Impact of individual- and neighborhood-level risk factors on brain responses to smoking cues among and across racial groups

吸烟是可预防死亡的主要原因，在美国有50万人死于吸烟。 然而，这一负担并不是平等承担的。例如，虽然非洲裔美国人（AAs） 与非西班牙裔白人（NHWs）的吸烟率相当，他们更有可能死亡 与吸烟有关的疾病。此外，AA的戒烟率低于NHWs。 因此，AA有更大的终身暴露于烟草烟雾，这增加了风险 与烟草有关的疾病。治疗效果存在种族差异的原因 并没有完全被理解，甚至出现在同等治疗的临床试验中。 我们目前了解到，吸烟是通过几个 神经生物学过程，包括积极情绪的增强，消极情绪的减少 情绪和/或压力，以及避免尼古丁戒断。因此，神经生物学评估 可能会为更有效的戒烟干预措施的发展提供信息。一个有前途 神经生物学指标，线索反应性，与成瘾强度相关，并已被 显示出预示着停止。 然而，很少有研究探讨线索反应的种族差异。因此， 关于可能导致吸烟和/或戒烟差异的神经生物学机制 在种族/民族群体中取得成功。进一步的无线索反应性研究已经检查了 烟草差异的邻居级相关性之间的关系（例如，邻域 贫穷、犯罪）和线索反应。理论上，暴露于慢性疾病的居民 社区压力源，包括劣势，暴力和犯罪，使用尼古丁作为自我， 抗压力的药物邻里劣势及其相关因素与 不仅吸烟率更高，而且戒烟的可能性也降低， 开始吸烟的可能性。因此，有可能是高浓度和长期暴露于 个人和社区层面的压力源，这是不成比例的普遍存在 在AA中，有助于形成对吸烟相关刺激的反应的种族模式。 使用从休斯顿招募的非裔美国人和非西班牙裔白色吸烟者的数据， 德克萨斯州和密尔沃基、威斯康星州，这项研究将调查种族之间的关系， 个人因素，薄荷香烟的使用（考虑到不成比例的流行， 薄荷香烟之间的AA），和邻里水平的压力，包括邻里 贫穷和犯罪，以及线索反应。研究结果将有助于阐明关键的个人-和 预测和/或修改线索反应性水平的邻域水平因子。

Smoking is the leading cause of preventable deaths, with half a million occurring in the U.S. However, this burden is not borne equally. For example, although African Americans (AAs) have a comparable smoking prevalence to non-Hispanic Whites (NHWs), they are more likely to die from smoking-related diseases. Further, AAs have lower smoking cessation rates than NHWs. Consequently, AAs have greater lifetime exposure to tobacco smoke, which increases the risk of tobacco-related disease. The reasons underlying these racial disparities in treatment efficacy are not completely understood and appear even among clinical trials with equal treatments. We currently understand smoking to be initiated and maintained through several neurobiological processes, including enhancement of positive emotion, reduction of negative emotion and/or stress, and avoidance of nicotine withdrawal. Thus, neurobiological assessment might inform the development of more effective smoking cessation interventions. A promising neurobiological metric, cue reactivity, is associated with addiction intensity and has been shown to be predictive of cessation. However, few studies have examined racial differences in cue reactivity. Thus, little is known about neurobiological mechanisms that might underlie differences in smoking and/or cessation success across racial/ethnic groups. Further no cue reactivity research has examined the relationship between neighborhood-level correlates of tobacco disparities (e.g., neighborhood poverty, crime) and cue reactivity. It is theorized that residents who are exposed to chronic neighborhoods stressors, including disadvantage, violence, and crime, use nicotine as self- medication against stress. Neighborhood disadvantage and its correlates are associated with not only higher prevalence of smoking, but also decreased likelihood of quitting, and higher likelihood of smoking initiation. Hence, it is possible that heightened and chronic exposure to stressors at both the individual and neighborhood levels, which is disproportionately prevalent among AAs, help shape the racial patterning of responses to smoking-related stimuli. Using data of African American and non-Hispanic White smokers recruited from Houston, Texas and Milwaukee, Wisconsin, this study will investigate the relationship between race, individual factors, mentholated cigarette usage (given the disproportionate popularity of mentholated cigarettes among AAs), and neighborhood-level stressors, including neighborhood poverty and crime, and cue reactivity. Study results will help elucidate the key individual- and neighborhood-level factors that predict and/or modify cue reactivity levels.