Fini Elham H, Pahlavan Farideh, Vega Natalie Ortiz, Bibo Adriana, Kaur Harpreet, Ghasemi Hamid, Aldagari Sand, Hung Albert, Kannan Latha, Yazdani Hessam, Zhai R Grace, Link Nichole, Ackerman-Biegasiewicz Laura K G, Klein-Seetharaman Judith
School of Sustainable Engineering and the Built Environment, Ira A. Fulton Schools of Engineering, Arizona State University, 660 S. College Avenue, Tempe, AZ 85287-3005, USA.
School of Sustainable Engineering and the Built Environment, Ira A. Fulton Schools of Engineering, Arizona State University, 660 S. College Avenue, Tempe, AZ 85287-3005, USA.
J Hazard Mater. 2025 Mar 15;486:136849. doi: 10.1016/j.jhazmat.2024.136849. Epub 2024 Dec 14.
Asphalt, widely used in infrastructure, emits complex chemical mixtures throughout its service life, posing significant risks to human health and the environment. This expanded understanding extends the concern from a construction-related hazard to a broader public health issue, especially affecting vulnerable populations like children who play on blacktop surfaces. Despite increased awareness, the specific mechanisms behind asphalt emissions, their impact on asphalt deterioration, and their effects on the human nervous system remain poorly understood. Our study addresses these knowledge gaps by examining the long-term health effects of asphalt emissions, focusing on neurological impacts. We investigate how environmental stressors and asphalt's chemical composition influence emission types and severity, using a combination of in vitro experiments, Drosophila melanogaster models, and advanced computational analyses. FTIR analysis reveals that as asphalt ages, emissions evolve from aliphatic to aromatic compounds, increasing toxicity. Our results demonstrate significant neurological damage from asphalt emissions, with effects worsening with age and being more pronounced in females, as shown in the Drosophila model, emphasizing the need for gender-specific health risk research. In vitro studies using 3T3L1 cells show that VOC exposure disrupts lipid droplet formation and metabolism, processes linked to neurodegenerative disorders. To mitigate emissions, our novel approach introduces wood-based biochar as a functional carbon to enhance intermolecular interactions within asphalt. GC-MS analysis indicates that biochar reduces VOC emissions by up to 76 %, while molecular dynamics (MD) simulations highlight biochar's effectiveness in hindering free-radical diffusion. Density functional theory (DFT) calculations confirm biochar's role, with adsorption energies of -20.4 kcal/mol, demonstrating strong and stable interactions that decelerate oxidative aging and mass loss. These findings offer a comprehensive understanding of emission mechanisms and propose a sustainable strategy to enhance asphalt durability while reducing environmental and health risks. This in turn provides evidence-based recommendations for the asphalt industry, emphasizing proactive measures toward long-term exposure mitigation. SYNOPSIS: Asphalt emits chemicals throughout its service life, posing neurological risks, especially to vulnerable groups, and needs emission mitigation.
广泛应用于基础设施建设的沥青，在其整个使用周期内都会释放复杂的化学混合物，对人类健康和环境构成重大风险。这种认识的扩展将关注点从与施工相关的危害延伸到了更广泛的公共卫生问题，尤其影响到在柏油路面玩耍的儿童等弱势群体。尽管人们的认识有所提高，但沥青排放背后的具体机制、它们对沥青老化的影响以及对人类神经系统的影响仍知之甚少。我们的研究通过考察沥青排放的长期健康影响，重点关注神经学影响，来填补这些知识空白。我们结合体外实验、黑腹果蝇模型和先进的计算分析，研究环境压力源和沥青的化学成分如何影响排放类型和严重程度。傅里叶变换红外光谱分析表明，随着沥青老化，排放物从脂肪族化合物演变为芳香族化合物，毒性增加。我们的结果表明，沥青排放会造成显著的神经损伤，在果蝇模型中，这种影响会随着年龄增长而恶化，且在雌性中更为明显，这凸显了开展针对性别的健康风险研究的必要性。使用3T3L1细胞进行的体外研究表明，挥发性有机化合物暴露会破坏脂滴的形成和代谢，而这些过程与神经退行性疾病有关。为了减少排放，我们的新方法引入了木质生物炭作为功能性碳，以增强沥青内部的分子间相互作用。气相色谱 - 质谱分析表明，生物炭可将挥发性有机化合物排放量降低多达76%，而分子动力学模拟突出了生物炭在阻碍自由基扩散方面的有效性。密度泛函理论计算证实了生物炭的作用，其吸附能为-20.4千卡/摩尔，表明存在强烈且稳定的相互作用，减缓了氧化老化和质量损失。这些发现全面地揭示了排放机制，并提出了一项可持续战略，以提高沥青耐久性，同时降低环境和健康风险。这反过来为沥青行业提供了基于证据的建议，强调了针对长期暴露缓解采取积极措施的重要性。摘要：沥青在其整个使用周期内都会释放化学物质，带来神经学风险，尤其是对弱势群体，因此需要减少排放。
