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Dementia Slows Down: An Unanticipated Benefit of Environmental Policies?

Dementia Slows Down:

An Unanticipated Benefit of Environmental Policies?

Ted Schettler

Science and Environmental Health Network


The risk of dementia grows as we grow older and since people live longer now than in the past we expect to encounter this dreaded diagnosis more often. Surprisingly though, US and European studies that account for changes in population age distribution over two decades or more report that the incidence of dementia is decreasing. [1] [2] [3] [4] [5] The Framingham Heart Study, for example, found that the age-adjusted incidence of dementia was 3.6 per 100 people over five years in the late 1970s-1980s, falling to 2.0 per 100 people over five years in the late 2000s-early 2010s—a 20 percent decline per decade since 1977.[6]


Analysts speculate that this welcome news is due to some combination of more education, improved medications, and behavior changes like better diets, more exercise, and less smoking. There’s little doubt they contribute. In the Framingham study, the decline in dementia was greatest among people with at least a high school education. Beyond that, improvements in recorded cardiovascular risk factors did not mainly account for the findings. Something more seemed to be going on.


Arguably, environmental policies initiated in the 1970s leading to sharply lower population-wide exposures to air pollution and lead are prime candidates to explain more fully the slowdown in dementia onset.


Air pollution and cognitive decline: what’s the evidence?


In 2003 Lilian Calderón-Garcidueñas and her colleagues showed that the brains of dogs, even puppies a few months old, living in Mexico City’s notorious air pollution had inflammatory changes and protein deposits that looked like the pathology of Alzheimer’s disease.[7] Similar findings did not begin to appear in dogs from a low-pollution city until they were at least several years old.


Autopsy studies in people showed similar results—strikingly increased levels of inflammatory markers and abnormal protein plaques in the brains of Mexico City residents.[8] Even the brains of children and adolescents who had died accidental deaths showed marked inflammatory changes.[9] [10]


Since then, a growing number of studies and analyses more tightly link high air pollution exposures to increased risk of cognitive decline, dementia, strokes, and changes in brain structure.[11] [12] [13] [14] [15] [16] Particulate matter and traffic-related emissions are implicated, making it increasingly clear that commonly-encountered air pollution increases the risk of cognitive decline and dementia.


Lead and cognitive decline: what’s the evidence?


In addition to lead’s lasting damage to the developing brains of children, recent studies show that higher lifetime lead exposures increase the risk of more rapid cognitive decline in older adults. The first reports of subtle behavioral and psychological abnormalities in adults associated with chronic, lower-level lead exposures, typically in the workplace, began to emerge in the 1970s.[17] [18] These were largely based on blood lead concentrations as the measure of exposure.


A newer technology, X-ray fluorescence analysis (XRF), enables measurement of lead concentrations in bone, a better estimate of lifetime exposures than blood levels. Using XRF, recent studies report links between higher lifetime lead levels and more rapid cognitive decline later in life.


The first, a 2000 study in former lead workers, found more rapid decline in cognitive function due to past occupational exposures to lead, as estimated by bone levels, long after exposures had ceased.[19] Since then, others have published similar findings in people from the general population.[20] [21] [22]


Laboratory studies in rodents and primates show that relatively low-level early life exposure to lead modifies gene expression resulting in over-production of an amyloid protein later in life. [23] [24] [25] This is the protein that largely comprises plaques in the brains of people with Alzheimer’s disease. Although its role is contested, it is a primary target of pharmaceutical research into ways to reduce its production and deposition.


A small exploratory study in young adults whose blood lead levels in infancy had been measured also found a correlation between prenatal lead exposures and the expression of genes that influence amyloid production and deposition. [26]


Reducing exposures to air pollution and lead:


In the US, in response to growing, widespread air pollution, the 1970 Clean Air Act amendments for the first time required comprehensive federal and state regulations for stationary and mobile sources of air emissions. Airborne lead was among the pollutants addressed, and the US EPA first announced regulations to limit the amount of lead in gasoline in 1973. Beginning in 1971, lead-based house paint had already begun to be phased out in the US with the passage of the Lead-Based Paint Poisoning Prevention Act because of childhood lead poisonings from ingestion of paint chips. The phase-out of lead in gasoline was completed in most areas of the country by the early 1990s.


Trends in air pollution and blood lead levels:


During the 45 years since the 1970 Clean Air Act amendments, air quality has dramatically improved in most of the US. According to the US EPA, aggregate national emissions of six common pollutants—particles, ozone, lead, carbon monoxide, nitrogen dioxide, and sulfur dioxide—dropped by an average of 69 percent from 1970-2014.[27] Between 1980 and 2014, national concentrations of air pollutants improved 98 percent for lead, 85 percent for carbon monoxide, 80 percent for sulfur dioxide, 60 percent for nitrogen dioxide, and 33 percent for ozone. Fine particle concentrations fell by 36 percent and coarse particle concentrations fell by 30 percent between 2000—when trend data for fine particles began—and 2014. But these improvements are not evenly distributed. Air pollution in some communities in various regions of the US frequently and chronically exceeds regulatory health-protective levels.


With removal of lead from gasoline and most kinds of paint, childhood and adult lead levels dramatically declined. According to the CDC, average blood lead levels in US toddlers fell from about 16 micrograms/dL in 1974 to less than 2 micrograms/dL today. Yet, as we know, some families and communities continue to confront excessive lead exposures from deteriorating paint and drinking water contamination.


In adults, blood lead levels began to fall in the mid-1970s from an average of about 15 micrograms/dL to 9 micrograms/dL in 1980, a reduction of nearly 40 percent.[28] This was largely attributable to reduction in lead in gasoline. By 1990, the average adult blood lead level fell further to 3 micrograms/dL. The CDC also reports a steady decline in the number of adults with blood lead levels higher than 25 micrograms/dL since 1994 when systematic tracking began, although an estimated 10/100,000 workers still exceed that level.[29]




Benefits of improved air quality generally focus on avoided premature death and cardiovascular and pulmonary disorders. For lead, enduring harm to the developing brains of infants and children is the primary motivation for further reduction of even low-level exposures.


As populations age, projected increases in dementia-related disability, family stress, and costs of care are staggering. Better diets, more exercise, and avoiding smoking surely help delay and even prevent dementia onset. Initial reports of integrated approaches to dementia treatment show promise too.[30]


As evidence mounts, we can also more confidently include slowdown in dementia among the benefits of public policies that reduced population-wide exposure to air pollution and lead many years ago. Add those policies to the list of changes over the last 40 years that help explain why age-adjusted dementia incidence is declining.


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[3] Matthews F, Arthur A, Barnes L, et al. A two-decade comparison of prevalence of dementia in individuals aged 65 years and older from three geographical areas of England: results of the Cognitive Function and Ageing Study I and II. Lancet 2013;382:1405-1412.

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[9] Calderón-Garcidueñas L, Solt AC, Henríquez-Roldán C, et al. Long term air pollution exposure is associated with neuroinflammation, an altered innate immune response, disruption of the blood-brain barrier, ultrafine particulate deposition, and accumulation of amyloid beta-42 and alpha-synuclein in children and young adults. Toxicol Pathol. 2008; 36(2):289-310.

[10] Calderón-Garcidueñas L, Reynoso-Robles R, Vargas-Martínez J, et al. Prefrontal white matter pathology in air pollution exposed Mexico City young urbanites and their potential impact on neurovascular unit dysfunction and the development of Alzheimer’s disease. Environ Res. 2016; 146:404-417.

[11] Power M, Weisskopf M, Alexeeff S, et al. Traffic-related air pollution and cognitive function in a cohort of older men. Environ Health Perspect. 2011;119:682–687.

[12] Weuve J, Puett RC, Schwartz J, et al. Exposure to particulate air pollution and cognitive decline in older women. Arch Intern Med. 2012;172:219–227.

[13] Wilker E, Preis S, Beiser A, Wolf P, et al. Long-term exposure to fine particulate matter, residential proximity to major roads and measures of brain structure. Stroke. 2015; 46(5):1161-166.

[14] Peters R, Peters J, Booth A, Mudway I. Is air pollution associated with increased risk of cognitive decline? A systematic review. Age Aging. 2015; 44(5):755-760.

[15] Weuve J. Invited commentary: how exposure to air pollution may shape dementia risk, and what epidemiology can say about it. Am J Epidemiol. 2014; 180(4):367-371. Available at:

[16] Oudin A, Forsberg B, Adolfsson A, Lind N, et al. Traffic-related air pollution and dementia incidence in Northern Sweden: a longitudinal study. Environ Health Perspect. 2016; 124(3):306-312.

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[21] Weisskopf M, Wright R, Schwartz J, Spiro A, et al. Cumulative lead exposure and prospective change in cognition among elderly men: the VA Normative Aging Study. Am J Epidemiol. 2004; 160(12): 1184-1193.

[22] Bandeen-Roche K, Glass T, Bolla K, Todd, A, Schwartz B. Cumulative lead dose and cognitive function in older adults. 2009; 20(6):831-839.

[23] Bihaqi S, Bahmani A, Subaiea G, Zawia N. Infantile exposure to lead and late-age cognitive decline: relevance to AD. Alzheimers Dement. 2014; 10(2):187-195.

[24] Basha M, Wei W, Bakheet S, Benitez N. The fetal basis of amyloidogenesis: exposure to lead and latent overexpression of amyloid precursor protein and beta-amyloid in the aging brain. J Neurosci. 2005; 25(4):823-829.

[25] Wu J, Basha M, Brock B, Cox D, 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. J Neurosci. 2008; 28:3–9.

[26] Mazumdar M, Xia W, Hofmann O, Gregas M, et al. Prenatal lead levels, plasma amyloid β levels, and gene expression in young adulthood. Environ Health Perspect. 2012; 120(5):702-707.

[27] See

[28] Annest J, Pirkle J, Makuc D, Neese J, et al. Chronological trend in blood lead levels between 1976 and 1980. N Engl J Med. 1983; 308(23):1373-1377.

[29] See

[30] Bredesen D, Amos E, Canick J, et al. Reversal of cognitive decline in Alzheimer’s disease. Aging (Albany NY). 2016; 8(6):1250-1258. Open access at