Postnatal Methylmercury Effects on Neurodevelopment
产后甲基汞对神经发育的影响
基本信息
- 批准号:9223392
- 负责人:
- 金额:$ 7.69万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2017
- 资助国家:美国
- 起止时间:2017-04-01 至 2019-03-31
- 项目状态:已结题
- 来源:
- 关键词:9 year oldAddressAdolescenceAdolescentAdultAffectAgeAge-YearsArchivesAttentionBrainChildChild DevelopmentChildhoodCognitiveConsumptionCross-Sectional StudiesDataDevelopmentDietDisease OutbreaksDoseEatingEnrollmentEpidemiologyEvaluationExposure toFemale of child bearing ageFishesGuidelinesHairHumanInfantIntakeIntelligenceJapanLifeMaternal ExposureMeasurementMeasuresMethylmercury CompoundsModelingMothersNatureNutritionalOutcomePoisoningPositioning AttributePregnancyPropertyProspective cohortPsychomotor PerformancePublic HealthRecruitment ActivityResearchRiskSafetySamplingSeychellesTimeUncertaintybasecognitive testingcohortdesignemerging adultepidemiology studyexecutive functionfetalfollow-upin uterolongitudinal analysismembermethylmercury exposureneurodevelopmentneurotoxicneurotoxicitypostnatalprenatalprenatal exposureretention rateyoung adult
项目摘要
Methylmercury (MeHg) exposure from fish consumption during childhood may adversely affect developmental
outcomes. The brain is not fully developed until halfway through the third decade of life and is therefore
potentially susceptible to MeHg exposure well beyond the fetal period. It is currently not known if it is safe for
children to eat fish. While epidemiological evidence supports the hypothesis that postnatal MeHg exposure is
adversely associated with children's development, studies have not been specifically designed to study
postnatal MeHg exposure. Nearly all studies have been cross-sectional evaluations in which MeHg exposure
was measured only at the time of cognitive testing (convenience samples). No studies have employed the
more definitive and powerful approach of longitudinal assessment of postnatal MeHg exposure in relation to
cognitive outcomes throughout childhood and adolescence. We are in a position to study this issue
longitudinally in the Republic of Seychelles where dietary MeHg exposure is among the highest in the world. In
1989-90 we enrolled a prospective cohort of 779 mother-infant pairs (“Main Cohort”). We have 24 years of
postnatal exposure and neurodevelopmental data in this cohort, which has been characterized more
extensively than any other cohort. In cross-sectional analyses we have found adverse associations between
recent postnatal MeHg exposure and various developmental endpoints at different ages, but especially with
measures of psychomotor and executive function, attention, and general intelligence at 9 years of age and
older. These cognitive domains have their greatest development postnatally and are therefore more likely to be
affected by postnatal MeHg exposure. These intriguing results need to be studied using longitudinal analyses
that better address the variability in postnatal exposure and its impact on neurodevelopment over time. The
aim of this proposed study is to examine the longitudinal associations of cumulative postnatal MeHg
exposure with neurodevelopment. We hypothesize that greater accumulated postnatal exposure is
adversely associated with neurodevelopmental outcomes in later childhood and adolescence. We will use a
previously-developed cumulative exposure metric based on repeated measurement of children's hair MeHg
values. So far, this metric has only been examined in relation to one developmental outcome at 9 years of age.
We now have an additional 15 years of exposure and developmental data on this cohort. We will leverage
these data and examine three cumulative postnatal exposure metrics (early life, late adolescent, and lifetime)
in relation to cognitive domains that have shown adverse associations in cross-sectional analyses. Longitudinal
models will evaluate the consistency of associations over time. Billions of people depend daily on the
nutritional properties of fish. It is therefore critical to examine whether children's exposure to MeHg from
consumption of fish is associated with adverse developmental consequences. This study will provide the most
comprehensive assessment to date of the risks or safety of fish consumption in childhood.
儿童期食用鱼类导致的甲基汞(MeHg)暴露可能对发育产生不利影响
结果。大脑直到生命的第三个十年的一半才完全发育,因此,
在胎儿期之后,可能对甲基汞暴露敏感。目前尚不清楚它是否安全。
孩子们吃鱼。流行病学证据支持产后接触甲基汞的假设,
与儿童的发展不利,研究没有专门设计研究
产后甲基汞暴露。几乎所有研究都是横断面评估,其中甲基汞暴露
仅在认知测试时测量(方便样本)。没有研究使用
更明确和有力的方法,纵向评估出生后甲基汞接触,
儿童期和青少年期的认知结果。我们有能力研究这个问题
在塞舌尔共和国,食物中的甲基汞暴露量是世界上最高的。在
1989- 1990年,我们招募了779对母婴的前瞻性队列(“主要队列”)。我们有24年的
该队列的出生后暴露和神经发育数据,
比其他任何群体都要多。在横截面分析中,我们发现
最近出生后的甲基汞暴露和不同年龄的各种发育终点,但特别是
9岁时的精神和执行功能、注意力和一般智力指标,
老了这些认知领域在出生后有最大的发展,因此更有可能是
受产后甲基汞暴露影响。这些有趣的结果需要用纵向分析来研究
更好地解决出生后暴露的变化及其对神经发育的影响。的
本研究的目的是探讨出生后累积甲基汞的纵向关联
暴露于神经发育。我们假设,更大的累积产后暴露是
与儿童后期和青春期的神经发育结果有不良关系。我们将使用一个
先前根据反复测量儿童头发甲基汞制定的累积接触度量
价值观到目前为止,这一指标仅在9岁时与一个发育结果相关。
我们现在有了这个队列额外的15年暴露和发育数据。我们将利用
这些数据,并检查三个累积的出生后暴露指标(早期生活,青少年后期,和终身)
与在横断面分析中显示出不利关联的认知领域有关。纵向
模型将评估关联随时间的一致性。数十亿人每天依赖于
鱼的营养价值。因此,至关重要的是要检查儿童接触甲基汞是否来自
食用鱼类与不利的发育后果有关。这项研究将提供最
对儿童食用鱼类的风险或安全性进行全面评估。
项目成果
期刊论文数量(0)
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科研奖励数量(0)
会议论文数量(0)
专利数量(0)
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Sally W Thurston其他文献
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{{ truncateString('Sally W Thurston', 18)}}的其他基金
BAYESIAN BIOMARKER MODELS FOR CANCER GENETICS STUDIES
用于癌症遗传学研究的贝叶斯生物标记模型
- 批准号:
6659844 - 财政年份:2002
- 资助金额:
$ 7.69万 - 项目类别:
BAYESIAN BIOMARKER MODELS FOR CANCER GENETICS STUDIES
用于癌症遗传学研究的贝叶斯生物标记模型
- 批准号:
6331506 - 财政年份:2002
- 资助金额:
$ 7.69万 - 项目类别:
BAYESIAN BIOMARKER MODELS FOR CANCER GENETICS STUDIES
用于癌症遗传学研究的贝叶斯生物标记模型
- 批准号:
6779205 - 财政年份:2002
- 资助金额:
$ 7.69万 - 项目类别:
BAYESIAN MEASUREMENT ERROR MODELS FOR EPIDEMIOLOGY
流行病学贝叶斯测量误差模型
- 批准号:
2909983 - 财政年份:1999
- 资助金额:
$ 7.69万 - 项目类别:
BAYESIAN MEASUREMENT ERROR MODELS FOR EPIDEMIOLOGY
流行病学贝叶斯测量误差模型
- 批准号:
2638407 - 财政年份:1998
- 资助金额:
$ 7.69万 - 项目类别:
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