Dec. 19 (UPI) -- The fact that fewer and fewer Americans are being diagnosed with dementia is a bit of good news that puzzles researchers.
After all, risk factors for the condition -- including diabetes and obesity -- are becoming increasingly common in the United States. So why hasn't this translated into a rise in dementia as well?
Researchers at the University of Toronto think they may have the answer: lifetime lead exposure. In a review published Thursday in the Journal of Alzheimer's Disease, they note that declining lead exposure levels in the United States and Canada, as well as parts of Europe, may explain why rates of dementia in these countries are falling.
The new study, researchers say, demands future research into possible links between lead and onset of conditions such as Alzheimer's disease.
"While the negative impact of lead exposure on the IQ of children is well-known, less attention has been paid to the cumulative effects of a lifetime of exposure on older adults' cognition and dementia," co-author Esme Fuller-Thomson, director of the Institute of Life Course and Aging at the University of Toronto, said in a press release. "Given previous levels of lead exposure, we believe further exploration of the of this hypothesis is warranted."
Generally, human lead exposure -- as measured by blood lead levels, or BLLs -- has dropped significantly in the U.S., since the country began phasing out leaded gasoline in 1973, Fuller-Thompson and co-author ZhiDi (Judy) Deng, noted.
According to the researchers, mean BLL in the U.S. was 12.8 µg/dL from 1976 to 1980, but it dropped to 2.8 µg/dL from 1988 to 1991 and, finally, to 0.84 µg/dL in 2013-14.
Additionally, the percentage of American children between 1 and 5 years old, with what the Centers for Disease Control and Prevention describes as "actionable" BLL, blood levels greater than 5 µg/dL was 99.8 percent in 1976-1980 but dropped to 0.5 percent in 2013-14. And, based on research published in the 1990s, measures of tibia bone lead levels in American adults born before 1925 were at least five times higher, or up to 28 µg/g, than those of people born between 1965 and 1982, which were up to 5 µg/g.
Lead is a known neurotoxin, and research on people exposed to lead at work suggest a link between lead exposure and dementia, Fuller-Thompson and Deng noted. In addition, studies have shown a higher incidence of dementia among older adults with a greater exposure to traffic-related pollution.
"The levels of lead exposure when I was a child in 1976 were 15 times what they are today," Fuller-Thomson said. "Back then, 88 percent of us had blood lead levels above 10 micrograms per deciliter. To put this numbers in perspective, during the Flint Michigan water crisis of 2014, one percent of the children had blood lead levels above 10 micrograms per deciliter."
Fuller-Thomson and Deng are particularly interested in a potential link between lifetime lead exposure and a recently identified subtype of dementia called Limbic-predominant Age-related TDP-43 Encephalopathy, or LATE. Research suggests LATE is the cause of approximately 20 percent of dementia cases.
Other plausible explanations for the improving trends in dementia include higher levels of education, lower prevalence of smoking and better control of hypertension among older adults. However, even when these factors are statistically accounted for, many studies still find incidences of dementia declining.
To confirm links between lead exposure and the onset of dementia, Fuller-Thompson and Deng recommend that future research compares blood lead levels in the 1990s to current Medicare records by assessing lead levels in teeth and tibia bones when conducting post-mortems of brains for dementia.
Noted Deng, "if lifetime lead exposure is found to be a major contributor to dementia, we can expect continued improvements in the incidence of dementia for many more decades as each succeeding generation had fewer years of exposure to the neurotoxin."