Environmental Toxins as Stressors

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Toxic chemicals and their fumes are physical stressors, as they can directly cause symptoms such as hyperventilation, nausea and vomiting, and in severe poisoning cases, convulsions, unconsciousness, and death (Nadakavukaren, 2000; Weiss, 1997). Toxins Eire also considered environmental stressors, because they are present in environments where we live and work. Pollution, industrial chemicals, and consumer products are forms of environmental stressors. In fact, the medical profession adopted the term "environmental illness" to describe various allergies, chemical sensitivities, and "sick building syndromes" associated with air pollution (Arnetz, 1998).

Psychological factors, such as anxiety concerning potential poisoning, can produce the same physical symptoms as actual toxins, including hyperventilation, headache, and nausea (Wessely, 2002). Depression, a disorder that currently affects almost 10% of people in the United States (National Institute of Mental Health, 2002), is associated with environmental toxins. Depressive symptoms can result both directly from exposure to metals or pesticides (Weiss, 1998), and indirectly, when people feel pessimistic or stressed about the quality of the environment and their ability to effect change.

Environmental, physical, and psychological stressors interact in diseases like asthma. Every year, millions of people suffer asthma attacks, or breathing difficulties due to inflammation or mucus that obstructs their airways (Sarafino, 1998). Almost 300 children die each year from the disorder, making it the second leading childhood killer after accidents; 150,000 are hospitalized (EPA, 2002a). Although asthma is usually caused by irritation from allergens or air pollution (environmental stressors), it can also result from strenuous exercise (physical) or emotional (psychological) responses (Gevirtz, 2000; Sarafino, 1998).

Another example of the interaction between physical, environmental, and psychological stressors was observed following the terrorist attacks on September 11, 2001, and the subsequent anthrax incidents. Public fears about the attacks resulted in 2,300 false reports of anthrax exposure in early October 2001. Wessely (2002) observed that the social, psychological, and economic effects of "mass sociogenic illness" caused by psychological reactions and associated anxiety may be as significant as that which results from actual attacks.

As we write this chapter in summer 2002, the events of September 11, 2001, have faded from most people's everyday thoughts. Yet individuals who worked on rescue efforts at "Ground Zero" in New York or who live in the area are still experiencing serious respiratory illnesses, including asthma and bronchitis caused by exposure to massive amounts of particulate matter and dust (Prezant et al., 2002). Those exposed are at higher risk for cancer because of contact with benzene, PCBs (polychlorinated biphenyls, common industrial chemicals), and asbestos as the buildings collapsed and the debris settled (Ritter, 2002). Many experienced severe psychological trauma from witnessing the attack, or contending with its consequences. Such ongoing adverse impacts do not have the same dramatic appeal as hijacked planes flying into skyscrapers, and thus have not received much media attention. However, the number of casualties or illnesses resulting from environmental toxins far surpasses the few thousand deaths of that day. The World Health Organization (2000) estimates that 3 million deaths occur annually from respiratory and cardiac disease caused by various sources of air pollution. A recent analysis by the Environmental Protection Agency (EPA, 2002d) revealed that two thirds of people living in the United States (200 million people) are at an elevated risk for developing cancer due to exposure to toxic emissions released by automobiles and trucks, power plants, and other industrial sources. As we will see, environmental toxins can also cause neurological, cognitive, and emotional damage.

Many of the substances contained in vehicular and industrial emissions act as persistent bio-accumulative and toxic pollutants (PBTs; EPA, 2002c; also known as persistent organic pollutants; McGinn, 2002). They are persistent, meaning that they can remain in the environment for long periods of time (years or decades) without breaking down or losing their potency. Bioaccumulation means that such substances become more and more concentrated as they move through the food chain, becoming most toxic and potentially fatal later in the consumption cycle. In the 1950s, for example, phytoplankton in Clear Lake, California, absorbed low levels of a pesticide. The chemicals became more concentrated in the fish that ate the phytoplankton, and reached lethal levels in the birds that ate the fish (Nadakavu-karen, 2000). Because humans are at the end of many food chains, at least 40 states have issued advisories, especially to pregnant women, about eating fish that may contain high levels of PBTs.

Behavioral toxicology is the investigation of adverse cognitive and behavioral effects of PBTs (Weiss, 1998). All PBTs, including industrial emissions, heavy metals such as mercury and lead, and pesticides, are stored in fats and other tissues, and build up with repeated exposure (thus the term, bio-accumulative). These substances can be directly toxic by killing or damaging cells, or produce indirect effects by altering endocrine or immune system functioning. The developing nervous system is particularly vulnerable to the effects of toxins, and its study is reflected in the subdiscipline of developmental neurotoxicology.

As many as 1 in 10 women are at risk of bearing children with learning disabilities and other neurological problems because of mercury exposure, putting 375,000 babies at risk annually (Motavalli, 2002b). Mercury, which impacts both pre- and postnatal brain development, acts directly as a neurotoxin. That is, mercury specifically damages or kills neurons, cells in the nervous system. Exposure to neurotoxins is associated with disordered cognitive development, including lowered IQ scores, impairments of memory and attention, and coordination deficits, or in more severe poisoning cases, mental retardation and cerebral palsy (G. J. Myers & Davidson, 2000). Other forms

of industrial chemicals such as PCBs also act as direct neurotoxins. J. L. Jacobson and S. W. Jacobson (1996) reported a difference of as much as 6.2% on IQ scores in children exposed to PCBs. The comparably harmful effects of lead, including retardation, attention deficits, and learning disabilities, are generally well known due to intensive public awareness campaigns. Lead damages neurological systems by interrupting the development of connections between nerve cells.

Even minimal amounts of toxins are cause for concern. As little as one seventieth of a teaspoon of mercury can disperse to contaminate a 25 acre lake for one year (McGinn, 2002). Although consumption of tainted fish is the most common source of exposure, airborne mercury is also quite common. Yet coal-fired power plants and municipal waste incinerators are still releasing mercury. Perhaps more disturbing is the fact that the medical and dental industries use and generate considerably more mercury-containing waste than other sources (Sattler, 2002), and mercury thermometers continue to be sold in most states. Because of consumer ignorance or carelessness in disposing of thermometers, mercury can be found in landfills where it can leach into water supplies.

Numerous PBTs in the form of industrial-use chemicals, manufacturing by-products, and emissions continually contaminate the air, wa-

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ter, and soil. We consume tainted animals or their by-products (milk, cheese, and eggs), and PBTs "are found in everything from plastic wrap to computer terminals" (McGinn, 2002, p. 76). Many active ingredients of common agricultural, home, and garden pesticides also qualify as PBTs. All of these chemicals are a cause for concern because of their potential for causing psychological disabilities including retardation, attention deficit hyperactivity disorder, dyslexia, and autism; these disorders currently affect between 3% and 8% of children (Weiss & Landrigan, 2000). Thus, when Sue's next-door neighbor sprays pesticides on his lawn while carrying his young child in a snuggly on his back, she worries about the long-term implications for the child's development.

During the prenatal period, chemicals enter the placenta from the maternal bloodstream, affecting fetal growth and brain development (Weiss, 1997). PBTs are also present in the fat of breast milk. Breast milk contains levels of toxins that are even greater than that in the mother's blood, so breast-fed infants consume significant concentrations (Weiss, 1997). Young children also encounter higher levels of PBTs than adults, due to what Weiss (2000) called the spatial ecology of childhood. For example, because young children spend considerable time on floors, they stir up and breathe dust and residues, and their contact with dust may be 10 times greater than adults'. Children naturally explore their environments by putting contaminated items into their mouths. Perhaps most disturbingly, many children's toys contain phthalates (pronounced THAL-ates), which are additives that make plastics more pliable. In nonhuman animals, phthalates cause reproductive system abnormalities, birth defects, and cancer (McGinn, 2002). Finally, the fact that children ingest relatively more juice, fruit, and water than adults gives them increased exposure to residues and contaminants in those substances. Thus, "tolerance levels" set by the EPA for pesticide residues on food (EPA, 2002e) do not adequately protect children. The Food Quality Protection Act of 1996 requires regulators to consider these factors as well as possible cumulative effects in setting tolerance levels. However, tests conducted by the Environmental Working Group (2000) determined that dangerous levels of pesticides, including some that have been banned from production, continue to be found on popular foods such as apples. In their words, "two in 25 apples have pesticide levels so hazardous that a two year-old eating half an apple or less would exceed the government's daily safe exposure level" (II 2).

Although most parents are aware of the risks of poisoning through accidental ingestion of household chemicals, an estimated 73,000 children suffered common household pesticide-related poisonings or expo sures in the United States in 2000 alone (EPA, 2002b). Early signs of excessive exposure to some pesticides include nervousness, restlessness, and anxiety; not surprisingly, these symptoms are often improperly diagnosed (Weiss, 1998). More apparent indicators of acute poisoning are headache, weakness, and dizziness. Some pesticides cause severe abdominal pain, vomiting, diarrhea, difficult breathing, and potentially convulsions, coma, and death (Nadakavukaren, 2000; Weiss, 1997).

Moreover, long-term psychological impairment is common. One follow-up assessment demonstrated significantly lower IQ scores and greater deficits in visual-motor integration in children who had initially shown signs of central nervous system effects, such as lack of coordination, poor reflexes, "incoherence, loss of consciousness, [and] lethargy," following pesticide poisoning (Bellinger & Adams, 2001, p. 179). In rural populations where pesticides are regularly applied, frequent contact can produce deficits in balance, hand-eye coordination, and short-term memory in children. Prenatal exposure to a pesticide called chlorpyrifos interferes significantly with neurological development, resulting in brain atrophy and mental retardation.

However, conclusive evidence regarding the effects of environmental toxins, particularly for chronic low level exposure in humans, remains "disturbingly sparse" (Weiss, 1997, p. 246; see Table 5.1). Environmental toxins now bathe the entire planet, and even in the most remote places, people show measurable levels of PBTs in their tissues (Nadakavukaren, 2000); thus no unexposed "control" group exists to compare with exposed populations. Behavioral and cognitive effects from toxins are generally subtle and difficult to diagnose, so they may go unnoticed. In the words of a former director of the National Institute of Environmental Health Sciences, "Suppose that thalidomide, instead of causing the birth of children with missing limbs, had instead reduced their intellectual potential by 10%. Would we be aware, even today, of its toxic potency?" (Rail, as quoted by Weiss, 1998, p. 37).

Despite the lack of good control groups, it is highly likely that toxins combine with other factors to impact the developing brain (Bellinger & Adams, 2001; Weiss, 2000). A relatively small number of children experience clinical poisoning severe enough to require medical intervention (Weiss, 2000). A larger population is affected by subclinical poisoning, detectable by neuropsychological testing. Latent, or "silent," toxicity, "only emerges with additional challenges such as other pesticides, other environmental chemicals, or other health problems, and may not become apparent until additional challenges to function, such as the demands of the classroom, supervene" (p. 377; see Fig. 5.3). Early brain damage (i.e., fetal or neonatal) may not be observable until later in life when the brain is less adaptable (Weiss,

TABLE 5.1

Classification of Environmental Chemicals According to Availability of Data Regarding Childhood Exposure and Developmental Effects

Amount of Information on Childhood Exposures

Little or None

Amount of Information on Developmental Effects

Some

Considerable

Little or none hazardous waste sites municipal

Some incinerators arsenic solvents manganese pesticides cadmium inorganic

PC Bs (low dose) methyl mercury (low dose)2

PCBs (high dose) methyl mercury (high dose)

mercury fluoride

Considerable inorganic lead (high/low dose):

Note: From Bellinger, D. C. & H. F. Adams (2001). Environmental pollutant exposures and children's cognitive abilities. In R. J. Sternberg & E. L. Grigorenko (Eds.), Environmental Effects on Cognitive Abilities, p. 159. © Lawrence Erlbaum Associates, Mahwah, New Jersey. Reprinted with permission.

1PC8s (polychlorinated biphenyls): PCBs are a diverse class of polycyclic hydrocarbon chemicals, now banned in the United States, but once used in a wide variety of industrial processes and products, including dielectric fluids in capacitors and transformers, hydraulic fluids, plasticizers, and adhesives. Current exposures are due primarily to residual contamination of soils and water. The consumption of sport fish taken from contaminated water bodies is a major pathway of exposure.

2Methyl Mercury: Mercury is a heavy metal that occurs naturally in the earth's crust and is released into the atmosphere by geologic processes such as volcanoes. The primary human activities that result in dispersal of mercury into the environment are emissions from power plants and waste incinerators, smelting processes, and industries such as paper mills and cement production. Dental amalgam, the material traditionally used to restore cavities, contains 50% elemental mercury and may produce chronic low-dose exposure. Inorganic mercury can be biotransformed to the organic form, methyl mercury, by bacteria in water body sediments. Methyl mercury undergoes "biomagnification," with tissue concentrations highest among organisms near the top of the food chain. Thus, fish consumption is the primary pathway of human exposure to methyl mercury.

zLead: Lead is a heavy metal that has been mined and smelted for thousands of years. For decades, lead was added to residential paint to increase its durability and to gasoline to boost octane rating. The current primary sources and pathways include leaded paint still in place within homes, soil, and dust contamination resulting from these past uses, drinking water (primarily plumbing fixtures), industrial point sources such as smelters, and food processing procedures.

1998). Thus, diseases including schizophrenia, Alzheimer's, and Parkinson's may originate in prenatal toxic exposure.

As you are probably aware from personal experience, stressors do not affect the body independently, but interact with each other. If you are sick with the flu and stuck in traffic, things will feel worse than if you were dealing with either stressor alone. Similarly, the negative im-

Toxicity Pyramid for Pesticides

/ \ Clinical Pesticide Poisoning

Subclinical Pesticide Poisoning

Latent Pesticide Toxicity

FIG. 5.3. The toxicity pyramid for pesticides is designed to show that, although only a small proportion of children will manifest clear signs of excessive exposure, many more will show effects detectable by neurobehavioral testing, and even more will endure latent or silent toxicity that only emerges with additional challenges such as other pesticides, other environmental chemicals or other health problems. From Weiss, B. (2000). Vulnerability of children and the developing brain to neurotoxic hazards. © Environmental Health Perspectives, 108 (supplement 3), p. 377. Reprinted with permission.

pact of environmental stressors is often compounded by social factors. For example, environmental racism (also known as environmental injustice, as discussed in chap. 3) occurs because relative to higher status groups, minority and low income populations are exposed to more environmental pollution, and environmental and public health laws are often inadequately enforced in their communities (Bullard & Johnson, 2000). Economically disadvantaged and minority groups are more likely to live in regions containing toxic waste sites (Nadakavu-karen, 2000), and lower income families often live in older houses where lead paint was used; roughly one third of urban African American children exhibit elevated levels of lead in their blood (e.g., McGinn, 2002).

Weiss (2000) advanced a conceptual model of how these factors interact. Intellectual development may be more compromised in someone born in a violent neighborhood following poor prenatal care and exposure to pesticides, than someone raised in a more privileged environment who is also exposed to toxins. Weiss' (2000) model illustrates how individual risk factors, none of which alone might exert obvious influence, can jointly produce damaging impacts on development (Weiss, 2000; see Fig. 5.4).

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