Aging and Vulnerability to Environmental Chemicals: Age-related Disorders and their Origins in Environmental Exposures / Edition 1 available in Hardcover
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- RSC Publishing
The world's aging populations, with age-related disorders affecting every organ system, are generating medical care costs rising at an unsustainable rate. Although such disorders are expected, we are now beginning to ask whether exposures to toxic environmental chemicals hasten or account for their onset. This book provides a detailed review of current knowledge about the possible associations between a variety of chemical contaminants and adverse effects later in life. It will serve as a guide to policy decisions about protecting us from chemical exposures that distort the aging process. It provides a guide to current understanding of how our contaminated environment may be influencing the aging process and contains examples of approaches that will help us undertake further research on this topic. It will help alert policy makers to the implications of chemical pollution for aging populations and will help formulate initiatives for environmental protection. The book provides a comprehensive view of how environmental exposures may alter the health of our aging population. For readers engaged in environmental research, or aging research, it will highlight a number of questions that need more attention For other readers, they will learn something about the kind of exposures they should avoid or that they should prompt policy makers to reduce or eliminate.
About the Author
Dr. Bernard Weiss is Professor of Environmental Medicine at the University of Rochester School of Medicine and Dentistry, where he has been a member of the faculty since 1965. He is also a member of its Environmental Health Sciences Center. Before coming to Rochester, he served on the faculty of the Johns Hopkins School of Medicine, and, earlier, held an appointment at the U.S. Air Force School of Aviation Medicine. Dr. Weiss has served as a member of many committees and panels devoted to toxicology and environmental health, including those organized by the U.S. Environmental Protection Agency's Science Advisory Board, and the National Academy of Sciences. He is especially concerned with risk assessment issues arising from the effects of environmental chemicals on brain development and brain aging, and with the role played by sex differences. He is the editor or co-editor of seven books and monographs and author or co-author of over 250 articles. His special interests and publications lie primarily in areas that involve chemical influences on behavior; these include the neurobehavioral toxicology of metals such as lead, mercury and manganese; developmental toxicants such as dioxin; solvents such as toluene and methanol; endocrine disruptors such as phthalates; and air pollutants such as ozone. His current research projects, supported by NIH, examine the effects of Bisphenol A on brain sexual differentiation.
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Aging and Vulnerability to Environmental Chemicals
Age-related Disorders and their Origins in Environmental Exposures
By Bernard Weiss
The Royal Society of ChemistryCopyright © 2013 The Royal Society of Chemistry
All rights reserved.
Exposure to Lead and Cognitive Dysfunction
JENNIFER WEUVE AND MARC G. WEISSKOPF
1.1 Lead Exposure: Long at Hand and in Mind
Humans' use of lead dates back at least to 7000 BC. And knowledge of lead's neurotoxicity has been with us since the observations of Nicander, Vitruvius, and the ancient Greek physician, Dioscorides, who wrote that "[l]ead makes the mind give way". Nonetheless, between 1925 and 1980, human exposure to lead in the US environment reached historically high levels owing to the dominance of leaded gasoline for automobile fuel and the widespread use of lead-based paint. In the present US environment, as a result of long-sought regulations that removed lead from gasoline and minimized the use of lead-based paint, exposure to lead happens sporadically, and most individuals' exposures occur at low doses. Nonetheless, exposure to lead remains relevant to the cognitive function of aging adults, because exposures in the past were substantial. These exposures may influence adult cognition either through their effects on the developing nervous system or, because lead is stored in the skeleton for periods of years and decades, through re-exposure to lead in adulthood with age-related bone turnover.
In this chapter, we describe historical and contemporary sources of lead exposure and scientific findings on its effects on cognitive function in adults. We give particular consideration to the history of lead's use in gasoline and the incremental acknowledgement of its neurotoxicity by industrial and regulatory stakeholders. It is this history that underlies an epidemic of elevated lead exposure that spanned several generations and may be responsible for cognitive decrements in many adults. This history is also instructive for how future additives to gasoline and other widely used consumer products should be scrutinized.
1.2 How Humans were and Continue to be Exposed to Lead
1.2.1 Historical Exposures
18.104.22.168 Early Uses: the Emergence of Lead into the Environment
Unlike metals such as iron, copper, and manganese, lead is not essential to physiological function. Yet humans have been introducing lead into their environments — and often directly into their bodies — for millennia. In ancient Chinese, Mediterranean, and Middle Eastern societies, lead was a key ingredient in glassware, pots and vessels, solder, paints, cosmetics, eye medicines, and contraceptive methods. It was also used in food and wine as a sweetener and preservative. The Romans, taking advantage of its malleability and availability, made lead the centerpiece of their infrastructure with their extensive web of lead pipes, promoting lead to a quotidian status unprecedented in human civilizations. These uses were joined by new ones — e.g., as an ingredient in inks, ammunitions, and even poisons — and continued throughout the early twentieth century. Then, in the 1920s, humans in the burgeoning US automotive industry, aided and abetted by others in the US government, developed a use for lead that would expose much more of the population, at much higher doses than ever before.
22.214.171.124 How Leaded Gasoline Became the Major Source of Exposure to Lead
The market for automobiles in the US had grown increasingly competitive by the early 1920s, and General Motors (GM) sought to distinguish its automobiles from Ford's reliable but sedate Model T by unveiling new models every year and, critically, improving engine power and efficiency. A challenge central to this latter goal was eliminating the pinging "knock" that arose when the fuel ignited prematurely in high-performance, high-compression engines. In 1921, Thomas Midgley, Jr., an engineer at GM, discovered that adding tetraethyl lead (TEL) to gasoline decreased this knock. Curiously, several years earlier, GM's engineers had established that ethyl alcohol (grain alcohol) was also an effective anti-knock agent. However, the competitive advantage of having a proprietary fuel and GM's entwinement with the production of TEL fuel meant that the lead-based agent prevailed while the alcohol-based agent was maligned. This occurred even though, since TEL's first synthesis by a German chemist in 1854, it had a "known deadliness."
In response to protests from industrial hygienists, physiologists, and chemists, the Surgeon General inquired with GM and the DuPont company, a manufacturer of TEL, who responded with evidence-free reassurances. Nonetheless, seeking a governmental "stamp of approval" for their product, GM and DuPont entered into an agreement to study TEL's safety with oversight from the Bureau of Mines. This oversight was merely symbolic, because GM and DuPont negotiated contractual control over all TEL data and any communications regarding it. The first gallon of leaded gasoline was sold in 1923.
The momentum behind the ambition of GM and its affiliates was nearly staunched when, in October 1924, five employees at Standard Oil's TEL facility died violent, psychotic deaths, and 35 other workers were smitten with serious neurologic symptoms such as hallucinations, tremors, and palsies. Even though Standard Oil dismissed suspicions with such claims as the victims "had probably worked too hard", officials in New Jersey, Philadelphia, New York state, and New York City were unconvinced and officially banned the sale of leaded gasoline for varying periods – in New York City, the ban lasted for 3 years.
By this time, the Bureau of Mines had formally exonerated leaded gasoline, and yet at the TEL plants, poisonings and deaths continued, many of them closely guarded by industry. Still, the neurotoxicity of lead in these occupational settings was difficult to miss. Among workers at the Standard Oil plant, the TEL building was known as "The Looney Gas Building," and at the DuPont plant, the TEL building was known as "The House of Butterflies," in tribute to its occupants' tendency to have hallucinations involving insects. Yielding to the perception that a governmental body (the Bureau of Mines) was in the pocket of industry, and thus any ill effects of TEL were being ignored, in 1925, the Surgeon General assembled a conference of public health and industry scientists. The argument that prevailed was that TEL would contribute so substantially to the progress of the US as to advance civilization itself, thus making TEL a "gift from God." And although public health advocates argued that it was incumbent on industry to demonstrate TEL's safety, ultimately, the Surgeon General commissioned a "Blue Ribbon Panel" to investigate lead's harm, giving this panel only seven months to do so. It is not surprising then that the committee concluded that "... at present, there are no good grounds for prohibiting the use of ethyl gasoline. ..." However, the committee recognized that seven months was insu?cient for the job. Presciently, it predicted that, given the insidious and cumulative toxicity of lead poisoning, "[l]onger experience may show that even such slight storage of lead [in the body] as was observed in these studies may lead eventually in susceptible individuals to recognizable or to chronic degenerative diseases. ..." This was the last time for several decades that the US government would come close to considering major regulatory action on leaded gasoline.
126.96.36.199 Lead-Based Paints Added to the Burden of Lead Exposure
Running in parallel to the emergence of leaded gasoline was the emergence of lead-based paint. Humans have been adding lead to paint for centuries, and the neurologic hazards to children of exposure to lead-based paint have been known since at least the early 1900s. The players in the saga of lead-based paint were the archetypes seen in the saga of leaded gasoline. The paint saga differed in its focus on children, both as potential victims of exposure and as subjects in advertising for lead-based paint manufacturers. In a perverse twist, the medical director for the Ethyl Gasoline Corporation advocated reducing children's exposures to lead by eliminating lead from paint, but clearly saw no problem with lead in gas.
188.8.131.52 Leaded Gasoline and Lead-Based Paint Were Phased out, but Many Were Exposed
The US Environmental Protection Agency, born in 1970, instituted regulations that initiated the gradual phase-down of lead content in gasoline for on-road vehicles, beginning in 1976 and concluding with a complete ban in 1995. (Excluded from this phase-down were fuels used for off-road vehicles and marine vessels, and in farming and aviation. In addition, it was only in 2008 that the National Association for Stock Car Racing completely switched its racing fuels to unleaded varieties.)
In 1978, the Consumer Products Safety Commission banned the sale and use of lead-based paint. By then, human exposures to lead, primarily from leaded gasoline and paint, had reached common and chronic proportions. As of 1980, the estimated per capita consumption of lead-based products in the US was 5.2 kilograms per American per year, around 10 times the estimated exposures of ancient Romans. Over the 20th century, the US had burned an estimated 7 million tons of lead in its gasoline, the source of about 90% of the lead emitted into the environment.
While leaded gasoline and paint were being removed from public consumption, interventions were occurring on other sources of exposure. For example, in the 1970s, many US-based food can manufacturers voluntarily ceased using leaded solder in their cans, which resulted in a substantial reduction in human exposure from this source between 1979 and 1989. In 1995, the US Food and Drug Administration formally banned the use of lead-based solder in all canned food sold in the US, including imported food.
The removal of lead from gasoline, paint, and other sources markedly reduced Americans' lead exposures. For example, in early 1976, at the start of the phase-down of lead in gasoline, the average blood lead level in the civilian, non-institutionalized US population was 15 µg dL-1, well above what is defined today as an elevated level for children (around 5 µg dL-1). (In some areas in the early 1970s, including rural areas, the average blood lead levels among children exceeded 20 µg dL-1) By 1980, the average blood lead level had sunk to 10 µg dL-1, and it had plummeted to 2.8 µg dL-1 about a decade after that. Nonetheless, millions of children and adults had been exposed to biologically relevant doses of lead, often for many years, and emerging evidence was suggesting that while removing the exposures had established health benefits, the legacies of those exposures could go on to influence myriad health risks, including risks for impaired cognition in adulthood.
1.2.2 Contemporary Sources of Exposure
Lead exposure results from inhalation of air contaminated with lead, or ingestion of food, water, or dust that contains lead. The highest exposures to lead have always been occupational, where workers can experience extremely high levels of exposure. The action level for medical removal from the workplace in the Occupational Safety and Health Administration's (OSHA) standard for blood lead is 50 µg dL-1 or above for construction and 60 µg dL-1 or above for all other occupation settings; that is, when workers are found to have blood lead levels above these levels, they are required to be removed from that work environment until two consecutive blood lead measurements are below 40 µg dL-1. This level is still over 10 times greater than the current average blood lead concentration of adults in the US population (see also Section 184.108.40.206).
In the US, while occupational lead exposure has generally been decreasing, it remains a problem in construction, and this sector has become the dominant source of lead exposure for adults (to a large extent the result of lead in paint). Lead paint can contain up to 50% lead by weight, and workers who remove paint are at extremely high risk of lead exposure. The majority of houses built before 1978 (estimated at 42–47 million houses in the US) have lead-based paint inside and outside, and lead paint was also used in commercial buildings and other structures such as bridges. Scraping and, in particular, sanding lead paint creates a fine lead dust that can be easily inhaled. Absorption of lead is highly efficient following inhalation, particularly if the particles are small. Hand-to-mouth behavior of construction workers, for example eating and smoking cigarettes without prior hand washing, can also lead to significant absorption of lead. Lead dust on the hands can be ingested and absorbed through the gastrointestinal tract as can lead dust on cigarettes, which can be heated during smoking, generating lead fumes that are especially well absorbed by the lungs. Much more commonly in countries outside the US, Canada, and Europe, workers in many other industries, such as battery manufacturing plants, are also at high risk of extremely high lead exposure.
Aside from occupationally exposed individuals, people who present with blood lead levels that exceed the Centers for Disease Control and Prevention (CDC) current pediatric action limit of 5 µg dL-1 were often exposed from sources such as contaminated traditional medications and cosmetics, accidental exposures to lead from commercial uses (e.g., leaded batteries), or use of lead- containing materials in several common hobbies. For example, persons who create pottery and stained glass often use materials that contain lead, which can result in exposure, as can chewing on or making lead bullets or lead fishing line sinkers. Current exposures can also occur as a result of past activities, unfortunately sometimes unwittingly. Recent reports revealed elevated blood lead levels among children in areas where houses were built on the site of former lead manufacturing plants, of which the residents were unaware. In other communities, tap water has been inadvertently contaminated due to partial replacement of service lines, or to water treatment processes that render the chemistry of the water more amenable to dissolving corroded lead in water pipes. Outside of the US, many more examples of very high lead exposures of non-workers are found. A very recent and devastating example of this was the death of an estimated 400 children, and severe lead poisoning of many more, in Nigeria as a result of artisanal gold ore processing in their family compounds.
Common current sources of environmental lead exposure in the United States and around the world include lead in plumbing (which can contaminate drinking water), lead paint in older housing, contaminated house dust, contaminated soil, lead crystal, and lead-glazed pottery. However, past exposures to lead are still an important consideration. By far the predominant past general environmental exposure to lead was through exposure to lead in air, which was very largely a result of lead in gasoline. Although a few countries, including Canada and Japan, led the US in banning leaded gasoline, bans in other parts of the world have occurred more recently or not at all, and in these countries, past cumulative exposures are likely to have been much higher.
Excerpted from Aging and Vulnerability to Environmental Chemicals by Bernard Weiss. Copyright © 2013 The Royal Society of Chemistry. Excerpted by permission of The Royal Society of Chemistry.
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Table of Contents
Parkinson's Disease; Cognitive dysfunction and lead; Cardiovascular disease, metabolic syndrome; Breast cancer; Prostate cancer; Kidney disease; Liver disease; Osteoporosis; Immune system disorders; Male reproductive tract disorders; Female reproductive tract disorders; Air Pollutants; Mercury; Manganese; Aluminium; Cadmium; PCBs and Dioxins; Bisphenol A; Obesogens; Subject Index