Lead toxicity is a major public health problem in the United States. Lead is accumulated in bone and as much as 95 percent of the body burden of lead is located within the skeleton. Processes which cause movement of calcium in and out of bone can be presumed to have the same effect on lead. Therefore, under physiologic conditions during which bone demineralization occurs, bone can become a secondary internal source of lead. Cross-sectional epidemiologic data from the second National Health and Nutrition Examination Survey (NHANES II) have shown significantly higher blood lead levels in postmenopausal women than in premenopausal women, suggesting that bone lead may be mobilized via osteoporosis bone loss in older women. To our knowledge, this has not been examined in with longitudinal study design. We will test the hypothesis that menopausal bone loss is associated with increased blood lead levels in women participating in the Healthy Women's Lifestyle Project (WHLP), a randomized clinical trial of weight and cholesterol reduction in 500 women. We will make measurements of blood lead levels and bone mineral density, on an annual basis as this cohort enters menopause. An epidemiologic analysis of data from this unique cohort will help answer important questions about bone lead release in older women.
Our specific aims are: 1) to test the hypothesis that as women enter menopause an inverse association develops between bone mass density and blood lead levels, such that as bone mass density decreases, blood lead levels increase; 2) to determine the association of blood lead levels in a population of peri-menopausal women, aged 44 to 55, with specific variables, such as age, diet, and reproductive and lifestyle factors, and 3) to test the hypothesis that over the course of menopause, an increase in blood lead levels is associated with a longitudinal change in blood pressure, greater than that expected from age alone as measured in matched controls. We propose to achieve these aims in a five-year prospective study. Significant findings consistent with our hypotheses will have implications for the role of bone-stored lead as a endogenous, secondary source of lead exposure, and a latent cause of age-related increase in blood pressure.
