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

个人和社区层面的危险因素对不同种族群体中吸烟线索的大脑反应的影响

• 批准号: 10664822
• 负责人: D. PHUONG DO
• 金额: $ 8.74万
• 依托单位: UNIVERSITY OF WISCONSIN MILWAUKEE
• 依托单位国家: 美国
• 财政年份: 2022
• 资助国家: 美国
• 起止时间: 2022-07-15 至 2025-06-30
• 项目状态: 未结题
• 来源: https://reporter.nih.gov/project-details/10664822
• 关键词: Address; Adult; Advertising; African American; African American population; Alaska Native; American Indians; Behavior; Biological; Black Populations; Brain; Brain imaging; Cessation of life; Characteristics; Chronic; Chronic Obstructive Pulmonary Disease; Chronic stress; Cigarette; Clinical Trials; Crime; Data; Data Analyses; Data Set; Development; Diabetes Mellitus; Disadvantaged; Discrimination; Disease; Disparity; Elements; Emotions; Environmental Risk Factor; Ethnic Origin; Ethnic Population; Exposure to; Financial Hardship; Health; Heart Diseases; High Prevalence; Individual; Knowledge; Laboratories; Link; Literature; Lung diseases; Malignant Neoplasms; Measures; Mediating; Menthol; Neighborhoods; Neurobiology; Nicotine Withdrawal; Not Hispanic or Latino; Outcome; Pattern; Play; Poverty; Predictive Factor; Process; Race; Reporting; Research; Risk; Risk Factors; Role; Self Medication; Shapes; Smoke; Smoker; Smoking; Smoking Behavior; Smoking Cessation Intervention; Socioeconomic Status; Source; Stimulus; Stress; Stroke; Texas; Tobacco; Treatment Efficacy; Violence; Wisconsin; addiction; cigarette smoking; cognitive process; cue reactivity; design; effective intervention; environmental tobacco smoke exposure; ethnic difference; evidence base; experience; high risk; human old age (65+); improved; neighborhood disadvantage; neurobiological mechanism; nicotine use; non-smoker; positive emotional state; preventable death; programs; racial difference; racial disparity; racial population; racism; recruit; response; secondary analysis; smoking addiction; smoking cessation; smoking cue; smoking initiation; smoking intervention; smoking prevalence; smoking-related disease; social factors; stressor; success; theories; tool; treatment disparity

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.

吸烟是可预防死亡的主要原因，美国有 50 万人因吸烟而死亡。 然而，这一负担并不是平等承担的。例如，尽管非裔美国人 (AA) 吸烟率与非西班牙裔白人 (NHW) 相当，他们更有可能死亡 远离与吸烟有关的疾病。此外，AA 的戒烟率低于 NHW。 因此，AA 一生中更多地接触烟草烟雾，从而增加了风险 与烟草有关的疾病。治疗效果中种族差异的根本原因 尚未完全被理解，甚至在具有同等治疗的临床试验中也出现了。 我们目前了解吸烟是通过以下几种方式引发和维持的： 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 可能有助于制定更有效的戒烟干预措施。一个有前途的 神经生物学指标，提示反应性，与成瘾强度相关，并且已被证实 被证明可以预测戒烟。 然而，很少有研究探讨线索反应性的种族差异。因此，鲜为人知 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/族裔群体的成功。此外，没有线索反应性研究检验过 烟草差异的邻里级相关因素之间的关系（例如，邻里 贫困、犯罪）和线索反应。据推测，接触慢性病的居民 邻里压力源，包括不利、暴力和犯罪，利用尼古丁作为自我调节剂。 抗压力药物。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，而且吸烟率也更高 开始吸烟的可能性。因此，有可能长期长期接触 个人和社区层面的压力源非常普遍 在 AA 中，有助于塑造对吸烟相关刺激反应的种族模式。 使用从休斯顿招募的非裔美国人和非西班牙裔白人吸烟者的数据， 德克萨斯州和威斯康星州密尔沃基，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（考虑到薄荷香烟的不成比例的受欢迎程度） AA 中的薄荷香烟），以及邻里层面的压力源，包括邻里 贫困和犯罪，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/或修改提示反应水平的邻域级因素。