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James R. Campbell,¹ Randy N. Rosier,² Leonore Novotny,² and J. Edward Puzas²

¹Department of Pediatrics and ²Department of Orthopedics, University of Rochester Medical Center, Rochester, New York, USA

Abstract
Osteoporosis is a decrease in bone mineral density (BMD) that predisposes individuals to fractures. Although an elderly affliction, a predisposition may develop during adolescence if a sufficient peak BMD is not achieved. Rat studies have found that lead exposure is associated with decreased BMD. However, human studies are limited. We hypothesized that the BMD of children with high lead exposure would be lower than the BMD of children with low lead exposure. We collected data on 35 subjects ; 16 had low cumulative lead exposure (mean, 6.5 µg/dL) , and 19 had high exposure (mean, 23.6 µg/dL) . All were African American ; there was no difference between the groups by sex, age, body mass index, socioeconomic status, physical activity, or calcium intake. Significant differences in BMD between low and high cumulative lead exposure were noted in the head (1.589 vs. 1.721 g/cm²) , third lumbar vertebra (0.761 vs. 0.819 g/cm²) , and fourth lumbar vertebra (0.712 vs. 0.789 g/cm²) . Contrary to our hypothesis, subjects with high lead exposure had a significantly higher BMD than did subjects with low lead exposure. This may reflect a true phenomenon because lead exposure has been reported to accelerate bony maturation by inhibiting the effects of parathyroid hormone-related peptide. Accelerated maturation of bone may ultimately result in a lower peak BMD being achieved in young adulthood, thus predisposing to osteoporosis in later life. Future studies need to investigate this proposed model. Key words: blood lead levels, bone mineral density, dual-energy X-ray absorptiometry, parathyroid hormone-related peptide. Environ Health Perspect 112:1200-1203 (2004) . doi:10.1289/ehp.6555 available via http://dx.doi.org/ [Online 7 April 2004]

Address correspondence to J.R. Campbell, Department of Pediatrics, MOB Suite 300, Rochester General Hospital, 1425 Portland Ave., Rochester, NY 14621 USA. Telephone: (585) 922-3919. Fax: (585) 922-3929. E-mail: James.Campbell@ViaHealth.org

We thank C. Muzytchuk for conducting the bone density measures, and R. O'Keefe, M. Zuscik, and S. Schaffer for their thoughtful commentary on the manuscript.

This work was supported by University of Rochester Environmental Health Sciences Center grants NIEHS P30 ES01247 and NIEHS PO1 ES011854.

The authors declare they have no competing financial interests.

Received 30 June 2003 ; accepted 7 April 2004.