Lead exposure during adulthood may cause persistent deficits in certain forms of learning and memory, according to a new study from the University of Washington School of Public Health.

The study exposed male mice to lead for three months during late adolescence and adulthood, and researchers found that the lead-exposed mice exhibited impairments in their ability to record information about their environment and spatial orientation. Sub-chronic exposure refers to having multiple or continuous exposures lasting for about 10 percent of an organism’s lifetime.

“There are many people in the U.S. who were, through lead contamination in the environment or the workplace, exposed to higher levels of lead throughout their life,” said Anna Engstrom, a toxicologist who conducted the study as a graduate student in the School’s Department of Environmental and Occupational Health Sciences. “However, we do not fully understand the contribution of these long-term exposures to cognitive decline or neurodegeneration.”

Study findings, published online Sept. 29 in Neuroscience Letters, showed that sub-chronic exposure to lead is sufficient to impair key processes in adult neurogenesis — a unique process that generates new neurons throughout adulthood — in the hippocampus of the brain. Previous studies have shown that disturbances in this process may cause deficits in certain forms of learning and memory, accelerate cognitive decline and contribute to the development of Alzheimer’s disease.

Engstrom and Zhengui Xia, professor of environmental and occupational health sciences at the School of Public Health, exposed mice to either normal drinking water or to drinking water with 0.2 percent lead acetate, beginning at 6 weeks of age. After 12 weeks of lead exposure, the animals were switched to normal drinking water for the remaining duration of the study.

In an open field test, mice were allowed to freely explore an arena for 20 minutes and their vertical and horizontal movements were recorded. The researchers did not observe any signs that lead exposure caused deficits in locomotor activity or in anxiety. However, lead did cause a slight, but significant, increase in hyperactivity.

In another test, researchers placed each mouse into the open arena with two objects for five minutes, then returned them to their cage for an hour. Researchers moved one of the two objects and later placed the mice back into the arena. The amount of time each mouse spent investigating the object in a new location was compared to the amount of time the animal spent investigating the object in a familiar location, as an indicator of short-term spatial memory.

Mice exposed to normal drinking water spent significantly more time exploring the new object location, indicating that the mice remembered where the original object had been placed. However, mice exposed to lead spent a similar amount of time exploring both the new and familiar object locations, suggesting these mice had impaired spatial short-term memory.

Additionally, researchers observed a significant decrease in the total number of adult-born mature neurons in lead-exposed mice. “While lead inhibition of adult cell proliferation may be reversible after exposure stops, lead impairment of neuronal differentiation may persist after the cessation of lead exposure,” the study authors wrote.

These findings suggest that the effect of lead on adult neurogenesis may be one mechanism underlying the long-term effects of lead on cognition. However, the study authors concluded that additional research is needed to better understand how lead exposure at different life stages impacts cognitive behavior later in life.