Alzheimer’s and Parkinson’s Diseases

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An estimated 5.4 million people in the United States have Alzheimer’s disease.[1] Two-thirds of those with the disease are women.[2] By 2050, researchers estimate that the number of people with the disease will nearly triple to 16 million.[3] Of Americans aged 65 and over, 1 in 8 has Alzheimer’s disease, and nearly half of people aged 85 and older have the disease.[4] Deaths from Alzheimer’s disease increased 66% between 2000 and 2008.[5]

Parkinson’s disease affects approximately 500,000 Americans, with about 50,000 new cases annually.[6] The prevalence of the disease is expected to double by 2030.[7] Lack of Parkinson’s disease registries, however, make it difficult to estimate the true incidence and trends over time.[8]

The Alzheimer’s Association estimates that national direct and indirect annual costs of caring for individuals with Alzheimer’s disease are $183 billion.[9] Estimates of the costs of Parkinson’s disease range from $13 billion to $28.5 billion per year.[10]

The link to chemical exposure

apprehensive-man-with-doctorThe risk of cognitive decline, dementia, and Parkinson’s disease increases with age, and most cases are likely to arise from multiple contributing factors. In recent years, the extent to which exposures to environmental chemicals and contaminants throughout the lifespan may play a role has received increased attention.

In one study, 21% of more than a thousand patients with cognitive disorders had medical histories that suggested they may have been exposed to chemicals either in their workplace or from some other environmental source. Clinicians found that a history of toxic exposure was associated with cognitive decline at significantly younger ages.[11] Unfortunately, few of the more than 100 industrial chemicals that are known to be toxic to the nervous system generally have been studied for specific impacts on the adult brain, but those few are illustrative.[12]

Pesticides

In the 1980s, case reports of individuals who developed Parkinson-like symptoms after injecting a synthetic drug contaminated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) sparked interest in looking for environmental chemicals that might have similar effects.[13] Early studies focused on chemicals with structural similarities to MPTP or its breakdown products, including the pesticide rotenone and the herbicide paraquat. Extensive laboratory and epidemiologic evidence now shows that exposure to certain kinds of pesticides increases the risk of Parkinson’s disease.[14][15] Although less well studied, pesticide exposures may also increase the risk of cognitive decline and dementia.[16][17]

Solvents

Solvents are another class of chemicals that appear to increase the risk of Parkinson’s disease in exposed workers. Solvents are used for cleaning, degreasing, extraction, surface coating, and laboratory work. They are components of paints, inks, glues, adhesives, and hydrocarbon fuels. Occupational exposure to solvents such as carbon disulfide, methanol, n-hexane, and trichloroethylene (TCE) is associated with an increased risk of Parkinson’s disease.[18][19][20] TCE is a particular concern. Not only is it frequently used as a degreasing agent in industry, but it is also a common surface and groundwater contaminant, resulting in widespread, low-level exposures in the general population.[21]

Lead and other metals

Lead, which is notorious for its impacts on the developing brains of children, also now appears likely to increase the risk of neurodegenerative disorders in people as they age.

A study of older men in the general population found that increasing levels of lead in their bones was associated with accelerated cognitive decline. The group with the highest lead levels had 15 years of additional cognitive aging compared to the group with the lowest levels when they were re-tested several years later.[22] Similar findings are also reported in women.[23]

Elevated bone lead levels are also associated with an increased risk of Parkinson’s disease.[24]

Studies in rodents designed to examine mechanisms by which early-life lead exposure might contribute to late-life neurodegeneration show that prenatal lead exposures modify the expression of certain genes later in life, resulting in increased production of Alzheimer-associated abnormal brain proteins.[25] The same delayed, late-life increase in Alzheimer’s disease-related proteins was reported in aged monkeys exposed in infancy to low levels of lead.[26]

New animal studies also have resurrected the 1960s controversy about the role of aluminum in neurodegenerative disease. One small study showed that when rodents were chronically exposed to dietary aluminum (similar to typical human exposure levels), aluminum accumulated in the brain.[27] A larger follow-up study in rats showed that the more aluminum a rat received in its diet, the more memory loss the rat exhibited.[28]

Excessive inhalation of manganese-containing fumes also can increase the risk of Parkinson-like symptoms.[29]

Polychlorinated biphenyls (PCBs)

Before they were effectively banned under TSCA in the late 1970s, polychlorinated biphenyls (PCBs) were used for many years as flame retardants, plasticizers in paints, lubricants and coolants in electrical equipment, and adhesives.[30][31] As a result of their widespread use, many people and wildlife throughout the world have been exposed.[32]

More than 30 years after they were effectively banned, PCBs continue to contaminate the environment because they are persistent, or not easily broken down, and move readily from land to air and water. They also bioaccumulate and continue to enter and contaminate the food supply, which is an ongoing source of human exposure.[33]

Biomonitoring data from the CDC show that the American public is still widely contaminated with PCBs.[34] Although the levels of PCBs in the general population are decreasing, certain subpopulations remain highly exposed, especially those regularly consuming contaminated fish.[35]

In the years following TSCA’s passage, we learned that, like most chemicals, PCBs can cross the placenta, directly exposing the fetus.[36] Numerous studies show that prenatal exposure to PCBs interferes with normal brain development.[37][38][39] More recently, we have learned that PCBs may increase the risk of both Alzheimer’s disease and Parkinson’s disease.

Three published epidemiologic studies have explored the effects of PCBs on cognitive decline or dementia, and each found that higher levels of exposure are associated with an increased risk of dementia or cognitive impairment. While PCB exposures were relatively high in two of the studies,[40][41] exposures in the third were closer to those in the general population.[42]

A retrospective mortality study of more than 17,000 workers occupationally exposed to PCBs reported a nearly threefold excess of Parkinson’s disease-related deaths and twice as many dementia-related deaths in women most highly exposed to PCBs.[43] Another postmortem study found higher levels of PCBs in the brains of people with Parkinson’s disease than in control subjects.[44] Animal and cellular studies also have shown that some PCBs produce Parkinson-like changes in the brain or brain cells.[45]

Thus, PCBs tell a cautionary tale: introduction of persistent, bioaccumulative, and toxic chemicals into commerce will predictably have adverse health and economic consequences for many years, even after they are banned.

How chemical policy reform can help

elderly-mother-with-daughter To be effective, TSCA reform must recognize the unique dangers posed by exposure to persistent, bioaccumulative, and toxic pollutants (PBTs), such as PCBs, PBDEs, and heavy metals, and include provisions to ban them except for critical uses. Communities and populations that bear disproportionately high burdens of PBT contamination must be the focus of exposure reduction efforts.

In addition, it is now clear that environmental chemicals can contribute to neurodegenerative changes in the adult and aging brain. Thus, in order to protect public health, TSCA reform also must include provisions for assessing the effects of industrial chemicals on the brain throughout the lifespan.

Citations:

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