A LONGITUDINAL STUDY OF LEAD EXPOSURE AND DENTAL CARIES

我们研究的长期目标是阐明物理和社会环境导致健康差异的潜在机制。我们以前的工作表明，铅暴露是龋齿风险因素的假设是合理的，并且可能对公共卫生产生重大影响，特别是对贫困环境中的个人（Watson等人，1997；Moss等人，1999）。我们将研究环境铅暴露导致的龋齿风险，研究对象为245名辛辛那提儿童，这些儿童自1979年底以来一直是辛辛那提铅队列研究的参与者。这项正在进行的针对15-16岁儿童的研究目前已进入资助的第三年（R01 ES08158，早期接触铅和青少年发展，p.i.: K. Dietrich）。这组非裔美国人和阿巴拉契亚白人儿童可以说是迄今为止关于产前和产后铅暴露（产前母亲血铅浓度，新生儿血铅浓度，从出生到5岁每季度评估一次血铅浓度，此后每半年评估一次）的研究中描述最详尽的纵向队列。这一队列在铅和儿童健康的主要纵向研究中是独一无二的，因为大量受试者在早期发育期间暴露于临床显著水平的铅。该队列的铅暴露峰值范围为5至80微克/分升以上。我们将收集与龋齿风险相关的额外数据，并对牙菌斑和牙釉质中的铅进行实验室微量分析评估。这将使我们能够测试一系列关于环境铅暴露与青少年龋齿发展风险相关的假设。该项目的工作将侧重于以下四个具体目标：1)证明环境铅暴露与龋齿风险之间的关联强度，并排除其他解释；2)利用微量分析技术评估恒牙釉质、乳牙釉质、乳牙本质和牙菌斑作为铅暴露生物标志物的效用；3)测试表明铅暴露a)降低唾液腺功能的机制假设；B)作为效果调节剂，降低唾液氟化物的保护作用；C)在牙釉质形成期间测量时，与龋齿的关系最为密切；4)通过检查铅、营养和社会因素的相互作用，更广泛地探索弱势群体口腔疾病差异的基础。

The long-term goal of our research is to elucidate underlying mechanisms by which the physical and social environments result in health disparities. Our previous work has shown that the hypothesis that lead exposure is a risk factor for dental caries is plausible and could have significant public health impact, especially for individuals in impoverished circumstances (Watson et al., 1997; Moss et al., 1999). We will study dental caries risk due to environmental lead exposure in a birth cohort of 245 Cincinnati children that have been participants in the Cincinnati Lead Cohort Study since late 1979. The on-going study of 15-16 year-olds is currently in its third year of funding (R01 ES08158, Early Exposure to Lead and Adolescent Development, P.I.: K. Dietrich). This group of African-American and white Appalachian children is arguably the most well-described longitudinal cohort ever studied for prenatal and postnatal lead exposure (prenatal maternal blood lead concentration, neonatal blood lead concentration, quarterly assessments of the concentration of lead in blood from birth to 5 years and semi-annually thereafter). This cohort is unique among the major longitudinal studies of lead and child health in that a substantial number of subjects were exposed to clinically significant levels of lead during early development. Peak lead exposure in this cohort ranges from 5 to over 80 micrograms/dL. We will collect additional data specifically related to dental caries risk and perform laboratory microanalytic assessments of lead in plaque and enamel. This will allow us to test a series of hypotheses that relate environmental lead exposure to risk for dental caries development in adolescents. The work of this project will focus on four specific aims related to 1) Demonstrating the strength of the association between environmental lead exposure and risk for dental caries and ruling out alternative explanations; 2) Assessing the utility of permanent tooth enamel, deciduous tooth enamel, deciduous tooth dentin and supragingival plaque as biomarkers for lead exposure using microanalytic techniques; 3) Testing mechanistic hypotheses that show lead exposure a) reduces salivary gland function; b) acts as an effect modifer to reduce the protective effect of salivary fluoride; c) is most strongly linked to caries when measured during enamel formation; 4) Exploring more broadly the basis for oral disease disparities in disadvantaged groups by examining the interplay of lead, nutrition, and social factors.