受热重油体内自由基演化诱导生焦历程及接力供氢抑焦自免疫机制研究

The free radical condensation to form coke in the initial heating stage is the bottleneck of heavy oil efficient partial upgrading. Thus, the free radical transformation chemistry is the key scientific issue to control the premature coke formation. However, there is a lack of deep research on the emergence and disappearance process of free radical in heavy oil upon heating. We have previously found that the internal hydrogen transferring in heavy oil upon heating is the essential chemical impetus to quench free radicals and could act as the “self-immunity system” for coke inhibition. Hence, it is hypothesized that the inherent and newly-generated free radicals in heavy oil could be continuously quenched by the active hydrogen from various natural hydrogen donors in heavy oil. In this project, the complicated heavy oil is separated into different fractions with molecular compositions are relatively simplified; the pyrolysis characteristics of heavy oil and fractions are firstly investigated. Subsequently, the variation of total active radical upon heating is traced by introducing hydrogen donor solvent as quantitative radical scavenger; the radical confined in large molecule structures is simultaneously monitored by electron spin resonance technique. By coupling these two methods, the intrinsic hydrogen abstracting effect of free radicals is revealed. Then, the hydrogen-donating effect is tracked using hydrogen accepting molecular probes with different activities in order to elucidate the developing process of hydrogen donating behavior. Meanwhile, the radical evolution and hydrogen donating effect during co-pyrolysis of three separate light fractions with asphaltene coke precursor fraction are explored to clarify the hydrogen transferring synergism for coke inhibition among different fractions. This project aims to unveil radical evolution to induce coke formation and hydrogen donating self-immunity mechanism to inhibit coke formation during thermal conversion of heavy oil, which is of great theoretical and practical significance to suppress the coke formation by combining with external hydrogen source as drugs during heavy oil partial upgrading.

重油受热初期自由基缩聚生焦是制约其高效热降黏输送的关键瓶颈，揭示热诱导生焦阶段重油自由基转化化学是控制初期生焦的根本科学问题。然而重油受热自由基的产生和消失历程仍缺乏深入研究。我们前期发现重油内部氢转移是湮灭自由基的重要化学抑焦“自免疫力”，因此推测热诱导生焦阶段重油依靠体内不同活性供氢体接力淬灭原生及新生自由基从而延缓生焦。针对此，本研究将重油细分为四类组分，考察其诱导生焦特性；利用充足供氢溶剂定量捕捉其活性自由基演变规律，结合ESR监控大分子裹挟自由基的变化状况，揭示自由基本征夺氢效应和诱导生焦历程；利用不同活性夺氢探针追踪天然供氢体的供氢效应，阐释接力供氢机制；探索轻组分与沥青质生焦前驱组分的混合热解自由基转变与供氢特性，剖析组分间协同氢转移作用。本课题旨在系统阐明受热重油自由基演化诱导生焦历程及接力供氢抑焦自免疫机制，为高效配合氢源药剂抑焦以定向调控重油降黏改质奠定理论与应用基础。

重油受热初期自由基缩聚生焦是制约其高效改质的关键瓶颈，揭示热诱导生焦阶段重油自由基转化化学是控制初期生焦的根本科学问题。然而受热重油自由基的产生和消失历程仍缺乏深入研究。我们前期发现重油内部氢转移是湮灭自由基的抑焦自免疫力，因此推测热诱导生焦阶段依靠体内不同活性供氢体接力淬灭固有和新出现的自由基从而延缓生焦。.本研究以加拿大油砂沥青常渣为原料，将渣油细分为不同亚组分，考察其热诱导生焦特性；利用过量供氢溶剂定量捕捉活性自由基在诱导生焦阶段的演变规律，结合ESR监控其中被重质大分子裹挟的高芳自由基的变化，揭示自由基本征夺氢机制；利用不同活性夺氢探针跟踪供氢体在诱导生焦阶段的供氢效应，阐释接力氢转移历程；探索轻组分与沥青质生焦前驱组分的混合热解自由基转变与供氢特性，剖析组分间协同氢转移抑焦效应。.研究表明，渣油生焦始于350℃且存在诱导期，遵循二级+自催化反应动力学，而胶质和沥青质生焦始于250℃、未表现出诱导期和自催化特征，说明生焦诱导期由原料和焦炭的溶解性差距决定。仅沥青质在250℃时产生活性自由基，其也是诱发渣油低温活性自由基的关键组分，当温度超过350℃时活性自由基链式爆发而后逐渐平稳。受热渣油低温生焦受多环芳香大分子物理缔合效应控制，高温生焦受自由基化学缩聚控制。高温生焦量与活性自由基浓度的线性正相关斜率由原料结构决定，而与稳定自由基浓度的线性正相关斜率还与温度密切相关，高温下稳定自由基诱发生焦的能力更强。三种轻组分能够通过物理胶溶和内部化学供氢的作用封闭沥青质大分子自由基而延缓生焦，渣油低温供氢特性主要源于胶质和沥青质，随温度升高芳香分接力参与供氢，胶质供氢能力始终发挥重要作用，沥青质供氢受自身强夺氢需求的增加而削弱，构成渣油供氢抑焦自免疫系统。本研究系统阐明了受热重油自由基演变及氢转移淬灭自由基机制，为高效配合氢源药剂抑焦以调控重油部分改质奠定理论与应用基础。