By then it will be too late to intervene. Within the next ten years, the oldest of these children will enter the age at which degenerative disease symptoms tend to emerge. Accumulating evidence from experimental and observational studies now suggests that childhood lead exposures may result in lasting neural, epigenetic, and behavioral changes not seen in exposed adults-changes that, together, may significantly alter exposed-children’s risks for neurodegenerative disease in old age.Īmerican children born in the 1960s, 1970s, and early 1980s experienced, en mass, lead exposures of a magnitude not seen before or since. Though its harm for the developing child’s brain is by now wellknown, the risk that lead poses for the exposed child later in life is still an active area of research. Lead, a heavy metal able to substitute for calcium in the body, is a potent neurotoxin. Individuals, and particularly children, living in highly urban areas, beside busy roads, or near lead-emitting industries had the highest exposures. In 1976, when the first America-wide lead-level surveillance began, the average American’s blood-lead level was three times higher than the current reference value for clinical attention. Lead was first added to gasoline in 1921 and, until phase-downs began in the mid-1970s, its use increased exponentially. Until the early-1990s, lead was ever-present in American communities, with lead use in paints, pipes, and gasoline resulting in high lead exposures across the population. įor millions of Americans now entering midlife and older age, childhood exposure to lead may be one profound, ubiquitous risk factor for age-related neurodegenerative disease.
With an aging global population, even small reductions in risk could significantly lower the future worldwide burden of neurodegenerative disease. Īlthough diseases like AD and PD appear to be fundamentally multifactorial in their etiology and mixed in their pathology -with many possible roads leading to the same dysfunctional outcome-the identification of common early-life risk factors holds significant promise for early intervention with at-risk individuals and for primary prevention to reduce risks for future generations. Following a Developmental Origins of Health and Disease (DOHaD) theoretical approach, some emerging theories now view abnormal age-related degeneration as the delayed consequence of disrupted neural development. As with many age-related conditions, neurodegenerative diseases are increasingly considered to result from an array of insults and risk factors operating differentially across the lifespan, with early life, pre- and post-natal emerging as a critical window for the development of risk. When do neurodegenerative diseases, like Alzheimer’s (AD) and Parkinson’s (PD), begin? The answer may be: at conception. More evidence is needed now to characterize the nature and magnitude of the degenerative risks facing adults exposed to lead as children and to identify interventions to limit long-term harm. Should childhood lead exposure prove pro-degenerative, the next twenty years will provide the last opportunities for possible early intervention to forestall greater degenerative disease burden across the aging lead-exposed population. Many will also enter the age in which lead stored in the skeleton may be remobilized at greater rates, particularly for women entering menopause and men and women experiencing osteoporosis. Within the next ten years, the generation of children with the highest historical lead exposures, those born in the 1960s, 1970s, and 1980s, will begin to enter the age at which dementia symptoms tend to emerge. Evidence from animal-model and human observational studies suggest that childhood lead exposure may raise the risk of adult neurodegenerative disease, particularly dementia, through a variety of possible mechanisms including epigenetic modification, delayed cardiovascular and kidney disease, direct degenerative CNS injury from lead remobilized from bone, and lowered neural and cognitive reserve. Millions of Americans now entering midlife and old age were exposed to high levels of lead, a neurotoxin, as children.
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