Final Paper Outline
Botkin, D. B., & Keller, E. A. (2014). Environmental science: Earth as a living planet (9th ed.). Hoboken, NJ: John Wiley & Sons, Inc
Chapter 8: Environmental Health, Pollution, and Toxicology
8.1 Some Basics
Environmental Health
The World Health Organization broadly defines environment health as human health and disease that is determined by or related to environmental factors such as toxic chemicals, toxic biological agents, or radiation. Also included in the realm of environmental health are direct and more often indirect adverse health effects resulting from housing (such as indoor air pollution from form- aldehyde ); urban development (including construction materials such as some paints); land use (including expo- sure to harmful trace metals such as arsenic from mining); or pesticides from agriculture and transport systems (in- cluding exposure to gasoline or diesel fuel).4
Disease may be defined as an impairment of an in- dividual’s health. The incidence of disease depends on several factors, including the physical environment, bio- logical environment, human-made environment, and lifestyle. Linkages between these factors are often related to other factors such as cultural customs and levels of urbanization and industrialization. Modern medicine in highly developed societies as found in the United States and western Europe has greatly reduced infectious dis- eases such as polio, cholera, dysentry, and typhoid fever. However, through modern agriculture, urbanization, and industrialization, we are exposed to more chemicals di- rectly or indirectly released into the environment that may cause acute or, more often, chronic health problems. In this chapter, we will explore some of the factors and linkages between factors that influence our health.
Terminology
What do we mean when we use the terms pollution, contamination, toxin, and carcinogen? A polluted en- vironment is one that is impure, dirty, or otherwise unclean. The term pollution refers to an unwanted change in the environment caused by the introduc- tion of harmful materials or the production of harmful conditions (heat, cold, sound). Contamination has a meaning similar to that of pollution and implies mak- ing something unfit for a particular use through the introduction of undesirable materials—for example, the contamination of water by hazardous waste. The term toxin refers to substances (pollutants) that are poi- sonous to living things. Toxicology is the science that studies toxins or suspected toxins, and toxicologists are scientists in this field. A carcinogen is a toxin that in- creases the risk of cancer. Carcinogens are among the most feared and regulated toxins in our society.
Synergism
An important concept we need to learn in considering pollution problems is synergism—the interaction of different substances, resulting in a total effect that is great- er than the sum of the effects of the separate substances. For example, both sulfur dioxide (SO2) and coal dust particulates are air pollutants. Either one taken separately may cause adverse health effects, but when they combine, as when SO2 adheres to the coal dust, the dust with SO2 is inhaled deeper than SO2 alone and causes greater damage to lungs. Another aspect of synergistic effects is that the body may be more sensitive to a toxin if it is simultane- ously subjected to other toxins.
Point, Area, and Mobile Sources
Pollutants are commonly introduced into the environ- ment by way of point sources, such as smokestacks, pipes discharging into waterways, a small stream entering the ocean (Figure 8.1), or accidental spills Area sources, also called nonpoint sources, are more diffused over the land and include urban runoff and mobile sources, such as au- tomobile exhaust. Area sources are difficult to isolate and correct because the problem is often widely dispersed over a region, as in agricultural runoff that contains pesticides.
Sudbury, Ontario
A famous example of a point source of pollution is provided by the smelters that refine nickel and copper ores at Sudbury, Ontario. Sudbury contains one of the world’s major nickel and copper ore deposits. A number of mines, smelters, and refineries lie within a small area. The smelter stacks used to release large amounts of particulates containing toxic metals—including arsenic, chromium, copper, nickel, and lead—into the atmosphere, much of which was then deposited locally in the soil. In addition, because the areas contained a high percentage of sulfur, the emissions included large amounts of sulfur dioxide (SO2). During its peak output in the 1960s, this complex was the largest single source of SO2 emissions in North America, emitting 2 million metric tons per year.
As a result of the pollution, nickel contaminated soils up to 50 km (about 31 mi) from the stacks. The forests that once surrounded Sudbury were devastated by decades of acid rain (produced from SO2 emissions) and the deposition of particulates containing heavy metals. An area of approximately 250 km2 (96 mi2) was nearly devoid of vegetation, and damage to forests in the region has been visible over an area of approximately 3,500 km2 (1,350 mi2); see Figure 8.2a. To control emissions from Sudbury, the Ontario government set standards to reduce emissions.5 During the past few decades, emis- sions of SO2 and metal particulates have been reduced by about 90%. Reducing emissions from Sudbury has allowed surrounding areas to begin to recover from the pollution (Figure 8.2b). Species of trees once eradicated from some areas have begun to grow again. Recent restoration ef- forts have included planting over 7 million trees and 75 species of herbs, moss, and lichens—all of which have contributed to the increase of biodiversity. Lakes dam- aged by acid precipitation in the area are rebounding and now support populations of plankton and fish.5 However, recovery of land aquatic ecosystems is a slow process.
The case of the Sudbury smelters provides a posi- tive example of emphasizing the key theme of thinking globally but acting locally to reduce air pollution. It also illustrates the theme of science and values: Scientists and engineers can design pollution-abatement equipment, but spending the money to purchase the equipment reflects what value we place on clean air.
Toxic Pathways
Chemical elements released from rocks or human processes can become concentrated in people (see Chapter 7) through many pathways (Figure 8.3). These pathways may involve what is known as biomagnification—the accumulation or increasing concentration of a sub- stance in living tissue as it moves through a food web (also known as bioaccumulation). For example, cadmium, which increases the risk of heart disease, may enter the environment via ash from burning coal. The cadmium in coal is in very low concentrations. However, after coal is burned in a power plant, the ash is collected in a solid form and disposed of in a landfill. The landfill is covered with soil and revegetated. The low concentration of cad- mium in the ash and soil is taken into the plants as they grow, but the concentration of cadmium in the plants is three to five times greater than the concentration in the ash. As the cadmium moves through the food chain, it becomes more and more concentrated. By the time it is incorporated into the tissue of people and other carni- vores, the concentration is approximately 50 to 60 times the original concentration in the coal.
8.2 Categories of pollutants
and Toxins
A partial classification of pollutants by arbitrary categories is presented below. We discuss examples of other pollut- ants in other parts of the book.
Infectious Agents
Infectious diseases—spread by interactions between in- dividuals and by the food, water, air, soil, and animals we come in contact with—constitute some of the oldest health problems that people face. Infectious disease may be caused by bacteria, virus, or fungus (but most of these organisms do not cause disease).
Bacteria compose a large group of unicellular micro- organisms lacking organelles with an organized nucleus (see Chapter 7). Some bacteria cause disease, but most do not. Viruses are very tiny organisms (particles smaller than bacteria) that consist of a combination of long molecules that carry genetic information (genes ) and a protein coat that protects the genes. Some viruses cause mild to severe illnesses in hosts (humans, animals, and plants). Because the original host may either die or eliminate the infec- tion, a virus needs to spread to another host to survive. Some transfer mechanisms for the human host include coughing (colds and influenza); fecal or oral emanations (hepatitis A, polio); sexual activity (HIV, hepatitis B); insect or rodent vector (yellow fever, dengue fever, West Nile, hantavirus); and animal bites (rabies).
Hantavirus is potentially a life-threatening disease that is spread from the feces and urine of rodents (espe- cially deer mice). Recently, there was a small outbreak in the Sierra Nevada (Yosemite National Park) among tent– cabin campers. Nine cases were confirmed, with three deaths. Most infections result from persons exposed to rodent droppings in their own homes or when cleaning places such as sheds that have been empty for some time and inhabited by mice.7
Fungi are a member of a large group of eukaryotic organisms that includes microorganisms such as molds as well as mushrooms. Fungal infections, especially but not limited to mold, are often carried by mold spores that are the asexual reproductive structures of fungi. In our homes and other buildings, mold may spread due to moisture in walls and foundation areas. Molds often become a prob- lem following floods but grow whenever there is sufficient moisture and heat. For example, following Hurricane Ka- trina in 2005 (which caused widespread flooding), there was a significant rise in reports of allergies and asthma in children in New Orleans—about three times the U.S. average. When people sensitive to mold inhale airborne mold spores, they may experience allergic reactions with asthma symptoms. Under specific growing conditions, molds may excrete toxic compounds (miotoxins). One miotoxin is called aflatoxin (a carcinogenic miotoxin), which is widespread in nature and has been known to contaminate peanuts, peanut butter, and milk. Other fungal infections are found in arid regions.
Valley fever or coccidioidomycosis is caused by breathing fungal spores that are naturally found in arid soil. It commonly occurs in the southern San Joaquin Valley of California. Agriculture that disturbs soil can ex- pose people to valley fever as soil erodes. Dust storms are another source of exposure because they erode soils. And dust storms become more severe when land is denuded of natural vegetation by overgrazing, wildfire, or devel- opment that exposes soil to wind erosion. Most people infected with valley fever have no symptoms or experience flu-like symptoms (often in the summer). Occasionally, serious lung disease occurs. Working on soils near Bakers- field, California, in the mid 1980s, one of your authors (Keller) developed valley fever and experienced mild flu- like symptoms for a week or so.
Today, infectious diseases have the potential to pose rapid threats, both local and global, by spreading in hours via airplane travelers. Terrorist activity may also spread diseases. Inhalation of anthrax caused by a bacterium sent in powdered form in envelopes through the mail killed several people in 2001.
Some diseases can be controlled by manipulating the environment, such as by improving sanitation or treating water. Although there is great concern about the toxins and carcinogens produced in industrial societies todaythe greatest mortality in developing countries is caused by environmentally transmitted infectious disease. In the United States, thousands of cases of waterborne illness and food poisoning occur each year. These diseases can be spread by people; by mosquitoes and fleas; or by contact with contaminated food, water, or soil. They can also be transmitted through ventilation systems in buildings. The following are selected examples of environmentally trans- mitted infectious diseases:
• Legionellosis, or Legionnaires’ disease, which often occurs where air-conditioning systems have been contaminated by disease-causing organisms (bacteria).
• Giardiasis, a protozoan infection of the small intestine, spread via food, water, or person-to-person contact.
• Salmonella, a food-poisoning bacterial infection that is spread via water or food.
• Malaria, a protozoan infection transmitted by mosquitoes. • Lyme borreliosis (Lyme disease), transmitted by ticks
(caused by at least three species of bacteria).
• Cryptosporidiosis, a protozoan infection transmitted via water or person-to-person contact (see Chapter 19).
• Anthrax, spread by terrorist activity (caused by a bacteria).
We sometimes hear about epidemics in developing nations. An example is the highly contagious Ebola virus in Africa, which causes external and internal bleeding and kills 80% of those infected. We may tend to think of such epidemics as problems only for developing nations, but such thinking may give us a false sense of security. True, monkeys and bats spread Ebola, but the origin of the virus in the tropical forest remains unknown.
Toxic Heavy Metals
The major heavy metals (metals with relatively high atomic weight; see Chapter 7) that pose health hazards to people and ecosystems include mercury, lead, cad- mium, nickel, gold, platinum, silver, bismuth, arsenic, selenium, vanadium, chromium, and thallium. Each of these elements may be found in soil or water not contaminated by people; each has uses in our modern industrial society; and each is also a by-product of the mining, refining, and use of other elements. Heavy met- als often have direct physiological toxic effects. Some are stored or incorporated in living tissue, sometimes per- manently. Heavy metals tend to be stored (accumulating with time) in fatty body tissue. A little arsenic each day may eventually result in a fatal dose—the subject of more than one murder mystery.
The quantity of heavy metals in our bodies is referred to as the body burden. The body burden of toxic heavy elements for an average human body (70 kg) is about 8 mg of antimony, 13 mg of mercury, 18 mg of arsenic, 30 mg of cadmium, and 150 mg of lead. The average body burden of lead (for which we apparently have no bio- logical need) is about twice that of the others combined, reflecting our heavy use of this potentially toxic metal.
Mercury, thallium, and lead are very toxic to people. They have long been mined and used, and their toxic properties are well known. Mercury, for example, is the “Mad Hatter” element. At one time, mercury was used to stiffen felt hats, and because mercury damages the brain, hatters in Victorian England were known to act pecu- liarly. Thus, the Mad Hatter in Lewis Carroll’s Alice in Wonderland had real antecedents in history.
Mercury in aquatic ecosystems offers an example of biomagnification. Mercury is a potentially serious pol- lutant of aquatic ecosystems such as ponds, lakes, rivers, and the ocean. Natural sources of mercury in the en- vironment include volcanic eruptions and erosion of natural mercury deposits, but we are most concerned with human input of mercury into the environment by, for example, burning coal in power plants, incinerating waste, and processing metals such as gold. Rates of in- put of mercury into the environment through human processes are poorly understood. However, it is believed that human activities have doubled or tripled the amount of mercury in the atmosphere, and it is increasing at about 1.5% per year.
A major source of mercury in many aquatic ecosystems is deposition from the atmosphere through precipitation. Most of the deposition is of inorganic mercury (Hg11, ionic mercury). Once this mercury is in surface water, it enters into complex biogeochemical cycles, and a process known as methylation may occur. Methylation changes in- organic mercury to methyl mercury [CH3Hg]1 through bacterial activity. Methyl mercury is much more toxic than inorganic mercury, and it is eliminated more slowly from animals’ systems. As the methyl mercury works its way through food chains, biomagnification occurs, result- ing in higher concentrations of methyl mercury farther up the food chain. In short, big fish that eat little fish contain higher concentrations of mercury than do smaller fish and the aquatic insects on which the fish feed.
Selected aspects of the mercury cycle in aquat- ic ecosystems are shown in Figure 8.4. The figure emphasizes the input side of the cycle, from deposition of inorganic mercury through formation of methyl mer- cury, biomagnification, and sedimentation of mercury at the bottom of a pond. On the output side of the cycle, the mercury that enters fish may be taken up by animals that eat the fish; and sediment may release mercury by a variety of processes, including resuspension in the water, where, eventually, the mercury enters the food chain or is released into the atmosphere through volatilization (con- version of liquid mercury to a vapor form).
Biomagnification also occurs in the ocean. Because large fish, such as tuna and swordfish, have elevated mercury levels, we are advised to limit our consumption of these fish, and pregnant women are advised not to eat them at all.
The threat of mercury poisoning is widespread. Millions of young children in Europe, the United States, and other industrial countries have mercury levels that exceed health standards.9 Even children in remote areas of the far north are exposed to mercury through their food chain.
During the 20th century, several significant incidents of methyl mercury poisoning were recorded. One, in Minamata Bay, Japan, involved the industrial release of methyl mercury.8 (See A Closer Look 8.1.)
Minamata Bay involved local exposure to mercury. Another example of mercury poisoning is being reported in the Arctic. However, in this case the contamination would be classified as mobile, occurring at the global level, in a region far from emission sources of the toxic metal. The Inuit people in Quanea, Greenland, live above the Arctic Circle, far from any roads and 45 minutes by helicopter from the nearest outpost of modern society. Nevertheless, they are some of the most chemically contaminated peo- ple on Earth, with as much as 12 times more mercury in their blood than is recommended in U.S. guidelines. The mercury gets to the Inuit from the industrialized world by way of what they eat. The whale, seal, and fish they eat contain mercury that is further concentrated in their tis- sues and blood. The process of increasing concentrations of mercury farther up the food chain is an example of biomagnification.9 A recent series of studies by a group of scientists working in conjunction with the U.S. National Park Service found surprising amounts of toxic substances in nine national parks, including mercury, dieldrin, and DDT; they also found serious indications of biomagni- fication through study of fish in the parks. Wind tends to carry contaminants upslope and into higher elevations where they vaporize and condense in cold weather. Hence high, more pristine areas may have greater pollution levels than lower elevations.10
What needs to be done to stop mercury toxicity from the local to the global level is straightforward. The answer is to reduce emissions of mercury by capturing it before emission or by using alternatives to mercury in industry. Success will require international cooperation and tech- nology transfer to countries such as China and India, which, with their tremendous increases in manufacturing, are the world’s largest emitters of mercury today.9
Organic Compounds
Organic compounds are carbon compounds produced naturally by living organisms or synthetically by industrial processes. It is difficult to generalize about the environ- mental and health effects of artificially produced organic compounds because there are so many of them, they have so many uses, and they can produce so many different kinds of effects.
Synthetic organic compounds are used in indus- trial processes, pest control, pharmaceuticals, and food additives. We have produced over 20 million synthetic chemicals, and new ones are appearing at a rate of about 1 million per year! Most are not produced commercially, but up to 100,000 chemicals are now being used or have been used in the past. Once used and dispersed in the environment, they may become a hazard for decades or even hundreds of years. Some synthetic compounds are called persistent organic pollutants or POPs. Many were first produced decades ago, when their harm to the environment was not known, and they are now banned or restricted (see Table 8.1). POPs are defined by several properties:11
• They have a carbon-based molecular structure, often
containing highly reactive chlorine.
• Most are manufactured by people—that is, they are synthetic chemicals.
• They are persistent in the environment—they do not easily break down in the environment.
• They are polluting and toxic. • They are soluble in fat and likely to accumulate in living
tissue.
• They occur in forms that allow them to be transported by wind, water, and sediments for long distances.
For example, consider polychlorinated biphenyls (PCBs), which are heat-stable oils originally used as an insulator in electric transformers.11 A factory in Alabama manufactured PCBs in the 1940s, shipping them to a General Electric factory in Massachusetts. They were put in insulators and mounted on poles in thousands of lo- cations. The transformers deteriorated over time. Some were damaged by lightning, and others were damaged or destroyed during demolition. The PCBs leaked into the soil or were carried by surface runoff into streams and rivers. Others combined with dust, were transported by wind around the world, and were deposited in ponds, lakes, or rivers, where they entered the food chain. First, the PCBs entered algae. Insects ate the algae and were in turn eaten by shrimp and fish. In each stage up the food web, the concentration of PCBs increased. Fish are caught and eaten, passing the PCBs on to people, where they are
concentrated in fatty tissue and mother’s milk.
Dioxin
Dioxin, a persistent organic pollutant, or POP, may be one of the most toxic human-made chemicals in the environment. The history of the scientific study of dioxin and its regulation illustrates the interplay of science and values.
Dioxin is a colorless crystal made up of oxygen, hy- drogen, carbon, and chlorine. It is classified as an organic compound because it contains carbon. About 75 types of dioxin and dioxin-like compounds are known; they are distinguished from one another by the arrangement and number of chlorine atoms in the molecule.
Dioxin is not normally manufactured intention- ally but is a by-product of chemical reactions, including the combustion of compounds containing chlorine in the production of herbicides.12 Dioxins are emitted into the air through such processes as incineration of municipal waste (the major source), incineration of medical waste, burning of gasoline and diesel fuels in vehicles, burning of wood as a fuel, and refining of metals such as cop- per. Releases of dioxins have decreased about 75% since 1987. However, we are only beginning to understand the many sources of dioxin emissions into the air, water, and land and the linkages and rates of transfer from dominant airborne transport to deposition in water, soil, and the biosphere.13
Studies of animals exposed to dioxin suggest that some fish, birds, and other animals are sensitive to even small amounts. As a result, it can cause widespread damage to wildlife, including birth defects and death. However, the concentration at which it poses a hazard to human health is still controversial. Studies suggest that workers exposed to high concentrations of dioxin for longer than a year have an increased risk of dying of cancer.14
The Environmental Protection Agency (EPA) has classified dioxin as a known human carcinogen, but its decision is controversial. For most of the exposed people, such as those eating a diet high in animal fat, the EPA puts the risk of developing cancer between 1 in 1,000 and 1 in 100. This estimate represents the highest possible risk for individuals who have had the greatest exposure. For most people, the risk will likely be much lower.15
The dioxin problem became well known in 1983 when Times Beach, Missouri, a river town just west of Saint Louis with a population of 2,400, was evacuated and purchased for $36 million by the government. The evacuation and purchase occurred after the discovery that oil sprayed on the town’s roads to control dust contained dioxin, and that the entire area had been contaminated. Times Beach was labeled a dioxin ghost town (Figure 8.5). The buildings were bulldozed, and all that was left was a grassy and woody area enclosed by a barbed-wire-topped chain-link fence. The evacuation has since been viewed by some scientists (including the person who ordered the evacuation) as a government overreaction to a perceived dioxin hazard. Following cleanup, trees were planted, and today Times Beach is part of Route 66 State Park and a bird refuge.
The controversy about the toxicity of dioxin is not over.16-19 Some environmental scientists argue that the regulation of dioxin must be tougher, whereas the indus- tries producing the chemical insist that the dangers of exposure are exaggerated.
Hormonally Active Agents (HAAs)
Persistent organic chemicals that interact with the hor- mone systems of an organism, whether or not they are linked to disease or abnormalities, are known as hormonally active agents (HAAs). What happens when HAAs—in particular, hormone disrupters (such as pes- ticides and herbicides)—are introduced into the system is shown in Figure 8.6. Natural hormones produced by the body send chemical messages to cells, where recep- tors for the hormone molecules are found on the outside and inside of cells. These natural hormones then transmit instructions to the cells’ DNA, eventually directing devel- opment and growth. We now know that chemicals, such as some pesticides and herbicides, can also bind to the receptor molecules and either mimic or obstruct the role of the natural hormones. Thus, hormonal disrupters may also be known as HAAs.20-25
An increasing body of scientific evidence indicates that certain HAAs in the environment may cause devel- opmental and reproductive abnormalities in animals, including humans. (See A Closer Look 8.2.) HAAs in- clude a wide variety of chemicals, such as some herbicides, pesticides, phthalates (compounds found in many chlo- rine-based plastics), and PCBs. Evidence in support of the hypothesis that HAAs are interfering with the growth and development of organisms comes from studies of wildlife in the field and laboratory studies of human dis- eases, such as breast, prostate, and ovarian cancer, as well as abnormal testicular development and thyroid-related abnormalities.20
Studies of wildlife include evidence that alligator populations in Florida that were exposed to pesticides, such as DDT, have genital abnormalities and low egg production. Pesticides have also been linked to reproductive problems in several species of birds, including gulls, cormorants, brown pelicans, falcons, and eagles. Studies are ongoing on Florida panthers; they apparently have abnormal ratios of sex hormones, and this may be affecting their reproductive capability. In sum, the studies of major disorders in wildlife have centered on abnormalities, including thinning of birds’ eggshells, decline in populations of various animals and birds, reduced viability of offspring, and changes in sexual behavior.21
With respect to human diseases, much research has been done on linkages between HAAs and breast cancer by exploring relationships between environmental estro- gens and cancer. Other studies are ongoing to understand relationships between PCBs and neurological behavior that result in poor performance on standard intelligence tests. Finally, there is concern that exposure of people to phthalates that are found in plastics containing chlorine is also causing problems. Consumption of phthalates in the United States is considerable, with the highest exposure in women of childbearing age. The products being tested as the source of contamination include perfumes and other cosmetics, such as nail polish and hairspray.21
In sum, there is good scientific evidence that some chemical agents, in sufficient concentrations, will affect human reproduction through endocrine and hormonal disruption. The human endocrine system is of primary importance because it is one of the two main systems (the other is the nervous system) that regulate and control growth, development, and reproduction. The human en- docrine system consists of a group of hormone-secreting glands, including the thyroid, pancreas, pituitary, ova- ries (in women), and testes (in men). The bloodstream transports the hormones to virtually all parts of the body, where they act as chemical messengers to control growth and development of the body.20
The National Academy of Sciences completed a re- view of the available scientific evidence concerning HAAs and recommends continued monitoring of wildlife and human populations for abnormal development and repro- duction. Furthermore, where wildlife species are known to be experiencing declines in population associated with abnormalities, experiments should be continued to study the phenomena with respect to chemical contamination. For people, the recommendation is for additional studies to document the presence or absence of associations be- tween HAAs and human cancers. When associations are discovered, the causality is investigated in the relationship between exposure and disease and indicators of susceptibil- ity to disease of certain groups of people by age and sex.21
As an example, consider the exposure of frogs to a common herbicide in A Closer Look 8.2.
Nuclear Radiation
Nuclear radiation is introduced here as a category of pollu- tion. We discuss it in detail in Chapter 17, in conjunction with nuclear energy. We are concerned about nuclear radiation because excessive exposure is linked to serious health problems, including cancer. (See also Chapter 21 for a discussion of radon gas as an indoor air pollutant.)
Thermal Pollution
Thermal pollution, also called heat pollution, occurs when heat released into water or air produces undesirable effects. Heat pollution can occur as a sudden, acute event or as a long-term, chronic release. Sudden heat releases may result from natural events, such as brush or forest fires and volcanic eruptions, or from human activities, such as agricultural burning. The major sources of chronic heat pollution are electric power plants that produce electricity in steam generators and release large amounts of heated water into rivers. This changes the average water temperature and the concentra- tion of dissolved oxygen (warm water holds less oxygen than cooler water), thereby changing a river’s species com- position (see the discussion of eutrophication in Chapter 19). Every species has a temperature range within which it can survive and an optimal temperature for living. For some species of fish, the range is small, and even a small change in water temperature is a problem. Lake fish move away when the water temperature rises more than about 1.5°C above normal; river fish can withstand a rise of about 3°C.
Heating river water can change its natural conditions and disturb the ecosystem in several ways. Fish spawn- ing cycles may be disrupted, and the fish may have a heightened susceptibility to disease. Warmer water also causes physical stress in some fish, making them easier for predators to catch, and warmer water may change the type and abundance of food available for fish at various times of the year.
There are several solutions to chronic thermal dis- charge into bodies of water. The heat can be released into the air by cooling towers (Figure 8.8), or the heated water can be temporarily stored in artificial lagoons until it cools down to normal temperatures. Some attempts have been made to use the heated water to grow organisms of com- mercial value that require warmer water. Waste heat from a power plant can also be captured and used for a variety of purposes, such as warming buildings (see Chapter 14 for a discussion of cogeneration).
Particulates
Particulates here refer to small particles of dust (includ- ing soot and asbestos fibers) released into the atmosphereby many natural processes and human activities. Modern farming and the burning of oil and coal add considerable amounts of particulates to the atmosphere, as do dust storms, fires (Figure 8.9), and volcanic eruptions. The 1991 erup- tions of Mount Pinatubo in the Philippines were the largest volcanic eruptions of the 20th century, explosively hurling huge amounts of volcanic ash, sulfur dioxide, and other vol- canic material and gases as high as 30 km (18.6 mi) into the atmosphere. Eruptions can have a significant impact on the global environment and are linked to global climate change and stratospheric ozone depletion (see Chapters 20 and 21). In addition, many chemical toxins, such as heavy metals, enter the biosphere as particulates. Sometimes, nontoxic particulates link with toxic substances, creating a synergetic threat. (See discussion of particulates in Chapter 21.)
Asbestos
Asbestos is a term for several minerals that take the form of small, elongated particles, or fibers. Industrial use of asbestos has contributed to fire prevention and has provided protec- tion from the overheating of materials. Asbestos is also used as insulation for a variety of other purposes. Unfortunately, however, excessive contact with asbestos has led to asbestosis (a lung disease caused by inhaling asbestos) and to cancer in some industrial workers. Experiments with animals have demonstrated that asbestos can cause tumors if the fibers are embedded in lung tissue.26 The hazard related to certain types of asbestos under certain conditions is considered so serious that extraordinary steps have been taken to reduce the use of asbestos or ban it outright. The expensive process of asbestos removal from old buildings (particularly schools) in the United States is one of those steps.
There are several types of asbestos, and they are not equally hazardous. Most commonly used in the United States is white asbestos, which comes from the mineral chrysolite. It has been used to insulate pipes, floor andceiling tiles, and brake linings of automobiles and other vehicles. Approximately 95% of the asbestos that is now in place in the United States is of the chrysolite type. Most of this asbestos was mined in Canada, and environmen- tal health studies of Canadian miners show that exposure to chrysolite asbestos is not particularly harmful. How- ever, studies involving another type of asbestos, known as crocidolite asbestos (blue asbestos), suggest that exposure to this mineral can be very hazardous and evidently does cause lung disease. Several other types of asbestos have also been shown to be harmful.26
A great deal of fear has been associated with nonoc- cupational exposure to chrysolite asbestos in the United States. Tremendous amounts of money have been spent to remove it from homes, schools, public buildings, and other sites, even though no asbestos-related disease has been recorded among those exposed to chrysolite in non- occupational circumstances. It is now thought that much of the removal was unnecessary and that chrysolite asbes- tos doesn’t pose a significant health hazard. Additional research into health risks from other varieties of asbestos is necessary to better understand the potential problem and to outline strategies to eliminate potential health problems.
For example, from 1979 to 1998 a strip mine near Libby, Montana, produced vermiculite (a natural mineral) that was contaminated (commingled) with a fibrous form of the mineral tremolite, classified as an asbestos. People in Libby, a town of about 3,000 population, were exposed to asbestos by workers in the mines (occupational exposure) who brought it home on clothes. Asbestos tailings from the mine were also found in landscaping material that for years was used in city parks, schoolyards, and homes. Hundreds of asbestos-related cases of disease have been documented in Libby and asbestos mortality in Libby is much higher than expected, compared to the United States as a whole and to other parts of Montana.27 In 2002 Libby was named a national Superfund site, and in 2009 the EPA declared Libby a public health emergency. Medical care is being provided, and cleanup of the now closed mine and Libby has been ongoing for the last several years.28
Electromagnetic Fields
Electromagnetic fields (EMFs) are part of everyday ur- ban life. Cell phones, electric motors, electric transmission lines for utilities, and our electrical appliances—toasters, electric blankets, computers, and so forth—all produce magnetic fields. There is currently a controversy over whether these fields produce a health risk.
Early on, investigators did not believe that magnetic fields were harmful because fields drop off quickly with distance from the source, and the strengths of the fields that most people come into contact with are relatively weak. For example, the magnetic fields generated by power transmission lines or by a computer terminal are normally only about 1% of Earth’s magnetic field; directly below power lines, the electric field induced in the body is about what the body naturally produces within cells.29
Several early studies, however, concluded that children exposed to EMFs from power lines have an in- creased risk of contracting leukemia, lymphomas, and nervous-system cancers.30 Investigators concluded that children so exposed are about one and a half to three times more likely to develop cancer than children with very low exposure to EMFs, but the results were ques- tioned because of perceived problems with the research design (problems of sampling, tracking children, and es- timating exposure to EMFs).
A later study analyzed more than 1,200 children, ap- proximately half of them suffering from acute leukemia. It was necessary to estimate residential exposure to magnetic fields generated by power lines near the children’s present and former homes. That study, the largest such investi- gation to date, found no association between childhood leukemia and measured exposure to magnetic fields.29-30
In other studies, electric utility workers’ exposure to magnetic fields has been compared with the incidence of brain cancer and leukemia. One study concluded that the association between exposure to magnetic fields and both brain cancer and leukemia is not strong and not statisti- cally significant.31
Saying that data are not statistically significant is another way of stating that the relationship between exposure and disease cannot be reasonably established, given the database that was analyzed. It does not mean that additional data in a future study will not find a statistically significant relationship. Statistics can predict the strength of the relationship between variables, such as exposure to a toxin and the incidence of a disease, but statistics cannot prove a cause-and-effect relationship between them.
In sum, despite the many studies that have evalu- ated relationships between cancer (brain, leukemia, and breast) and exposure to magnetic fields in our modern urban environment, the jury is still out.32, 33 There seems to be some indication that magnetic fields cause health problems for children,34, 35 but the risks to adults (with the exception of utility workers) appear relatively small and difficult to quantify.36-39
Noise Pollution
Noise pollution is unwanted sound. Sound is a form of energy that travels as waves. We hear sound because our ears respond to sound waves through vibrations of the eardrum. The sensation of loudness is related to the intensity of the energy carried by the sound waves and is measured in decibels (dB). The threshold for human hearing is 0 dB; the average sound level in the interior of a home is about 45 dB; the sound of an automobile, about 70 dB; and the sound of a jet aircraft taking off, about 120 dB (see Table 8.2). A tenfold increase in the strength of a particular sound adds 10 dB units on the scale. An increase of 100 times adds 20 units. The decibel scale is logarithmic—it increases exponentially as a power of 10. For example, 50 dB is 10 times louder than 40 dB and 100 times louder than 30 dB.
Environmental effects of noise depend not only on the total energy but also on the sound’s pitch, frequency, and time pattern and length of exposure to the sound. Very loud noises (more than 140 dB) cause pain, and high levels can cause permanent hearing loss. Human ears can take sound up to about 60 dB without damage or hearing loss. Any sound above 80 dB is potentially dangerous. The noise of a lawn mower or motorcycle will begin to damage hearing after about eight hours of exposure. In recent years, there has been concern about teenagers (and older people, for that matter) who have suffered some permanent loss of hearing following ex- tended exposure to amplified rock music (110 dB). At a noise level of 110 dB, damage to hearing can occur after only half an hour. Loud sounds at the workplace are another hazard. Even noise levels below the hearing-loss level may still interfere with human communication and may cause irritability. Noise in the range of 50–60 dB is sufficient to interfere with sleep, producing a feel- ing of fatigue upon awakening.
8.3 Measuring The Amount of pollution
How the amount or concentration of a particular pollut- ant or toxin present in the environment is reported varies widely. The amount of treated wastewater entering Santa Monica Bay in the Los Angeles area is a big number, re- ported in millions of gallons per day. Emission of nitrogen and sulfur oxides into the air is also a big number, reported in millions of tons per year. Small amounts of pollutants or toxins in the environment, such as pesticides, are re- ported in units as parts per million (ppm) or parts per billion (ppb). It is important to keep in mind that the concentration in ppm or ppb may be by volume, mass, or weight. In some toxicology studies, the units used are milligrams of toxin per kilogram of body mass (1 mg/kg is equal to 1 ppm). Concentration may also be recorded as a percentage. For example, 100 ppm (100 mg/kg) is equal to 0.01%. (How many ppm are equal to 1%?)
When dealing with water pollution, units of concen- tration for a pollutant may be milligrams per liter (mg/L) or micrograms per liter (μg/L). A milligram is one-thou- sandth of a gram, and a microgram is one-millionth of a gram. For water pollutants that do not cause significant change in the density of water (1 g/cm3), a pollutant con- centration of 1 mg/L is approximately equivalent to 1 ppm. Air pollutants are commonly measured in units such as micrograms of pollutant per cubic meter of air (μg/m3).
Units such as ppm, ppb, or μg/m3 reflect very small concentrations. For example, if you were to use 3 g (one- tenth of an ounce) of salt to season popcorn in order to have salt at a concentration of 1 ppm by weight of the popcorn, you would have to pop approximately 3 metric tons of kernels!
8.4 Old and New Environmental health problems
When the Black Death (the bubonic plague) struck Lon- don in England in the 17th century, the disease spread so rapidly through the city that the bodies of the dead were stacked like logs on gravediggers’ wagons and dumped in mass graves that still can be found in London today. People of the time blamed the catastrophe of the disease on the wrath of God: Somehow people were not following the will of God faithfully and thus were being punished by disease. Of course, no one contemplated the thought that it was all those people crammed into London at that time that contributed to the spread of disease.
People did not know about infectious diseases and how they were, in fact, spread. However, it is clear that the Black Death had a strong social component related to hu- man society. In the 20th century, the blame for catastrophic disease or pandemic—defined as acute disease that spreads rapidly across wide regions of the planet affecting a high proportion of the population—shifted from God to hu- man-induced environmental damage. The argument went that, because people were penetrating deeply into the for- ests and jungles of the world, disrupting the natural order of the ecosystems, pandemic diseases were released. Some have likened this line of thinking to the modern analogue that God is punishing us for what we have done. Neither of these explanations is correct.40 The bubonic plague (a bacterial infection) remains with us, and several cases have been reported in recent years in the southwestern United States and in Oregon. The plague is also endemic to many parts of California (carried mostly by ground squirrels and their fleas). If not recognized early, the disease can be fatal. Fortunately, it is usually easily treated by antibiotics.
Epidemics and Pandemics
An epidemic is the breakout of a disease over smaller re- gions than a pandemic, sometimes at the scale of a village or two. Many epidemics have occurred from contact with disturbed environments, particularly in the tropics, and may cause much pain and suffering. Modern medicine studies the breakout of an epidemic as soon as possible, in order to prevent the disease from becoming a pandemic.
The idea that new diseases that cause pandemics may come from wilderness areas most likely results from the understanding that HIV, the virus that causes AIDs, most likely originated in the 1930s from the natural environment with which people interacted intimately through consumption of animals from the wilderness. Nevertheless, AIDs did not turn into a pandemic on the human scene until the disease evolved and changed and was transmitted by sexual activity. The disease-causing virus transformed what was a sluggish disease into one that had the explosive ability to be transmitted and that was deadly. Sex is a strong driver, which the disease exploited. The important factor was the change that occurred in the disease when it entered human society; then, what had been a relatively obscure regional disease ballooned into a global pandemic we now know as AIDs.
As is becoming evident, many human pandemics are social phenomena that exist because social conditions in urban areas have allowed the diseases to grow, evolve, and flourish. For a disease organism to flourish and develop into a global pandemic, the organism that attacks humans must be closely linked to our life cycles. For example, the resulting disease must not immobilize us immediately and quickly, or the infection will not have much chance to be passed on to large numbers of people. If poor sanitation exists and people are cramped into tight living areas, then diseases carried by water and feces, such as cholera, are much more likely to spread.
Social Conditions and the Spread of Disease
Two social conditions that are particularly worrisome with respect to future pandemics are environments where health care is provided to a large number of sick people with compromised immune systems, as in hospitals (Figure 8.10); and in large, commercial farms that raise chickens, turkeys, pigs, and other animals that we con- sume (Figure 8.11). It is believed that the next pandemic outbreak will, in fact, most likely come from diseases that evolve and cross over to humans from commercial animal farming activities.40, 41
First, let’s consider hospitals where many people visit because they are seriously ill and where they receive excellent medical care. People in hospitals are exposed to a variety of organisms, and this has led, in some cases, to the development of disease organisms (such as certain types of pneumonia) that may be resistant to most of the antibodies we have used in the past to control disease. It is frustrating to learn that hospitals encourage the emergence of disease-causing organisms in people already suffering from serious diseases. It appears, in some instances, that hospitals can become efficient disease factories that allow the proliferation and spread of dangerous organisms between patients and health care providers.
Most alarming is the fact that, in the hospital environment where people are packed in together, it is possible for organisms to evolve into even deadlier forms that resist the antibiotics that are often being used at hospitals. Antibiotics are substances, including penicillin or streptomycin and tetracycline, that are widely used in the prevention and treatment of infectious diseases. Antibiotics are derived or produced from certain fungi, bacteria, and other organisms found in nature that have the ability to destroy, inhibit, or neutralize the growth of other disease- causing microorganisms. Antibiotics are widely used today to fight disease and also in commercial food production of meat, including cattle, pigs, and chickens.
An example of a recent medical problem with disease resistance is a bacterium that commonly occurs in soils in many environments, including the more arid soils of Iran and Iraq. A particular soil bacterium has raised havoc in some veterans’ hospitals where the bacterium has evidently evolved and become the cause of serious disease—but it is also resistant to antibiotics. This disease infected soldiers returning from Iran and Iraq. The main point, however, is that when the veterans were treated in the facilities where lots of them congregated together, the disease, evidently, was able to evolve quicker than it would have in the natural environment where the bacterium is normally not a problem.40
The most serious concern, however, is not hospitals but large industrial farms where we deliberately pack as many animals as possible into a small area where production of meat can be maximized. For example, in 2011, a serious outbreak of E. coli occurred in Germany that was linked to importation of seeds from Egypt, but, most likely, contamination was thought to result from runoff from animal feed lots or from manure and sewage.41 The connection with the feedlots was apparent, since E. coli grows only in the intestines of humans or animals. Not all E. coli species are dangerous, but new ones are evolving that can resist antibiotics and cause serious health issues.
A second example comes from the considerable worry over pandemic strains of influenza (flu) from animals. Initially, the emergence of H1N1 was thought to be from Asia, and the crossover species was farm-bred birds. However, it turned out that the disease originated from pigs in Mexico. The disease did, in fact, trigger a global pandemic between 2004 and 2007, but the disease never evolved to the state of being deadly for a high percentage of the people infected. Thus, we dodged a bullet, but the emergence of the disease is a giant red flag concerning our animal farms. Probably, the only solution to the transmission of disease from crowded animal farms to people is to change our agricultural practices, moving from giant industrial farms to more diversified, smaller farms that raise fewer animals, use fewer antibiotics, and are sited on more land. For example, beef may be raised on pasture and on the open range rather than in giant feed lots that congregate thousands of animals in a relatively small place. Many perceive that the downside of this would be the price of meat. Around the world, as countries develop, the demand for meat is growing rapidly, and so, to meet these demands, the giant farms have been producing animal protein at an ever-increasing rate. What people will have to decide is whether they are willing to pay more for meat or accept a greater risk concerning their health and the emergence of pandemics from animal farms.
The human factor in the evolution and outbreak of pandemic diseases as a serious problem is linked to several themes of Environmental Science. The first is that human population growth is crowding millions of people into cities of countries where pollution, poor sanitation, and lack of disease-free drinking water create major environmental problems. The second theme, achieving a sustainable world population (carrying capacity), is an important goal to help avoid food crisis and human suffering. Third, health problems that develop in cities can expand to become global in extent. Fourth, science linked to values is important insofar as the decision to minimize existing and future environmental health problems has economic implications in a world where demand for meat is growing rapidly. Finally, we need to continue to take heed of the early warning of emerging diseases from the natural environment, urban environment (crowded conditions and hospitals), and our commercial farms where we raise meat.41 The decisions we make will reflect our values.
8.5 general Effects of pollutants
Almost every part of the human body is affected by one pollutant or another. For example, lead and mercury (remember the Mad Hatter) affect the brain; arsenic, the skin; carbon monoxide, the heart; and fluoride, the bones. Wildlife is affected as well. The effects of pollutants on wildlife populations are listed in Table 8.3.
The potential toxins and affected body sites for humans and other animals may be somewhat misleading. For example, chlorinated hydrocarbons, such as dioxin, are stored in the fat cells of animals, but they cause damage not only to fat cells but to the entire organism through disease, damaged skin, and birth defects. Similarly, a toxin that affects the brain, such as mercury, causes a wide variety of problems and symptoms, as illustrated in the Minamata, Japan, example (see A Closer Look 8.1).
Concept of Dose and Response
Five centuries ago, the physician and alchemist Paracel- sus wrote that “everything is poisonous, yet nothing is poisonous.” By this he meant, essentially, that too much of any substance can be dangerous, yet in an extremely small amount can be relatively harmless. Every chemical element has a spectrum of possible effects on a particu- lar organism. For example, selenium is required in small amounts by living things but may be toxic or increase the probability of cancer in cattle and wildlife when it is pres- ent in high concentrations in the soil. Copper, chromium, and manganese are other chemical elements required in small amounts by animals but toxic in higher amounts.
It was recognized many years ago that the effect of a certain chemical on an individual depends on the dose. This concept, termed dose response, can be represented by a generalized dose-response curve. When various concentra- tions of a chemical present in a biological system are plotted against the effects on the organism, two things are apparent: Relatively large concentrations are toxic and even lethal, but trace concentrations may actually be beneficial for life. Dos- es that are beneficial, harmful, or lethal may differ widely for different organisms and are difficult to characterize.
Fluorine provides a good example of the general dose- response concept. Fluorine forms fluoride compounds that prevent tooth decay and promote development of a healthy bone structure. Relationships between the concentration of fluoride (in a compound of fluorine, such as sodium fluoride, NaF) and health show a specific dose response. The optimal concentration of fluoride to reduce dental caries (cavities) is from about 1 ppm to just less than 5 ppm. Levels greater than 1.5 ppm do not significantly decrease tooth decay but do increase the occurrence of tooth discoloration. Concentrations of 4–6 ppm reduce the prevalence of osteoporosis, a disease characterized by loss of bone mass; and toxic effects are noticed between 6 and 7 ppm.
Dose-Response Curve (LD-50, ED-50, and TD-50)
Individuals differ in their response to chemicals, so it is difficult to predict the dose that will cause a response in a particular individual. It is more practical to predict in- stead what percentage of a population will respond to a specific dose of a chemical.
For example, the dose at which 50% of the popu- lation dies is called the lethal dose 50, or LD-50. The LD-50 is a crude approximation of a chemical’s toxicity. It is a gruesome index that does not adequately convey the sophistication of modern toxicology and is of little use in setting a standard for toxicity. However, the LD- 50 determination is required for new synthetic chemicals as a way of estimating their toxic potential. Table 8.4 lists, as examples, LD-50 values in rodents for selected chemicals.
The ED-50 (effective dose 50%) is the dose that causes an effect in 50% of the observed subjects. For example, the ED-50 of aspirin would be the dose that re- lieves headaches in 50% of the people observed.43
The TD-50 (toxic dose 50%) is defined as the dose that is toxic to 50% of the observed subjects. TD-50 is often used to indicate responses such as reduced enzyme activity, decreased reproductive success, or onset of specific symptoms, such as hearing loss, nausea, or slurred speech.
For a particular chemical, there may be a whole fam- ily of dose-response curves, as illustrated in Figure 8.12. Which dose is of interest depends on what is being evaluat- ed. For example, for insecticides we may wish to know the dose that will kill 100% of the insects exposed; therefore, LD-95 (the dose that kills 95% of the insects) may be the minimum acceptable level. However, when considering human health and exposure to a particular toxin, we often want to know the LD-0—the maximum dose that does not cause any deaths. For potentially toxic compounds, such as insecticides that may form a residue on food or food additives, we want to ensure that the expected levels of human exposure will have no known toxic effects. From an environmental perspective, this is important because of concerns about increased risk of cancer associated with exposure to toxic agents.43
For drugs used to treat a particular disease, the ef- ficiency of the drug as a treatment is of paramount importance. In addition to knowing what the effective dose (ED-50) is, it is important to know the drug’s rela- tive safety. For example, the effective dose (ED) and the toxic dose (TD) may overlap. That is, the dose that causes a positive therapeutic response in some individuals might be toxic to others. A quantitative measure of the relative safety of a particular drug is the therapeutic index, defined as the ratio of the LD-50 to the ED-50. The greater the therapeutic index, the safer the drug is believed to be.44 In other words, a drug with a large difference between the lethal and therapeutic dose is safer than one with a smaller difference.
Threshold Effects
Recall from the discussion of mercury in Minamata that a threshold is a level below which no effect occurs and above which effects begin to occur. If a threshold dose of a chemical exists, then a concentration of that chemical in the environment below the threshold is safe. If there is no threshold dose, then even the smallest amount of the chemical has some negative effect (Figure 8.13).
Whether or not there is a threshold for environ- mental toxins is an important environmental issue. For example, the U.S. Federal Clean Water Act originally stated a goal to reduce to zero the discharge of pollutants into water. The goal implies there is no such thing as a threshold—that no level of toxin will be legally permitted. However, it is unrealistic to believe that zero discharge of a water pollutant can be achieved or that we can reduce to zero the concentration of chemicals shown to be carcinogenic.
A problem in evaluating thresholds for toxic pollutants is that it is difficult to account for synergistic effects. Little is known about whether or how thresholds might change if an organism is exposed to more than one toxin at the same time or to a combination of toxins and other chemicals, some of which are beneficial. Exposures of people to chemicals in the environment are complex. For example, very small exposures to HAAs at certain times have been found to interfere with the endocrine system and cause reproductive problems in both humans and animals. We are only beginning to understand and conduct research on the possible interactions and consequences of multiple exposures.45
Ecological Gradients
Dose response differs among species. For example, the kinds of vegetation that can live nearest to a toxic source are often small plants with relatively short lifetimes (grass- es, sedges, and weedy species usually regarded as pests) that are adapted to harsh and highly variable environ- ments. Farther from the toxic source, trees may be able to survive. Changes in vegetation with distance from a toxic source define the ecological gradient.
Ecological gradients may be found around smelters and other industrial plants that discharge pollutants into the atmosphere from smokestacks. For example, ecological gradient patterns can be observed in the area around the smelters of Sudbury, Ontario, discussed earlier in this chapter. Near the smelters, an area that was once forest is now a patchwork of bare rock and soil occupied by small plants.
Tolerance
The ability to resist or withstand stress from exposure to a pollutant or harmful condition is referred to as tolerance. Tolerance can develop for some pollutants in some pop- ulations, but not for all pollutants in all populations. Tolerance may result from behavioral, physiological, or genetic adaptation.
Behavioral tolerance results from changes in behavior. For example, mice learn to avoid traps.
Physiological tolerance results when the body of an individual adjusts to tolerate a higher level of pollutant. For example, in studies at the University of California En- vironmental Stress Laboratory, students were exposed to ozone (O3), an air pollutant often present in large cities (Chapter 21). The students at first experienced symptoms that included irritation of eyes and throat and shortness of breath. However, after a few days, their bodies adapted to the ozone, and they reported that they believed they were no longer breathing ozone-contaminated air, even though the concentration of O3 stayed the same. This phenomenon explains why some people who regularly breathe polluted air say they do not notice the pollution. Of course, it does not mean that the ozone is doing no damage; it is, especially to people with existing respiratory problems. There are many mechanisms for physiologi- cal tolerance, including detoxification, in which the toxic chemical is converted to a nontoxic form, and internal transport of the toxin to a part of the body where it is not harmful, such as fat cells.
Genetic tolerance, or adaptation, results when some individuals in a population are naturally more resistant to a toxin than others. They are less damaged by exposure and more successful in breeding. Resistant individuals pass on the resistance to future generations, who are also more successful at breeding. Adaptation has been observed among some insect pests following exposure to some chemical pesticides. For example, certain strains of malaria-causing mosquitoes are now resistant to DDT, and some organisms that cause deadly infectious diseases have become resistant to common antibiotic drugs, such as penicillin.
Acute and Chronic Effects
Pollutants can have acute and chronic effects. An acute effect is one that occurs soon after exposure, usually to large amounts of a pollutant. A chronic effect occurs over a long period, often from exposure to low levels of a pol- lutant. For example, a person exposed all at once to a high dose of radiation may be killed by radiation sickness soon after exposure (an acute effect). However, that same total dose received slowly in small amounts over an entire life- time may instead cause mutations and lead to disease or affect the person’s DNA and offspring (a chronic effect).
8.6 risk Assessment
Risk assessment in toxicology can be defined as the pro- cess of determining potential adverse health effects of exposure to toxic materials (recall the discussion of mea- surements and methods of science in Chapter 2). We also discussed risk-benefit analysis in Chapter 3 and ad- dressed risk in terms of possible outcomes weighed against benefits or value (cost). You may wish to review that dis- cussion. Risk assessment in toxicology generally includes four steps:46
1. Identification of the hazard. This step consists of testing materials to determine whether exposure is likely to cause health problems. One method used is to investigate populations of people who have been previously exposed. For example, to understand the toxicity of radiation produced from radon gas, researchers studied workers in uranium mines. Another method is to perform experiments to test effects on animals, such as mice, rats, or monkeys. This method has drawn increasing criticism from groups who believe such experiments are unethical. Another approach is to try to understand how a particular chemical works at the molecular level on cells. For example, research has been done to determine how dioxin interacts with living cells to produce an adverse response. After quantifying the response, scientists can develop mathematical models to assess dioxin’s risk.16,17 This relatively newapproach might also be applicable to other potential
2. Dose-responseassessment.Thisnextstepinvolvesidentifying relationships between the dose of a chemical (therapeutic drug, pollutant, or toxin) and the health effects on people. Some studies involve administering fairly high doses of a chemical to animals. The effects, such as illness, or symptoms, such as rashes or tumor development, are recorded for varying doses, and the results are used to predict the response in people. This is difficult, and the results are controversial for several reasons:
• The dose that produces a particular response may be very small and subject to measurement errors.
• Whether thresholds are present or absent may be debatable.
• Experiments on animals such as rats, mice, or mon- keys may not be directly applicable to humans.
• The assessment may rely on probability and statistical analysis. Although statistically significant results from experiments or observations are accepted as evidence to support an argument, statistics cannot establish that the substance tested caused the observed response.
3. Exposure assessment. This step evaluates the intensity, duration, and frequency of human exposure to a particular chemical pollutant or toxin. The hazard to society is directly proportional to the total population exposed. The hazard to an individual is generally greater closer to the source of exposure. Like dose- response assessment, exposure assessment is difficult, and the results are often controversial, in part because of difficulties in measuring the concentration of a toxin in doses as small as parts per million, billion, or even trillion. Some questions that exposure assessment attempts to answer follow:
• How many people were exposed to concentrations of a toxin thought to be dangerous?
• How large an area was contaminated by the toxin?
• How long were people exposed to a particular toxin?
• What are the ecological gradients for exposure to the toxins that work at the cellular level.oxin?
4. Risk characterization. The goal of this final step is to delineate health risk in terms of the magnitude of the health problem that might result from exposure to a particular pollutant or toxin. To do this, it is necessary to identify the hazard, complete the dose-response assessment, and evaluate the exposure assessment, as has been outlined. This step involves all the uncertainties of the prior steps, and results are again likely to be controversial.
In sum, risk assessment is difficult, costly, and con- troversial. Each chemical is different, and there is no one method of determining responses of humans to specific EDs or TDs. Toxicologists use the scientific method of hypothesis testing with experiments (see Chapter 2) to predict how specific doses of a chemical may affect hu- mans. Warning labels listing potential side effects of a specific medication are required by law, and these warn- ings result from toxicology studies to determine a drug’s safety. Finally, risk assessment requires making scientific judgments and formulating actions to help minimize health problems related to human exposure to environ- mental pollutants and toxins.
The process of risk management integrates the assess- ment of risk with technical, legal, political, social, and economic issues.16,17 The toxicity of a particular material is often open to debate. For example, there is no agreement as to whether the risk from dioxin is linear. That is, do effects start at minimum levels of exposure and gradually increase, or is there a threshold exposure beyond which health prob- lems occur? 16,17,26 It is the task of people in appropriate government agencies assigned to manage risk to make judgments and decisions based on the risk assessment and then to take appropriate actions to minimize the hazard resulting from exposure to toxins. This might involve invoking the Precautionary Principle discussed in Chapter 1.
SUMMARY
• Environmental health is broadly defined as human health and disease associated with environmental factors, in- cluding toxic biological agents and toxic chemicals. In- cluded are adverse health effects of urban development, industrialization, and land use.
• Pollution produces an impure, dirty, or otherwise unclean state. Contamination means making something unfit for a particular use through the introduction of undesirable materials.
• Toxic materials are poisonous to people and other living things; toxicology is the study of toxic materials.
• A concept important in studying pollution problems is synergism, whereby the actions of different substances produce a combined effect greater than the sum of the effects of the individual substances.
• How we measure the amount of a particular pollutant introduced into the environment or the concentration of that pollutant varies widely, depending on the sub- stance. Common units for expressing the concentration of pollutants are parts per million (ppm) and parts per billion (ppb). Air pollutants are commonly measured in units such as micrograms of pollutant per cubic meter of air (μg/m3).
• Organic compounds of carbon are produced by living organisms or synthetically by people. Artificially pro- duced organic compounds may have physiological, genetic, or ecological effects when introduced into the environment. The potential hazards of organic com- pounds vary: Some are more readily degraded in the en- vironment than others; some are more likely to undergo biomagnification; and some are extremely toxic, even at very low concentrations. Organic compounds of serious concern include persistent organic pollutants, such as pesticides, dioxin, PCBs, and hormonally active agents.
• New diseases are emerging: some are from disturbed environments, but a more serious threat is our human environments, including hospitals where sick people are naturally crowded together and large industrial farms where we produce animals for consumption; new dis- eases may evolve in these places and spread to humans.
• The effect of a chemical or toxic material on an indi- vidual depends on the dose. It is also important to de- termine tolerances of individuals, as well as acute and chronic effects of pollutants and toxins.
• Risk assessment involves identifying the hazard, assess- ing the exposure and the dose response, and character- izing the possible results.
Botkin, D. B., & Keller, E. A. (2014). Environmental science: Earth as a living planet (9th ed.). Hoboken, NJ: John Wiley & Sons, Inc
