Alzheimer's and Parkinson's Disease
Alzheimer’s disease is estimated to affect nearly 4.5 million people in the U.S. About 5% of men and women aged 65– 74 have Alzheimer’s disease, while nearly half of those aged 85 and older may have the disease. By 2050, researchers estimate that this number will nearly triple to over 13 million.
About 50,000 new cases of Parkinson’s disease are reported annually in the U.S. Lack of patient registries, however, makes it difficult to estimate incidence and trends of the disease. The range of reported incidence of Parkinson’s disease varies from 4.5 to 21 per 100,000 people annually. The prevalence of Parkinson’s is expected to double by 2030.
The Alzheimer’s Association estimates that national direct and indirect annual costs of caring for individuals with Alzheimer’s disease are nearly $150 billion. The cost of Parkinson’s disease in the U.S. is estimated to be $13–28.5 billion per year.
The link to chemical exposure
As described previously, the scientific literature identifies more than 100 industrial chemicals that are known to affect the human brain and nervous system, causing memory, cognitive, and functional symptoms. (Philippe Grandjean and Philip J. Landrigan, “Developmental Neurotoxicity of Industrial Chemicals,” Lancet, 368, no. 9553 (December 2006): 2167–78.) While most of these studies have not focused on the aging brain, recent findings on lead, aluminum, PCBs, pesticides, particulate air pollution, and solvents suggest that chemicals affecting the developing brain may be harming the aging brain as well, leading to cognitive disorders like Alzheimer’s disease and Parkinson’s-like symptoms.
For example, in one recent study, 21% of more than a thousand patients presenting to a university clinic for cognitive disorders had medical histories that suggested they may have been exposed to chemicals in their workplace or from an environmental source. Clinicians found that a history of toxic exposure was associated with cognitive decline at significantly younger ages. (Donald E. Schmechel, Jeffrey Browndyke, Andrew Ghi, “Strategies for Dissecting Genetic-Environmental Interactions in Neurodegen-erative Disorders,” Neurotoxicology, 27, no. 5 (September 2006): 637–57.)
Another study divided a population of elderly men into four groups, based on the amount of lead found in the bones of their kneecaps. Researchers found that each increasing amount of bone lead was associated with accelerated cognitive aging; the most exposed group had 15 years of additional cognitive aging compared to the lowest exposed group. This study suggests that lead has a substantial impact on cognitive aging across the population. (Marc G. Weisskopf, et al., “Cumulative Lead Exposure and Prospective Change in Cognition among Elderly Men,” American Journal of Epidemiology, 160, no. 12 (2004): 1184–93.)
A series of animal studies on lead suggest that early-life lead exposure may contribute to late-life neurodegeneration. Rodents exposed to lead prenatally exhibited increases in Alzheimer-associated abnormal brain proteins later in life. In contrast, exposure to lead during old age did not cause increases in the Alzheimer’s disease-related proteins. 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. (Jinfang Wu, et al., “Alzheimer’s Disease (AD)-Like Pathology in Aged Monkeys after Infantile Exposure to Environmental Metal Lead (Pb): Evidence for a Developmental Origin and Environmental Link for AD,” The Journal of Neuroscience, 28, no. 1 (2008): 3–9.) (M. Riyaz Basha, Wei Wei, Saleh A. Bakheet, et al, “The Fetal Basis of Amyloidogenesis: Exposure to Lead and Latent Overexpression of Amyloid Precursor Protein and Beta- Amyloid in the Aging Brain,” The Journal of Neuro-science, 25, no. 4 (2005): 823–829.)
New animal studies have also 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. 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. (J.R. Walton, “A Longitudinal Study of Rats Chronically Exposed to Aluminum at Human Dietary Levels,” Neuroscience Letters, 412 (2007): 29-33.) (J.R. Walton, “Human Range Dietary Aluminum Equivalents Cause Cognitive Deterioration in Aged Rats,” (presented at the 24th International Neurotoxicology Conference, San Antonio, Texas, November, 2007).)
PCBs and the developing brain
Polychlorinated biphenyls (PCBs), may also be playing a role in the incidence of both Alzheimer’s and Parkinson’s disease. PCBs are a group of chemicals that have been shown to harm the developing brain. PCBs were used for many years as paint additives, lubricants, and insulators in electrical equipment before they were banned in 1976. Only three published epidemiologic studies have explored the effects of PCBs on cognitive decline or dementia in older human subjects. Each of these studies found an association of adult PCB exposure with dementia or cognitive impairment.
PCBs have also been tied to Parkinson’s disease. A retrospective mortality study of over 17,000 workers occupationally exposed to PCBs reported a nearly threefold greater incidence of Parkinson’s disease–related deaths than expected. Twice as many dementia-related deaths were seen in the women most highly exposed to PCBs—but not in men, even though men are generally at higher risk of Parkinson’s disease. Another postmortem study found higher levels of PCBs in the brains of people with Parkinson’s disease than in controls. (Kyle Steenland, Misty J. Hein, Rick Cassinelli, et al, “Polychlorinated Biphenyls and Neurodegenerative Disease Mortality in an Occupational Cohort,” Epidemiology, 17, no. 1 (2006): 8–13.) Animal and cellular studies have also shown that some PCBs produce Parkinson- like changes in the brain or brain cells.
Solvents and Parkinson’s disease
A variety of solvents are used for cleaning, degreasing, extraction, surface coating, and laboratory work. Solvents are also components of paints, inks, glues, adhesives, and hydrocarbon fuels. Several solvents, including carbon disulfide, methanol, n-hexane, and trichloroethylene (TCE), have been reported to be associated with Parkinson’s disease. One recent report describes Parkinsonism in 30 workers associated with long-term occupational exposure to TCE. (Don M. Gash, et al.,“Trichloroethylene: Parkinsonism and Complex 1 Mitochondrial Neurotoxicity,” Annals of Neurology, 63, no. 2 (2007): 184–92.) TCE is a particular concern because of widespread exposure: it is frequently used as a degreasing agent in industry, and is also a common surface- and groundwater contaminant, resulting in widespread, low-level exposures in the general population.
TSCA, Alzheimer’s and Parkinson’s
When TSCA was enacted in 1976, it banned new production and use of PCBs because of the accumulating evidence indicating they could cause cancer. Now we are learning that PCBs are among the chemicals that may be contributing to neurological disease as well. More than 30 years after the ban, PCBs continue to contaminate the environment because they are persistent and not easily broken down. And because they are fat-soluble and bioaccumulative, they also continue to enter and contaminate the general food supply, which serves as an ongoing source of human exposure. Biomonitoring data from the Centers for Disease Control and Prevention (CDC) show that the American public is still widely contaminated with PCBs. While the levels of PCBs in the general population are going down, hotspots of PCB contamination still exist across the U.S. (Centers for Disease Control and Prevention, Third National Report on Human Exposure to Environmental Chemicals, Department of Health and Human Services, 2005.)
To be effective, TSCA reform must recognize the unique dangers posed by exposure to persistent, bioaccumulative toxins (PBTs), like PCBs, and include provisions to phase out all non-essential uses of them. Communities and populations that bear disproportionately high burdens of PBT contamination need to be the focus of exposure reduction efforts. (This entire section is informed by Environmental Threats to Healthy Aging: With a Closer Look At Alzheimer’s and Parkinson’s Disease, by J. Stein, et al., (Boston: Greater Boston Physicians for Social Respon-sibility and the Science and Environmental Health Network, 2008).)
