Effects of Early Life Exposure to Household Air Pollution on DNA Methylation and Respiratory Disease in Guatemalan Children from the Household Air Pollution Intervention Network (HAPIN) Trial

根据家庭空气污染干预网络 (HAPIN) 试验,生命早期接触家庭空气污染对危地马拉儿童 DNA 甲基化和呼吸道疾病的影响

基本信息

  • 批准号:
    10660568
  • 负责人:
  • 金额:
    $ 67.64万
  • 依托单位:
  • 依托单位国家:
    美国
  • 项目类别:
  • 财政年份:
    2023
  • 资助国家:
    美国
  • 起止时间:
    2023-05-15 至 2028-04-30
  • 项目状态:
    未结题

项目摘要

PROJECT SUMMARY Household air pollution (HAP) from solid fuel use causes an estimated 400,000 chronic obstructive pulmonary (COPD) deaths each year. Although lung function and lower respiratory disease in childhood are determinants of COPD risk later in life, there are few studies of the influence of early life HAP exposure on respiratory health later in childhood. We propose a HAP study design that is sensitive to emerging chronic respiratory effects by incorporating three key features: 1) assessment of exposure during early life windows of susceptibility, 2) a strong exposure contrast introduced by a randomized intervention, and 3) sensitive endpoints that predict chronic disease later in life. Gestation and infancy are critical windows of susceptibility due to the rapid lung development. Previous HAP intervention trials had only low to moderate effectiveness for reducing HAP exposure. The Household Air Pollution Intervention Network (HAPIN) trial (2017-2021) offers a time-sensitive, unique research opportunity because the liquefied petroleum gas (LPG) stove and fuel intervention lowered median gestational fine particulate matter (PM2.5) exposure in Guatemalan participants by 77%, from 98 to 23 µg/m3. The intervention continued until age 1 year and extensive health data were collected, including pneumonia incidence and severity. We have maintained follow-up of the cohort post-intervention, assessing HAP exposure and child growth at age 2 years plus lung function at age 3 years. We posit that childhood lung function and lower respiratory disease episodes are sensitive indicators of HAP health effects that relate to adulthood COPD. DNA methylation (DNAm) and pneumonia during infancy may influence these respiratory endpoints later in childhood. We propose to leverage our successful LPG cooking intervention in Guatemala to investigate effects of early life HAP exposure on longer-term respiratory health and explore DNAm as a biomarker. We hypothesize that the randomized LPG cooking intervention and lower PM2.5 and black carbon (BC) exposure will be associated with DNAm at age 1 year and greater lung function and fewer lower respiratory disease episodes at age 4-7 years. Aim 1. Estimate effects of a randomized LPG cooking intervention during gestation and infancy (age <1 year) (Aim 1.A) and HAP exposure (PM2.5 and BC) during and after the intervention (Aim1.B) on lung function trajectories (age 3-7 years) and lower respiratory disease incidence (ages of 4 to 7 years). Aim 2. Estimate effects of a randomized LPG cooking intervention (Aim 2.A) and HAP exposure (Aim 2.B) during gestation and early infancy (age <1 year) on DNAm biomarkers at the end of the intervention period (age 1 year). Aim 3. Determine whether DNAm at age 1 year (Aim3.A) and pneumonia episodes until age 1 year (Aim 3.B) are associated with lung function trajectories and lower respiratory disease incidence between ages of 3 to 7 years. Effects of early life HAP on lung function and lower respiratory disease later in childhood would have important implications for the early life origins of COPD in populations exposed to HAP, and identifying epigenetic changes that might underpin this relationship could lead to improved research and interventions.
项目摘要 来自固体燃料使用的家庭空气污染(HAP)导致约40万慢性阻塞性肺疾病患者。 每年的COPD死亡人数。虽然儿童期的肺功能和下呼吸道疾病是 COPD风险在以后的生活中,很少有研究表明早期生活中HAP暴露对以后呼吸健康的影响 在童年。我们提出了一个HAP研究设计,该设计对新出现的慢性呼吸影响敏感, 包括三个关键特征:1)评估早期生命敏感期内的接触情况,2) 随机干预引入的暴露对比,以及3)预测慢性 病后的生活由于肺的快速发育,妊娠期和婴儿期是易感性的关键窗口期。 以前的HAP干预试验对于减少HAP暴露只有低到中等的有效性。的 家庭空气污染干预网络(HAPIN)试验(2017-2021)提供了一个时间敏感,独特的研究 机会,因为液化石油气(LPG)炉灶和燃料干预降低了中位妊娠期 危地马拉参与者的细颗粒物(PM2.5)暴露量降低了77%,从98微克/立方米降至23微克/立方米。干预 持续到1岁,并收集了广泛的健康数据,包括肺炎的发病率和严重程度。 我们对干预后的队列进行了随访,评估了HAP暴露和2岁儿童的生长情况 3岁时的肺功能。我们认为,儿童肺功能和下呼吸道疾病 发作是与成年期COPD相关的HAP健康影响的敏感指标。DNA甲基化(DNAm) 婴儿期的肺炎可能影响儿童期以后的这些呼吸终点。我们建议 利用我们在危地马拉成功的液化石油气烹饪干预措施,调查生命早期HAP暴露的影响 长期的呼吸系统健康,并探索DNAm作为生物标志物。我们假设随机LPG 烹饪干预和较低的PM2.5和黑碳(BC)暴露将与1岁时的DNAm相关 4-7岁时肺功能更好,下呼吸道疾病发作更少。目标1.估计影响 在妊娠期和婴儿期(年龄<1岁)随机液化石油气烹饪干预(目标1.A)和HAP 干预期间和干预后(目标1.B)暴露(PM2.5和BC)对肺功能轨迹的影响(3-7岁) 和下呼吸道疾病发病率(4至7岁)。目标二。估计随机化LPG的影响 烹饪干预(目标2.A)和妊娠期和婴儿早期(年龄<1岁)的HAP暴露(目标2.B) 在干预期结束时(1岁)对DNAm生物标志物的影响。目标3.确定年龄时是否有DNA m 1岁(Aim 3.A)和1岁之前的肺炎发作(Aim 3.B)与肺功能相关 3至7岁儿童的发病率和下呼吸道疾病发病率。生命早期HAP对 肺功能和下呼吸道疾病在童年后期将有重要的影响, COPD在暴露于HAP人群中的起源,并确定可能支持这一点的表观遗传变化 这种关系可能会导致研究和干预措施的改进。

项目成果

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John Patrick Mccracken其他文献

John Patrick Mccracken的其他文献

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