Gene appears to alter lead's toxicity.

New data indicate that a mutant gene appears to modify the body's storage of lead -- thus changing what organs face the earliest risk of toxicity.

Because this gene, first described 8 years ago (SN: 2/21/87, p.123), occurs in perhaps 15 percent of U.S. whites but "is essentially nonexistent in African Americans," its effects "could have implications for environmental equity," points out Karl T. Kelsey of the Harvard School of Public Health in Boston, who directed the new study.

In most people, ALAD is the second in a series of enzymes that the body employs to create porphyrins, ring-shaped chemicals involved in the production of heme. Heme is the oxygen-carrying component of red blood cells. But some people carry an ALAD-2 gene producing a variant form of the enzyme, one that binds lead tightly.

Kelsey and his coworkers decided to investigate how the gene might affect storage of the bone-seeking heavy metal in 691 construction workers, most of them white men. In the March Environmental Health Perspectives, they report that workers with and without the variant gene had similarly low concentrations of lead in their blood (about 7.75 micrograms per deciliter).

However, individuals with the variant gene shunted proportionately more of their stored lead into the spongier trabecular bone (of kneecaps and vertebrae, for instance) than did those with the normal gene. This bone tends to mineralize, taking up and releasing its calcium -- and lead -- more readily than the denser cortical tissue that makes up shins and other long bones.

In addition, the kidneys of people with ALAD-2 appeared to suffer more stress than those of people with the normal gene. Kidney damage can be a symptom of lead toxicity.

Taken together with earlier studies by others, Kelsey says, his group's findings appear to indicate that in people with the variant gene, lead binds better in the red cells, causing individuals with high exposures (unlike the construction workers) to develop higher concentrations of lead in their blood. But the data also suggest that this tightly bound lead "is less bioavailable to the long bones, which is where long-term lead deposition usually occurs."

Moreover, he notes, a study investigating attention deficits in children exposed to lead, published last year, hints that the ALAD-2 gene may help keep lead from the brain, where it can diminish IQ and neurological function.

Kelsey now plans to study the gene's effect on lead transfer from mothers to nursing babies.