Blood lead level and dental caries in school-age children

Environmental Health Perspectives, Oct, 2002 by Allison Gemmel, Mary Tavares, Susan Alperin, Jennifer Soncini, David Daniel, Julie Dunn, Sybil Crawford, Norman Braveman, Thomas W. Clarkson, Sonja McKinlay, David C. Bellinger

The association between blood lead level and dental caries was evaluated in cross-sectional analyses of baseline data for 543 children 6-10 years old screened for enrollment in the Children's Amalgam Trial, a study designed to assess potential health effects of mercury in silver fillings. Approximately half of the children were recruited from an urban setting (Boston/Cambridge, MA, USA) and approximately half from a rural setting (Farmington, ME, USA). Mean blood lead level was significantly greater among the urban subgroup, as was the mean number of carious tooth surfaces. Blood lead level was positively associated with number of caries among urban children, even with adjustment for demographic and maternal factors and child dental practices. This association was stronger in primary than in permanent dentition and stronger for occlusal, lingual, and buccal tooth surfaces than for mesial or distal surfaces. In general, blood lead was not associated with caries in the rural subgroup. The difference between the strength of the associations in the urban and rural settings might reflect the presence of residual confounding in the former setting, the presence of greater variability in the latter setting in terms of important caries risk factors (e.g., fluoride exposure), or greater exposure misclassification in the rural setting. These findings add to the evidence supporting a weak association between children's lead exposure and caries prevalence. A biologic mechanism for lead cariogenicity has not been identified, however. Our data are also consistent with residual confounding by factors associated with both elevated lead exposure and dental caries. Key words: blood lead, dental caries, epidemiology, tooth, toxicology. Environ Health Perspect 110:A625-A630 (2002). [Online 16 September 2002] http://ehpnet1.niehs.nih.gov/docs/2002/110pA625-A630gemmel/abstract.html

More than 40% of children develop caries in primary dentition by 6 years of age, and more than 85% develop caries in the permanent dentition by age 17 (Kaste et al. 1996). Despite a reduction in the prevalence of caries in the permanent dentition, the prevalence in the primary dentition has remained essentially unchanged, particularly among low-income children (Caufield and Griffen 2000). Caries is regarded as an infectious disease, the result of a multifactorial process involving three elements: particular oral microflora and dietary exposures as well as a susceptible host (Schafer and Adair 2000). Although Mutans streptococci are the critical cariogenic bacteria in the oral cavity, and fermentable carbohydrates (e.g., refined sugars) the critical dietary factor, the determinants of variability in host susceptibility are less certain. Structurally sound enamel and adequate salivary flow and composition are clearly important (Schafer and Adair 2000). Several sociodemographic correlates of increased risk have been identified as risk factors for both caries incidence and treatment, including living in poverty and being African American or Mexican American. These are presumably surrogate markers for key health-related behaviors, environmental exposures, and access to medical care (Kaste et al. 1996; Vargas et al. 1998).

The epidemiology of dental caries in children overlaps considerably with the epidemiology of lead poisoning, which is primarily a disease of inner-city poor children (Brody et al. 1994). Pediatric lead poisoning is associated with an increased risk of adverse effects in a variety of target organs, with the central nervous, hematopoietic, and renal systems receiving the greatest attention [National Research Council 1993; U.S. Centers for Disease Control and Prevention (CDC) 1991]. Because lead is a divalent cation, its metabolism is affected by the same factors that affect calcium metabolism, and lead's tendency to "follow the calcium stream" was recognized decades ago (Aub et al. 1925). Mineralized tissues are thus longterm storage sites for lead (Drasch et al. 1987; Drasch and Ott 1988). Because deciduous teeth provide a readily accessible bone biopsy, the concentrations of lead in the whole primary teeth, the enamel, or the dentin (particularly circumpulpal) have served as proxy measures for skeletal lead, and thus for total body lead burden, in epidemiologic studies of childhood lead toxicity (Needleman et al. 1979; Rabinowitz et al. 1991; Smith et al. 1983; Winneke et al. 1983).

Bone is not simply a physiologic "sink" for lead, however, and might itself be a target organ for lead toxicity, although little is known about either the form that this toxicity might take or its mechanism (Pounds et al. 1991). Some findings are consistent with an adverse effect of lead on odontoblast function (Appleton 1991). The risk of hypoplastic enamel defects (i.e., defective matrix formation) in primary teeth is increased among children who were never screened for lead poisoning (Needleman et al. 1992), and higher postnatal lead exposure is associated with pitting hypoplasia of permanent teeth (Lawson et al. 1971). In the rat, increased maternal lead exposure produces a decrease in stimulated parotid function, suggesting salivary hypofunction, and a concomitant increase in dental caries in offspring (Watson et al. 1997). An association between increased lead levels and increased caries prevalence has been reported in several epidemiologic studies (Brudevold et al. 1977; Gil et al. 1994, 1996; Moss et al. 1999). In a study of 251 children 9-12 years old, Brudevold et al. (1977) found that children with higher levels of enamel lead had more caries than did children with lower enamel lead levels. Among 25,000 participants in the Third National Health and Nutrition Examination Survey (NHANES III), an association was reported between blood lead level and the risk of carious lesions in teeth (Moss et al. 1999). Among children (5-17 years old), an increase of 5 [micro]g/dL in blood lead level was associated with nearly a doubling of the risk of dental caries, and the population-attributable risk associated with blood lead levels in the middle tertile of the distribution was nearly 10%. In a study of 248 school-age children, having a blood lead level greater than 10 [micro]g/dL, measured between 18 and 37 months of age, was modestly associated with an increased risk of caries, but overall the data failed to support any of the hypotheses regarding possible mechanisms of lead cariogenicity (Campbell et al. 2000). In the analyses reported by both Campbell et al. (2000) and Moss et al. (1999), adjustments were made for a variety of potentially confounding factors, including socioeconomic status, ethnicity, and geographic region.