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

吸烟是可预防的死亡的主要原因，美国有50万人死于吸烟。 然而，这一负担并不是平均承担的。例如，尽管非裔美国人(AA)有 吸烟率与非西班牙裔白人(NHW)相当，他们更有可能死亡 与吸烟相关的疾病。此外，AAA的戒烟率比NHW低。 因此，aa终生暴露在烟草烟雾中的几率更大，从而增加了患病风险。 与烟草有关的疾病。治疗效果的种族差异背后的原因 即使在同等治疗的临床试验中也没有完全被理解和出现。 我们目前了解吸烟是通过以下几个途径开始和维持的 神经生物学过程，包括增强积极情绪，减少消极情绪 情绪和/或压力，以及避免尼古丁戒断。因此，神经生物学评估 可能有助于开发更有效的戒烟干预措施。一个有希望的人 神经生物学指标，线索反应性，与成瘾强度有关，并已被 被证明是戒烟的预兆。 然而，很少有研究考察线索反应的种族差异。因此，人们对此知之甚少 关于可能导致吸烟和/或戒烟差异的神经生物学机制 跨种族/民族群体的成功。进一步的无线索反应性研究已经检验了 邻域水平的烟草差异相关因素(例如邻域)之间的关系 贫穷、犯罪)和暗示的反应性。从理论上讲，长期接触慢性病的居民 社区压力源，包括劣势、暴力和犯罪，使用尼古丁作为自我 缓解压力的药物。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了，而且 开始吸烟的可能性。因此，有可能增加和长期接触 个人和社区层面的压力源，这是不成比例的普遍现象 在AAs中，有助于形成对吸烟相关刺激反应的种族模式。 使用从休斯顿招募的非洲裔美国人和非西班牙裔白人吸烟者的数据， 德克萨斯州和威斯康星州的密尔沃基，这项研究将调查种族， 个人因素，薄荷醇香烟的使用(鉴于 AA中的薄荷醇香烟)，以及邻里层面的压力源，包括邻里 贫穷和犯罪，并提示反应性。研究结果将有助于阐明关键个人--以及 预测和/或修改线索反应水平的邻域水平因素。

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.