Scholarlink

Background <p>Graphite nanoplatelets (GNPs) are increasingly used in advanced materials, yet their environmental transformation and resulting health impacts remain poorly understood. This study investigated how long-term aquatic aging alters the physicochemical properties and pulmonary toxicity of GNPs.</p> Results <p>Pristine GNPs (PGNPs) were aged for 26 months in water containing sand under constant agitation to simulate natural mechanical and chemical weathering, yielding aged GNPs (AGNPs) with increased surface oxidation level, smaller lateral dimensions, and improved hydrophilicity. These alterations enhanced the intrinsic oxidative potential of AGNPs by 1.28–1.40-fold relative to PGNPs. Following a single intratracheal instillation in mice (25–100&#xa0;µg/mouse), AGNPs induced significantly stronger pulmonary inflammation at both 24&#xa0;h and 7 days, characterized by elevated neutrophil infiltration, increased levels of lactate dehydrogenase, total protein, and pro-inflammatory cytokines in bronchoalveolar lavage fluid. Although both materials showed a similar clearance pattern, AGNPs showed a slightly prolonged retention compared to PGNPs (half-life: AGNPs 10 days, PGNPs 5.5 days). Differentiated THP-1 macrophages and A549 cells exposed to AGNPs showed higher cytotoxicity, intracellular reactive oxygen species (ROS) generation, and cytokine release than PGNPs, confirming the <i>in vivo</i> findings. Correlation analysis revealed that ROS levels were strongly associated with inflammatory and cytotoxic endpoints (Pearson <i>r</i> &gt; 0.90), indicating that oxidative stress is a key mechanism of GNP-induced toxicity.</p> Conclusions <p>These findings demonstrate that simulated aquatic aging enhances the oxidative potential and pulmonary toxicity of GNPs through mechanically and chemically induced surface oxidation, highlighting the need to consider environmental transformation in nanomaterial hazard assessment and life-cycle-based safety assessment.</p> Graphical Abstract <p></p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Simulated aquatic aging exacerbates pulmonary toxicity of graphite nanoplatelets by mechanically and chemically induced surface oxidation, enhancing oxidative potential

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年4月18日

查看全文
  • Karthika Viswanathan,
  • Youn-Joo Jung,
  • Maruthupandy Muthuchamy,
  • Soyeon Jeon,
  • June-Woo Park,
  • Wan-Seob Cho

摘要

Background

Graphite nanoplatelets (GNPs) are increasingly used in advanced materials, yet their environmental transformation and resulting health impacts remain poorly understood. This study investigated how long-term aquatic aging alters the physicochemical properties and pulmonary toxicity of GNPs.

Results

Pristine GNPs (PGNPs) were aged for 26 months in water containing sand under constant agitation to simulate natural mechanical and chemical weathering, yielding aged GNPs (AGNPs) with increased surface oxidation level, smaller lateral dimensions, and improved hydrophilicity. These alterations enhanced the intrinsic oxidative potential of AGNPs by 1.28–1.40-fold relative to PGNPs. Following a single intratracheal instillation in mice (25–100 µg/mouse), AGNPs induced significantly stronger pulmonary inflammation at both 24 h and 7 days, characterized by elevated neutrophil infiltration, increased levels of lactate dehydrogenase, total protein, and pro-inflammatory cytokines in bronchoalveolar lavage fluid. Although both materials showed a similar clearance pattern, AGNPs showed a slightly prolonged retention compared to PGNPs (half-life: AGNPs 10 days, PGNPs 5.5 days). Differentiated THP-1 macrophages and A549 cells exposed to AGNPs showed higher cytotoxicity, intracellular reactive oxygen species (ROS) generation, and cytokine release than PGNPs, confirming the in vivo findings. Correlation analysis revealed that ROS levels were strongly associated with inflammatory and cytotoxic endpoints (Pearson r > 0.90), indicating that oxidative stress is a key mechanism of GNP-induced toxicity.

Conclusions

These findings demonstrate that simulated aquatic aging enhances the oxidative potential and pulmonary toxicity of GNPs through mechanically and chemically induced surface oxidation, highlighting the need to consider environmental transformation in nanomaterial hazard assessment and life-cycle-based safety assessment.

Graphical Abstract