Residential Air Pollution and Preeclampsia
Residential Air Pollution and Preeclampsia
批准号:
8570629
负责人:
GREGORY A WELLENIUS
金额:
$26.78万
依托单位:
依托单位国家:
美国
项目类别:
财政年份:
2013
资助国家:
美国
项目状态:
已结题
起止时间:
2013-08-09 至 2015-07-31
关键词:
AddressAffectAir PollutionBirthCarbon BlackCase-Control StudiesClinicalCohort StudiesDataDiagnosisDiseaseEarly DiagnosisEpidemiologyEvaluationEventExposure toFetal GrowthFirst Pregnancy TrimesterGestational AgeHealthHospitalsHypertensionInfantLinkLow Birth Weight InfantMaternal ExposureMedical RecordsMethodsModelingMonitorMorbidity - disease rateMothersOutcomeParticulate MatterPatientsPlacentationPollutionPre-EclampsiaPregnancyPremature BirthPrenatal careProteinuriaPublic HealthPublishingRecording of previous eventsRecordsResolutionRhode IslandRiskSample SizeSeveritiesSourceSyndromeTimeWomanbasecardiovascular risk factorcase controlcohortfetalhigh riskimprovedmortalitynovelnovel strategiespopulation basedpublic health relevancetrafficking
中文摘要
描述(由申请人提供):子痫前期是一种以妊娠后半期新发高血压和蛋白尿为特征的疾病,影响3-8%的妊娠。它是孕产妇和胎儿发病和死亡的主要原因,分娩仍然是唯一已知的治疗方法。细颗粒物(PM2.5)空气污染与心血管疾病和死亡风险增加有关,交通污染被认为是一个关键来源。产妇暴露于空气污染也可能与胎儿生长缓慢、出生体重较低、早产和出生时胎龄小的风险较高有关。先兆子痫是早产和胎龄小的主要原因之一,因此可能是导致这些结果的早期事件。然而,很少有研究评估空气污染与子痫前期风险之间的关系。为了严格解决这一假设,我们提出了一种新的双管齐下的方法,包括:1)一项大型队列研究,基于2002年至2011年期间罗德岛妇幼医院88,000名单胎婴儿的详细行政和生命记录数据,其中包括出院诊断为先兆子痫的4,000名患者;2)在该队列中嵌套的一项大型病例对照研究(1000例/1000例对照),详细审查了从产前护理到分娩的医疗记录,首次获得以下数据:A)孕妇整个妊娠期间的居住史,b)子痫前期的临床特征和发病时间。在这两项研究中,我们将使用一种基于卫星和地面监测的新型高分辨率(1公里网格)时空模型来估计整个孕期居民对PM2.5的暴露,并通过扩展我们已验证的黑碳时空模型来估计居民对交通源污染的暴露。因此,拟议的项目结合了以往研究的最强特征,并提供了新的改进。鉴于无处不在的环境空气污染暴露、子痫前期的公共卫生重要性、初步的流行病学证据以及暴露与子痫前期之间联系的生物学合理性,这一假设值得进一步评估暴露、健康结果及其相互关系的改进方法。
英文摘要
DESCRIPTION (provided by applicant): Preeclampsia is a disease characterized by new onset of hypertension and proteinuria during the second half of pregnancy, affecting 3-8% of pregnancies. It is a leading cause of maternal and fetal morbidity and mortality, and delivery remains the only known treatment.!Fine particulate matter (PM2.5) air pollution has been persuasively linked to increased risk of cardiovascular morbidity and mortality, with pollution from traffic identified as a key source. Maternal exposure to air pollution may also be associated with slower fetal growth, lower birth weight, and higher risk of preterm birth and small size for gestational age at birth. Preeclampsia is one of the leading causes of preterm birth and small size for gestational age, and thus may be an early event leading to these outcomes. However, few studies have evaluated the association between air pollution and risk of preeclampsia. To rigorously address this hypothesis, we propose a novel two-pronged approach consisting of: 1) a large cohort study based on detailed administrative and vital records data on 88,000 singleton births between 2002 and 2011 at the Women and Infants Hospital of Rhode Island, including >4,000 patients with a discharge diagnosis of preeclampsia, and 2) a large, case-control study (1000 cases/1000 controls) nested within this cohort with detailed review of medical records from prenatal care to delivery to obtain, for the first time, data on: a) maternal residential histry throughout the pregnancy, and b) clinical features and timing of onset of preeclampsia. In both studies we will estimate residential exposure to PM2.5 throughout pregnancy using a novel, high-resolution (1 km grid) spatial-temporal model informed by both satellite and ground based monitoring, and residential exposure to pollution derived from traffic sources by extending our validated spatial-temporal model of black carbon. Thus, the proposed project combines the strongest features of previous studies and offers novel refinements. Given ubiquitous exposure to ambient air pollution, the public health importance of preeclampsia, suggestive preliminary epidemiologic evidence, and the biologic plausibility of a link between exposure and preeclampsia, this hypothesis warrants further evaluation with improved methods for assessing exposures, health outcomes, and their interrelationships.
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