Air Pollution and the Lung in Health and COPD: Obstructive, Restrictive and Vascular Pathways

空气污染与健康和慢性阻塞性肺病中的肺部：阻塞性、限制性和血管通路

• 批准号: 9012513
• 负责人: Mary B Rice
• 金额: $ 17.67万
• 依托单位: BETH ISRAEL DEACONESS MEDICAL CENTER
• 依托单位国家: 美国
• 财政年份: 2016
• 资助国家: 美国
• 起止时间: 2016-03-01 至 2021-02-28
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/9012513
• 关键词: Acute; Address; Admission activity; Adult; Aerosols; Affect; Air; Air Pollutants; Air Pollution; American; Area; Autopsy; Award; Behavior Therapy; Biometry; Biopsy; Blood Vessels; Boston; Caliber; Cardiac; Chest; Chronic; Chronic Obstructive Airway Disease; Chronic lung disease; Cicatrix; Clinical; Clinical Research; Clinical Sciences; Critical Care; Data; Development; Development Plans; Disease; Environment; Environmental Epidemiology; Environmental Exposure; Epidemic; Epidemiologist; Epidemiology; Exposure to; Fellowship; Forced expiratory volume function; Fossil Fuels; Framingham Heart Study; Future; General Population; Goals; Health; Home environment; Hospitals; Image; Image Analysis; Israel; Journals; Lung; Lung diseases; Measurable; Measurement; Measures; Medical center; Medicine; Mentors; Mentorship; Modeling; Monitor; Morphology; Nitrogen Dioxide; Obstructive Lung Diseases; Optics; Ozone; Participant; Particulate Matter; Pathway interactions; Patients; Pattern; Peak Expiratory Flow Rate; Peripheral; Physicians; Play; Pollution; Population; Predisposition; Prospective Studies; Public Health Education; Public Health Schools; Publications; Pulmonary Emphysema; Pulmonary Function Test/Forced Expiratory Volume 1; Pulmonary Mass; Pulmonary vessels; Questionnaires; Recruitment Activity; Research; Research Personnel; Resources; Respiratory Signs and Symptoms; Respiratory physiology; Rice; Risk; Risk Factors; Role; Sampling; Scanning; Severities; Site; Smoker; Smoking; Spirometry; Staging; Structural defect; Structure; Symptoms; Testing; Thick; Tobacco smoke; Total Lung Capacity; Training; Translating; Translational Research; United States Environmental Protection Agency; Vascular Diseases; Vascular remodeling; Ventricular; Vital capacity; Woman; Work; X-Ray Computed Tomography; alveolar destruction; ambient air pollution; attenuation; base; career; career development; catalyst; cohort; constriction; exercise capacity; experience; extrastriate visual cortex; interstitial; light weight; lung volume; medical schools; mortality; multidisciplinary; novel; particle; pollutant; population based; prevent; professor; public health relevance; quantitative imaging; respiratory; skills; tool; trafficking

 DESCRIPTION (provided by applicant): Dr. Mary Rice is a pulmonologist whose long-term career goal is to become an independent translational investigator focused on understanding how environmental exposures affect the development and progression of chronic lung disease. Her research efforts have focused on the study of short- and long-term exposure to ambient air pollution and lung function in the Framingham Heart Study. In this population-based study of adults, she has found that previous-day air pollution exposure within current standards is associated with lower lung function, and long-term pollution exposure is associated with accelerated lung function decline. Her research has resulted in a first place award in a national pulmonary fellows' research competition and two first author publications in the American Journal of Respiratory and Critical Care Medicine. Dr. Rice proposes new research that will move the field forward, and build on these findings and the skills she acquired during her Master's in Public Health training, to understand how pollution at these concentrations may affect the development and progression of chronic lung disease. Her immediate career objectives are (1) to obtain formal and applied training in environmental epidemiology, biostatistics, and the use of quantitative chest CT analysis in research, and (2) to gain practical skills in building a cohort with chronic obstructive pulmonary disease (COPD), and assessing pollution exposure, respiratory symptoms and lung function in this population. Environment: With the guidance of her co-mentors, Drs. Murray Mittleman and George Washko, Dr. Rice has formulated a comprehensive career development plan to accomplish these goals. Dr. Mittleman MD DrPH, Harvard Professor of Epidemiology at Beth Israel Deaconess Medical Center (BIDMC) and the Harvard School of Public Health (HSPH), will serve as Dr. Rice's primary mentor, as he has for nearly 3 years during her research fellowship. Dr. Mittleman is a renowned physician epidemiologist with expertise in the study of acute and chronic effects of pollution exposure. He has a long track record of mentoring trainees to independence and has won awards for his mentorship role. Dr. Washko, the proposed co-mentor, is a pulmonologist and Director of the Chest Imaging Lab at Brigham and Women's Hospital, and Associate Director of the Framingham Heart Study Pulmonary Research Center. He is a pioneer in the use of quantitative imaging analysis in the study of chronic obstructive pulmonary disease (COPD). Dr. Rice will be based within the Division of Pulmonary and Critical Care at BIDMC, which is deeply committed to promoting her as a future leader in translational research focused on understanding the environmental origins of chronic lung disease, and COPD in particular. Dr. Rice will be supported by the Harvard Catalyst Clinical and Translational Science Award, which will provide research space and resources at the BIDMC Clinical Research Center for her new study of the respiratory effects of pollution exposure in people with COPD. This study will provide data for a future R01 proposal. Additionally, the proposed career development plan will take advantage of advanced classes and seminars at HSPH and Harvard Medical School, and a multidisciplinary advisory board with world-class expertise in air pollution exposure assessment, respiratory epidemiology and environmental biostatistics. Research: In her first two aims, Dr. Rice proposes analyses of long-term exposure to traffic and fine particulate matter, estimated by a sophisticated model using satellite-based estimates of particle abundance in the atmospheric column, and (1) measures of emphysema, airway thickness, lung volumes and interstitial lung abnormalities, and (2) measures of pulmonary vascular morphology on chest CT in the Framingham Heart Study. This work builds on her prior work in this cohort to determine if long-term pollution exposure contributes to obstructive lung disease (with alveolar destruction and airway thickening), restrictive lung disease (with parenchymal scarring that stiffens and shrinks the lung), and/or pulmonary vascular disease (with constriction or pruning of the peripheral vasculature). Prior studies of lung function indicate that long-term air pollution exposure may cause obstructive and restrictive effects, and limited evidence suggests pollution may increase right ventricular afterload and mass, possibly a result of pulmonary vascular change. Dr. Rice hypothesizes that years of exposure to traffic-related pollution, like tobacco smoke, contributes to emphysema, airway thickening, interstitial abnormalities, and a lower volume of small caliber peripheral pulmonary vessels. In her third aim, Dr. Rice proposes a new prospective study of people with COPD (n=30) to test associations between daily exposure to ambient air pollutants measured by central site in Boston and also by a novel, light-weight personal monitor, and daily measurements of respiratory symptoms and lung function at home, using state-of-the art spirometry tools. Although studies using administrative data have found that day-to-day increases in outdoor pollution levels are associated with increased risk of COPD admissions and respiratory mortality, little is known about how air pollution at today's levels affects lung function and symptoms in people with COPD, for whom even modest changes in lung function may have clinical importance. This research will advance understanding of how exposure to pollution at relatively low levels affects lung structure in the general population, and lung function and symptoms in people with COPD. Findings may inform air quality standards to protect the public and susceptible populations. Data on personal pollution exposure in COPD may ultimately translate to behavioral interventions to prevent COPD exacerbations.

 描述（由应用程序提供）：玛丽·赖斯（Mary Rice）博士是一名脉动女人，其长期职业目标是成为一名专注于了解环境暴露如何影响慢性肺病的发展和发展的独立翻译调查员。她的研究工作集中在弗雷明汉心脏研究中的短期和长期暴露于环境空气污染和肺功能的研究上。在这项基于人群的成年人研究中，她发现，在当前标准范围内，前一天的空气污染暴露与较低的肺功能有关，并且长期污染暴露与加速肺功能下降有关。她的研究在全国肺研究员的研究竞赛中获得了第一名，并在《美国呼吸道和重症监护医学杂志》上获得了两位第一作者出版物。赖斯博士提出的新研究将推动该领域的前进，并以这些发现以及她在公共卫生培训的硕士学位中获得的技能为基础，以了解这些浓度下的污染如何影响慢性肺部疾病的发展和发展。她的直接职业目标是（1）获得环境流行病学，生物统计学以及在研究中使用定量胸部分析的正式和应用培训，以及（2）获得实用 与慢性阻塞性肺疾病（COPD）建立队列的技能，并评估该人群中污染暴露，呼吸道症状和肺功能。环境：在她的联合官员的指导下。赖斯博士Murray Mittleman和George Washko制定了一项全面的职业发展计划，以实现这些目标。贝丝以色列执事医学中心（BIDMC）和哈佛大学公共卫生学院（HSPH）的哈佛流行病学教授Mittleman Md Drph博士将担任赖斯博士的主要导师，因为他在研究奖学金期间拥有将近3年的赖斯。 Mittleman博士是一位著名的身体流行病学家，在研究污染暴露的急性和慢性影响方面具有专业知识。他拥有精神学员的悠久记录，并因其精神训练而赢得了奖项。拟议的院长Washko博士是Brigham and妇女医院的肺科医生兼胸部成像实验室主任，也是Framingham心脏研究肺部研究中心的副主任。他是在慢性阻塞性肺疾病（COPD）研究中使用定量成像分析的先驱。 Rice博士将基于BIDMC的肺部和重症监护措施，该公司致力于促进她作为未来的翻译研究领导者，专注于理解慢性肺部疾病的环境起源，尤其是COPD。赖斯博士将获得哈佛大学催化剂临床和转化科学奖的支持，该奖项将在BIDMC临床研究中心提供研究空间和资源，以了解她对COPD污染暴露的呼吸影响的新研究。这项研究将为未来的R01提案提供数据。此外，拟议的职业发展计划将利用HSPH和Harvard医学院的高级课程和半小伙子，以及具有世界一流的空气污染暴露评估，呼吸流行病学和环境生物统计学方面的世界一流专业知识的多学科顾问委员会。研究：在她的前两个目标中，赖斯博士提出了长期暴露于交通和特定问题的分析，这是通过复杂的模型使用基于卫星的大气柱中颗粒丰度的估计来估算的，以及（1）肺气肿，气道厚度，气道厚度，肺部和肺部肺部的肺部和（2）骨骼的孔子孔的衡量。 学习。这项工作是基于她在这一队列中的先前工作的基础，以确定长期污染的暴露是否有助于阻塞性肺部疾病（肺泡破坏和气道增厚），限制性肺部疾病（具有实质性疤痕会使肺部僵硬并缩小肺部），以及/或肺部血管疾病（肺部疾病（伴有肺癌）（伴有或肿块或普罗尼）。先前对肺功能的研究表明，长期空气污染暴露可能会导致阻塞性和限制性作用，并且有限的证据表明污染可能会增加右心后载荷和质量，这可能是肺血管变化的结果。赖斯博士假设多年暴露于交通相关的污染（例如烟草烟雾）会导致肺气肿，气道增厚，间隙异常和较低体积的小口径外周血肺动脉尿。在她的第三个目标中，赖斯博士提出了对COPD患者（n = 30）的新的前瞻性研究，以测试每天接触波士顿中央现场测量的环境空气污染物，以及通过使用现有的艺术模拟工具，通过新颖的，轻量级的个人监测仪和每日测量呼吸道症状和肺部功能的测量。尽管使用行政数据的研究发现，室外污染水平的日常增加与COPD入院和呼吸道死亡率的增加有关，但对于当今水平的空气污染如何影响COPD的患者的肺功能和症状，即使对肺功能的适度变化也可能具有临床重要性。这项研究将进一步了解相对较低水平的污染如何影响普通人群的肺结构，以及COPD患者的肺功能和症状。调查结果可能会为空气质量标准提供信息，以保护公众和易感人群。 COPD中个人污染暴露的数据最终可能转化为行为干预措施，以防止COPD加剧。