Seniors can be affected by poor indoor air quality.
The population of Americans aged 65 and older is expected to double between 2010 and 2050,1 and by midcentury the proportion of the human population made up of people over age 80 is projected to have quadrupled since 2000.
So factors that affect this aging population are of increasing importance. Of particular concern are the neurological diseases and disorders typically associated with advanced age, among them Alzheimer’s and Parkinson’s diseases, dementia, and reduced cognitive function.
Investigators are studying the effects of not just present-day exposures and environmental influences such as physical and mental exercise, but also exposures that occurred much earlier in life, whose effects may only become apparent in old age.
It was long assumed that “once the brain received its allotted quota of nerve cells, its destiny was frozen. After that, the passage of time eroded our allotment steadily and irrevocably,” as professor emeritus Bernard Weiss of the University of Rochester School of Medicine and Dentistry wrote in 2007.3
Now, however, there is increasing evidence that the brain is capable of generating new neurons and other functional brain cells even during advanced age. There is also evidence that the older brain can respond quickly and positively to external influences such as physical exercise and intellectual stimulation.
This is prompting considerable interest in developing strategies for protecting and enhancing neurological function in the elderly.
The two most vulnerable periods for the brain, Weiss says, are early in life, when the organ is first developing, and later in life, when the body’s defenses and compensatory mechanisms begin to falter.
There is a large and growing body of evidence indicating these two vulnerable life stages can be linked when damage incurred during early development contributes to health disorders that may not become apparent until later in life.
Weiss also notes that declining defense mechanisms may magnify vulnerability to contemporary environmental exposures.
He says that when older adults experience cognitive problems, diagnoses rarely consider the possibility that environmental chemical exposure may be involved, simply because questions about such exposures are typically not asked as part of clinical intake.
Over the past 30 years, Weiss says, research attention has focused primarily on environmental influences on early developmental stages. Far less extensively researched, but a subject of increasing interest, are environmental chemical exposures that can affect the health of the aging brain.
In the past 10 years, however, a number of studies have looked at the effects of chronic low-level lead exposure on adult humans’ cognitive abilities. The findings of such studies suggest that lead that has accumulated in bones can be mobilized over time as part of the aging process, resulting in exposures that adversely affect adults’ cognitive skills later in life.
Other metals may adversely affect neurological function in later life by either acting directly on the brain or adversely impacting other organs or hormones that maintain healthy neurological function.
For example, cadmium can cause kidney disease, which is associated with cognitive problems. Like lead, cadmium is stored in the body, primarily in the kidneys and liver but also in joints and other tissues, where it has a biological half-time of decades.
Similarly, lead and mercury have been associated with liver disease, which itself is associated with adverse neurological health effects, including a condition that produces a type of neuronal plaque associated with Alzheimer’s disease.
Older brains may be affected by chemical exposures earlier in life.
Chemical exposures that adversely affect kidney and liver function can also hamper the body’s ability to detoxify and excrete environmental toxicants, thus letting them remain in the body—an effect that may be particularly problematic in advanced age when a body’s defense mechanisms are in decline.
There is evidence connecting certain metals (e.g., lead, manganese), pesticides (e.g., paraquat, maneb), and solvents (e.g., toluene, trichloroethylene) with neurological
symptoms characteristic of Parkinson’s disease. Many of the exposures studied have been occupational, and some were acute, rather than lower-level and chronic. Much more extensive research is needed to determine the precise role environmental exposures to these agents may play in prompting Parkinson’s disease.
More substantial evidence links various solvent exposures to other neurological conditions, including cognitive impairments, neuropathy, and what is sometimes called “pseudodementia,” when temporary neurological dysfunction produces symptoms similar to those of dementia.
Organic solvents, including toluene, have also been found to impair color vision, while other solvent exposures have been linked to hearing loss, particularly when combined with noise exposure.
Such exposures have been primarily studied when they occur occupationally, but some epidemiological studies suggest there is also potential for adverse effects from ambient environmental exposures.
These solvent and pesticide exposures can, of course, occur at any age. But because the neurological disorders with which they are linked mirror those associated with motor and sensory-function declines of aging, they can be mistaken in diagnosis for the effects of aging or diseases of old age like Parkinson’s and Alzheimer’s diseases.
It also appears that long-term nonacute exposures to solvents and pesticides can affect verbal memory, attention, and spatial skills, with effects that may not become apparent until later in life, when they, too, might be confused with or compounded by aging-related conditions.
More subtle environmental exposures are also thought to be implicated in neurological health effects that can manifest later in life. These include exposures to chemicals that may disrupt the normal function of hormones involved in regulating neurological health, chief among them thyroid hormones.
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Hormones are intimately involved with neurological function; a normal brain can’t develop without healthy thyroid hormone function, and the fetal brain is extremely receptive to thyroid hormone.
When environmental factors affect thyroid and other hormones, the result can be health effects associated with conditions that impair neurological function.
For example, there is evidence that exposure to persistent organic pollutants including dioxins and certain polychlorinated biphenyls, halogenated flame retardants, and pesticides can produce hormonally mediated effects that promote obesity and diabetes, which increase risk for vascular health problems.
There is also evidence that exposures to some of these same compounds may directly increase risk for hypertension and cardiovascular disease.
These cardiovascular conditions can, in turn, cause less dramatic neurovascular effects that sometimes result in memory loss, or what’s called “vascular dementia,” when reduced blood flow to the brain deprives brain cells of oxygen and causes the equivalent of small strokes.
Evidence of similar effects has been reported for exposure to chemicals that are pervasive due to widespread use but are not environmentally persistent.
Among these is bisphenol A (BPA).
Laura Vandenberg, an assistant professor of environmental health studies at the University of Massachusetts Amherst, explains that numerous animal studies indicate early-life exposure to BPA can produce health effects characteristic of metabolic syndrome.
Individuals with metabolic syndrome are at increased risk for hypertension, with its risk for adverse neurological effects. It is also often hard to exercise for those who are overweight or obese or who have cardiovascular disease or diabetes. Yet aerobic exercise in later life appears to be an essential component of maintaining, if not also enhancing, brain function in older age.
There is now substantial research investigating how physical activity and exercise affect brain function. This is also the area of research where it is perhaps the easiest to make direct comparisons between animal experiments and human studies.
One focus is to understand the mechanisms by which exercise protects and restores the brain.
Of particular interest is learning how physical exercise increases the production of new neurons, and how that may enhance performance of certain memory functions. Functions of interest include what’s called “relational binding”—for example, remembering the name of a person you recently met and where you met that person.
Physical exercise also appears to enhance “visual pattern separation,” which enables you to distinguish and remember different patterns—a process that increases memory accuracy.
Source: Environmental Health Perspectives
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