and negatively with PIF. Histopathological examination confirmed severe lung injury in the CS group. Significant differences in microbial composition were observed, particularly in Blastomonas, Rothia, and other microbiome (p < 0.05). Prolonged exposure to cigarette smoke and its heavy metals induces significant pulmonary dysfunction and alters the bronchoalveolar microbiota, resulting in pronounced lung injury in rats.