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<p>Epidemiological studies link traffic proximity to increased osteoporosis and fracture risk in older adults, but mechanistic relationships remain unclear. Following our recently published hypothesis regarding metal-induced bone fragility, we performed an exploratory study to investigate whether chronic exposures to metals in traffic-derived PM<sub>2.5</sub> during development compromise bone health in young adult mice. This opportunistic investigation utilised stored biological material from a concurrent sub-chronic exposure study. BALBc mice were divided into PM<sub>2.5</sub> exposed and control groups over 12 weeks. Starting at 6 weeks of age PM<sub>2.5</sub> exposed mice received daily intranasal administration of 10 µg/mL filtered particulates collected from Sydney roadside air while controls received saline. Metal accumulation was quantified using ICP-MS and bone structural properties were assessed via micro-CT. Mechanical properties were evaluated through three-point bending tests at 4 and 8 and 12 weeks of exposure. No significant differences were observed between groups across any parameter. Both groups exhibited comparable concentrations of endogenous and exogenous metals at all examined time points. Bone geometric properties and mechanical characteristics including yield stress and ultimate tensile strength and stiffness were similar between groups with normal age-related development in both. These findings suggest that metal accumulation in bone is not significant in early life and is not associated with a deterioration of mechanical properties under the specific conditions of this exploratory model. It is more likely that any adverse effects require a cumulative lifetime burden and age-related decline in protective mechanisms rather than immediate developmental vulnerability. This shifts the focus from early-life susceptibility to long-term risk and establishes a methodological pipeline for future longitudinal research.</p>

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Chronic developmental exposure to traffic-derived PM2.5 has limited skeletal effects in mice

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月28日

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  • Joudi Altaleb,
  • Min Feng,
  • Yushi Zhao,
  • Xing Zhou,
  • Hui Chen,
  • Brian G. Oliver,
  • Ian Mudway,
  • Ulrich Hansen,
  • Richard L. Abel

摘要

Epidemiological studies link traffic proximity to increased osteoporosis and fracture risk in older adults, but mechanistic relationships remain unclear. Following our recently published hypothesis regarding metal-induced bone fragility, we performed an exploratory study to investigate whether chronic exposures to metals in traffic-derived PM2.5 during development compromise bone health in young adult mice. This opportunistic investigation utilised stored biological material from a concurrent sub-chronic exposure study. BALBc mice were divided into PM2.5 exposed and control groups over 12 weeks. Starting at 6 weeks of age PM2.5 exposed mice received daily intranasal administration of 10 µg/mL filtered particulates collected from Sydney roadside air while controls received saline. Metal accumulation was quantified using ICP-MS and bone structural properties were assessed via micro-CT. Mechanical properties were evaluated through three-point bending tests at 4 and 8 and 12 weeks of exposure. No significant differences were observed between groups across any parameter. Both groups exhibited comparable concentrations of endogenous and exogenous metals at all examined time points. Bone geometric properties and mechanical characteristics including yield stress and ultimate tensile strength and stiffness were similar between groups with normal age-related development in both. These findings suggest that metal accumulation in bone is not significant in early life and is not associated with a deterioration of mechanical properties under the specific conditions of this exploratory model. It is more likely that any adverse effects require a cumulative lifetime burden and age-related decline in protective mechanisms rather than immediate developmental vulnerability. This shifts the focus from early-life susceptibility to long-term risk and establishes a methodological pipeline for future longitudinal research.