title: Influence of maternal lead ingestion on caries in rat pups.
abstract: Lead is one of the most toxic and pervasive pollutants in society, and although there has been some lowering of blood lead levels in recent years, the levels continue to be of concern for African Americans, central city residents, residents in the Northeast region of the United States, persons with low income, and those with low educational attainment. Notably, these are the persons and the region where the highest prevalence of dental caries is observed. Information relating lead toxicity to oral health is sparse, but the preponderance of epidemiological data shows a relation between lead in the environment and the prevalence of dental caries. Using our well-defined rat caries model we found that pre- and perinatal exposure to lead results in an almost 40% increase in the prevalence of caries and a decrease in stimulated parotid function of nearly 30%. Levels of lead in milk from lead-treated dams were approximately 10 times as high as the corresponding blood lead levels, suggesting that lead is being concentrated by mammary glands. These findings may help in part to explain the comparatively high levels of dental caries observed in the inner cities of the United States where exposure to lead is common. Environmental sources of lead include drinking water, lead-based paint and, to a lesser extent, automobile and industrial emissions. In humans lead is accumulated and stored in bones (half-life of approximately 62 years), and even maternal exposure to lead decades before pregnancy can subsequently result in exposure of the developing fetus to elevated levels of lead. Moreover, lead concentration in maternal blood has been shown to increase during pregnancy and lactation because of mobilization of stored lead from bone, and typically, lead is found in milk at a higher concentration than the level found in maternal plasma at the same time point.
authors.affiliation: Department of Clinical Dentistry, School of Medicine and Dentistry, University of Rochester, New York 14642, USA.
authors.forename: G E
authors.initials: GE
authors.lastname: Watson
authors.forename: B A
authors.initials: BA
authors.lastname: Davis
authors.forename: R F
authors.initials: RF
authors.lastname: Raubertas
authors.forename: S K
authors.initials: SK
authors.lastname: Pearson
authors.forename: W H
authors.initials: WH
authors.lastname: Bowen
mesh_terms: D000818:Animals; D003731:Dental Caries / Q000139:chemically induced*; D004785:Environmental Pollutants / Q000633:toxicity; D005260:Female; D006801:Humans; D007854:Lead / Q000097:blood / Q000493:pharmacokinetics / Q000633:toxicity*; D008431:Maternal-Fetal Exchange; D008892:Milk / Q000378:metabolism; D010306:Parotid Gland / Q000187:drug effects / Q000503:physiopathology; D011247:Pregnancy; D051381:Rats; D017207:Rats, Sprague-Dawley; D014481:United States; D014505:Urban Population
chemical_list: D004785:Environmental Pollutants; D007854:Lead