For decades, scientists have known that the human skeleton is a repository for lead in people who were exposed to high levels of this environmental toxin in their childhood, but thought this storage to be benign. Recently, a growing body of research is showing that the opposite is true, and that lead in bone actually sets off a bizarre chain reaction, first accelerating bone growth, and then eventually limiting it so that a high peak bone mass is not achieved. Preventing a high peak bone mass will predispose a young person to osteoporosis later in life.
Now, researchers in the Center for Musculoskeletal Research at the University of Rochester Medical Center are set to embark on the next phase of a four-year, $5 million research project funded by the National Institute of Environmental Health Sciences with a clinical study aimed at better understanding the deceptive role lead initially plays in bone development, growth and loss and how this all might lead to earlier onset of osteoporosis in those exposed to high levels of lead as a child.
A metabolic bone disease that predominantly occurs in women, osteoporosis affects one in three American women over the age of 65. It is characterized by low bone mass that eventually leads to fractures, mostly of the hip and vertebrae. These fractures can be life-threatening; experts say that more women die each year from hip fracture complications than from cancer of the ovaries, cervix and uterus combined. Close t
Contact: Germaine Reinhardt
University of Rochester Medical Center