Person:

Arora, Manish

Background: Periodontal disease is a complex, multifactorial, chronic inflammatory disease that involves degradation of periodontal structures, including alveolar bone. Cadmium adversely affects bone remodeling, and it is therefore possible that environmental Cd exposure may be a risk factor for periodontal-disease–related bone loss. Objective: We examined the relationship between environmental Cd exposure and periodontal disease in U.S. adults. Methods: We analyzed cross-sectional data from the third National Health and Nutrition Examination Survey (NHANES III). We defined periodontal disease as clinical attachment loss of at least 4 mm in > 10% of sites examined. We used multivariable-adjusted logistic regression analyses to estimate the association between creatinine-corrected urinary Cd levels and periodontal disease. Results: Of the 11,412 participants included in this study, 15.4% had periodontal disease. The age-adjusted geometric mean urine Cd concentration (micrograms per gram creatinine) was significantly higher among participants with periodontal disease [0.50; 95% confidence interval (CI), 0.45–0.56] than among those without periodontal disease (0.30; 95% CI, 0.28–0.31). Multivariable-adjusted analyses, which included extensive adjustments for tobacco exposure, showed that a 3-fold increase in creatinine-corrected urinary Cd concentrations [corresponding to an increment from the 25th (0.18 μg/g) to the 75th (0.63 μg/g) percentile] was associated with 54% greater odds of prevalent periodontal disease (odds ratio = 1.54; 95% CI, 1.26–1.87). We observed similar results among the subset of participants who had limited exposure to tobacco, but only after removing six influential observations. Conclusion: Environmental Cd exposure was associated with higher odds of periodontal disease.

Background: Although animal experiments have shown that cadmium exposure results in severe dental caries, limited epidemiologic data are available on this issue. Objectives: We aimed to examine the relationship between environmental cadmium exposure and dental caries in children 6–12 years of age. Methods: We analyzed cross-sectional data, including urine cadmium concentrations and counts of decayed or filled tooth surfaces, from the Third National Health and Nutrition Examination Survey. We used logistic and zero-inflated negative binomial (ZINB) regression to estimate the association between urine cadmium concentrations and caries experience, adjusting these analyses for potential confounders including environmental tobacco smoke (ETS). Results: Urine cadmium concentrations ranged from 0.01 to 3.38 ng/mL. Approximately 56% of children had experienced caries in their deciduous teeth, and almost 30% had been affected by caries in their permanent dentition. An interquartile range (IQR) increase in creatinine-corrected cadmium concentrations (0.21 μg/g creatinine) corresponded to a 16% increase in the odds of having experienced caries in deciduous teeth [prevalence odds ratio (OR) = 1.16; 95% confidence interval (CI), 0.96–1.40]. This association was statistically significant in children with low ETS exposure (prevalence OR = 1.30; 95% CI, 1.01–1.67). The results from the ZINB regression indicated that, among children with any caries history in their deciduous teeth, an IQR increase in cadmium was associated with 17% increase in the number of decayed or filled surfaces. We observed no association between cadmium and caries experience in permanent teeth. Conclusions: Environmental cadmium exposure may be associated with increased risk of dental caries in deciduous teeth of children.

Early life dietary transitions reflect fundamental aspects of primate evolution and are important determinants of health in contemporary human populations1,2. Weaning is critical to developmental and reproductive rates; early weaning can have detrimental health effects but enables shorter inter-birth intervals, which influences population growth3. Uncovering early life dietary history in fossils is hampered by the absence of prospectively-validated biomarkers that are not modified during fossilisation4. Here we show that major dietary shifts in early life manifest as compositional variations in dental tissues. Teeth from human children and captive macaques, with prospectively-recorded diet histories, demonstrate that barium (Ba) distributions accurately reflect dietary transitions from the introduction of mother’s milk and through the weaning process. We also document transitions in a Middle Palaeolithic juvenile Neanderthal, which shows a pattern of exclusive breastfeeding for seven months, followed by seven months of supplementation. After this point, Ba levels in enamel returned to baseline prenatal levels, suggesting an abrupt cessation of breastfeeding at 1.2 years of age. Integration of Ba spatial distributions and histological mapping of tooth formation enables novel studies of the evolution of human life history, dietary ontogeny in wild primates, and human health investigations through accurate reconstructions of breastfeeding history.

Background: Individuals previously exposed to lead remain at risk because of endogenous release of lead stored in their skeletal compartments. However, it is not known if long-term cumulative lead exposure is a risk factor for tooth loss. Objectives: We examined the association of bone lead concentrations with loss of natural teeth. Methods: We examined 333 men enrolled in the Veterans Affairs Normative Aging Study. We used a validated K-shell X-ray fluorescence (KXRF) method to measure lead concentrations in the tibial midshaft and patella. A dentist recorded the number of teeth remaining, and tooth loss was categorized as 0, 1–8 or ≥ 9 missing teeth. We used proportional odds models to estimate the association of bone lead biomarkers with tooth loss, adjusting for age, smoking, diabetes, and other putative confounders. Results: Participants with ≥ 9 missing teeth had significantly higher bone lead concentrations than those who had not experienced tooth loss. In multivariable-adjusted analyses, men in the highest tertile of tibia lead (> 23 μg/g) and patella lead (> 36 μg/g) had approximately three times the odds of having experienced an elevated degree of tooth loss (≥ 9 vs. 0–8 missing teeth or ≥ 1 vs. 0 missing teeth) as those in the lowest tertile [prevalence odds ratio (OR) = 3.03; 95% confidence interval (CI), 1.60–5.76 and OR = 2.41; 95% CI, 1.30–4.49, respectively]. Associations between bone lead biomarkers and tooth loss were similar in magnitude to the increased odds observed in participants who were current smokers. Conclusion: Long-term cumulative lead exposure is associated with increased odds of tooth loss.