Prenatal Low Level Tobacco & Phthalate Exposure & Childhood Respiratory Health

产前低浓度烟草

• 批准号: 8097393
• 负责人: ADAM J SPANIER
• 金额: $ 17.76万
• 依托单位: PENNSYLVANIA STATE UNIV HERSHEY MED CTR
• 依托单位国家: 美国
• 财政年份: 2008
• 资助国家: 美国
• 起止时间: 2008-07-01 至 2013-06-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8097393
• 关键词: Accounting; Affect; Allergic; Asthma; Biological Markers; Birth; Case-Control Studies; Child; Child health care; Childhood; Childhood Asthma; Clinic Visits; Clinical; Cosmetics; Cotinine; Data; Development; Disease; Dose; Dust; Enrollment; Environment; Environmental Epidemiology; Environmental Exposure; Environmental Health; Environmental Risk Factor; Epidemiology; Evaluation; Exhalation; Exposure to; Female of child bearing age; Fetus; Food Packaging; Funding; Growth and Development function; Hair; Health; Human Cell Line; IL8 gene; Individual; Infant; Infant Behavior; Interleukin-6; K-Series Research Career Programs; Knowledge; Lead; Life; Link; Lung diseases; Measures; Meconium; Medical; Mentors; Modeling; Molecular Epidemiology; Morbidity - disease rate; Mothers; Newborn Infant; Nicotine; Nitric Oxide; Outcome; Outcome Measure; Parents; Participant; Patient Self-Report; Pediatrics; Perinatal; Plastics; Pneumonia; Positioning Attribute; Pregnancy; Pregnant Women; Prevalence; Prevention; Relative (related person); Reporting; Research; Research Infrastructure; Research Personnel; Respiratory Tract Infections; Risk; Risk Factors; Role; Second Pregnancy Trimester; Serum; Smoke; Smoking; Source; Surveys; Symptoms; Techniques; Testing; Tobacco; Tobacco smoke; Toxic Environmental Substances; Toy; Training; United States National Institutes of Health; Urine; Wheezing; base; career; cohort; cytokine; early childhood; environmental toxicology; fetal tobacco exposure; improved; maternal serum; novel; patient oriented; phthalates; postnatal; prenatal; prenatal exposure; pulmonary function; rapid growth; respiratory; smoking prevalence

DESCRIPTION (provided by applicant) Asthma and respiratory infection pose major burdens to child health. Prenatal tobacco exposure is a key risk factor for wheeze in young children, but there is little data about the relationship of prenatal low level exposures to tobacco (e.g. passive exposure of nonsmoking pregnant women) with risk of childhood wheeze or respiratory infection. There is emerging, yet limited evidence for novel environmental risk factors for wheeze such as phthalates. Advances in biomarkers offer an ability to quantify indicators of internal dose directly, reduce exposure misclassification, and enhance our ability to link exposures with disease. The primary objective for this K23 proposal is to rigorously characterize the relationship of common environmental exposures with risk of wheeze and respiratory infection in early childhood using serial biomarkers of exposure. The specific aims are to: 1) Test which measure of prenatal tobacco smoke exposure (different biomarkers, parent-report) is most strongly associated with risk of wheeze, respiratory infection, and pulmonary inflammation (fraction of exhaled nitric oxide, FeNO) in the first three years of life; 2) Investigate the association of low levels of maternal passive tobacco smoke exposure during pregnancy with risk of wheeze, respiratory infection, and pulmonary inflammation (FeNO) in children of nonsmoking mothers in the first three years of life; and 3) Investigate the association of prenatal phthalate exposure with risk of wheeze, respiratory infection, and pulmonary inflammation in the first three years of life. This proposal is novel because it uses serial biomarkers to measure individual exposure burden and low levels of exposure objectively throughout pregnancy and early childhood. Additionally, we will be the first to explore the role of prenatal phthalate exposure with the risk of childhood wheeze, respiratory infection, and pulmonary inflammation using biomarkers. Through this K23, the applicant will develop expertise in pediatric environmental epidemiology to position him to help broaden the model of environmental toxicology and respiratory epidemiology in children. It will also provide the background and training needed to develop an independent research career in clinical pediatrics and enhance our understanding of how environmental risk factors affect the development and exacerbation of pediatric asthma and respiratory disease and integrate this knowledge into prevention and treatment efforts.

描述（由申请人提供） 哮喘和呼吸道感染是儿童健康的主要负担。产前烟草暴露是幼儿喘息的一个关键危险因素，但关于产前低水平烟草暴露（如非吸烟孕妇被动暴露）与儿童喘息或呼吸道感染风险之间关系的数据很少。有新的，但有限的证据表明，新的环境风险因素的喘息，如邻苯二甲酸酯。生物标志物的进步提供了直接量化内部剂量指标的能力，减少了暴露错误分类，并提高了我们将暴露与疾病联系起来的能力。K23建议的主要目的是使用暴露的系列生物标志物，严格描述常见环境暴露与儿童早期喘息和呼吸道感染风险之间的关系。具体目标是：1）产前烟草烟雾暴露的测量（不同的生物标志物，家长报告）与喘息、呼吸道感染和肺部炎症的风险最密切相关（呼出的一氧化氮分数，FeNO）在生命的前三年; 2）调查母亲在怀孕期间被动吸烟暴露水平低与喘息，呼吸道感染，和肺部炎症（FeNO）的非吸烟母亲的儿童在生命的前三年;和3）调查产前邻苯二甲酸酯暴露与喘息，呼吸道感染，和肺部炎症的风险在生命的前三年的关联。这一建议是新颖的，因为它使用一系列生物标志物来衡量个人的暴露负担和低水平的暴露客观整个怀孕和幼儿。此外，我们将是第一个使用生物标志物探索产前邻苯二甲酸酯暴露与儿童喘息，呼吸道感染和肺部炎症风险的作用。通过这个K23，申请人将发展儿科环境流行病学的专业知识，使他能够帮助扩大儿童环境毒理学和呼吸流行病学的模型。它还将提供发展临床儿科独立研究事业所需的背景和培训，并提高我们对环境风险因素如何影响儿童哮喘和呼吸系统疾病的发展和恶化的理解，并将这些知识融入预防和治疗工作中。