What Causes MCS?
Physiological and Psychological Hypotheses
Many people with MCS associate one large chemical exposure with their decline in health. Others who report sensitivity to chemicals are not able to cite one specific exposure, but report a series of low-level exposures; and still others do not know what triggered their problems. Many know only that they seem to become ill from common chemicals.
What People with MCS Say About the Cause
One person with MCS said, “I was aware that I arrived at work feeling well and after exposure to people smoking I experienced headaches that lasted the remainder of the day, and nausea, as well.” Some suspect, but can’t be sure of exactly which chemicals caused their problem. For example, one woman who has coped with MCS for six years said, “I do not know the names of chemicals—just that they were the chemicals in a copy machine. I sat four to five feet from a copy machine for three years. I then became sensitive to certain colognes and petro [petroleum]-based products.”
When I asked respondents from Phase II of my research study what they thought caused their problem, more than half said they suspected that they became sensitive by one identifiable exposure, one-quarter said that they had not, and another quarter did not know. The most commonly cited exposures thought to cause MCS were pesticides, remodeling, and workplace renovations. (See Appendix A for a full list of exposures thought to cause MCS.)
The remainder of this chapter will review various scientific hypotheses as to what causes MCS. I have tried to review theories in such a way as to condense academic findings into understandable language. Theories are broken down roughly into physiological and psychological causes; however, many feel that this is an artificial distinction because the brain and behavior are so intricately intertwined. For practical purposes, the division here is into theories that assume MCS is a physiological/medical condition versus those that describe it as a psychological problem.
Physiologically Based Theories
Probably the most general theory regarding the cause of MCS is that people’s bodies are breaking down in response to chemical insults. Much as animals have been found to develop tumors, suppressed immunity, and reproductive problems in response to contaminated habitats, human health is showing harmful effects of environmental degradation.
Systemic Breakdown in Response to Pollution
To many, it makes sense that humans would become weaker in the face of increased environmental contamination. This is the canary down the mineshaft theory. It suggests that increasing numbers of people will experience MCS and other toxic injuries as more and more people are subjected to chemical contamination. This is a generalized hypothesis and does not specify exactly how people’s bodies break down and become damaged or hypersensitive. But nervous system damage figures prominently in a number of theories. Claudia Miller has given a name to this theory – Toxic Induced Loss of Tolerance – and believes that the loss of ability to tolerate poisons is the mechanism for the development of many modern diseases. She has postulated that the shift to understand toxics as causes of illness may be as important as it once was for science to understand germ theory (Miller, 1997).
Limbic Kindling/Neurogenic Sensitization
One hypothesis receiving serious attention is that of limbic kindling through the olfactory-limbic system (Bell 1994; Bell, Miller, and Schwartz 1992). There is a direct pathway from the nose into the central part of the “old” animal brain, or limbic system, which is involved in governing sleep, mood, eating, aggression, and other very basic survival behaviors. It is called “kindling” because kindling in biology refers to the process of sensitizing nerve tissue. For example, if you put a frog’s nerve in a Petri dish, and stimulate it with electrical impulses that individually are too mild to fire the nerve (called “sub-threshold” impulses), eventually, due to the repeated stimulation, that nerve will fire.
Some individuals are thought to have sensitized or “kindled” to low-level chemicals, which trigger serious reactions mediated through limbic pathways. In other words, very small amounts of chemicals can induce reactions that normally would not be expected. Because the limbic system is connected to and involved in regulating so many body systems, its disruption could easily cause many of the symptoms reported by people with MCS. This theory also explains the “spreading” phenomenon where people acquire more and more sensitivities even without further chemical exposures, which has been demonstrated in animal research. Iris Bell (1994) and her colleagues (Bell, Miller, and Schwartz 1992), and Claudia Miller (1992) suggest that limbic kindling is one possible explanation for the development and worsening of MCS.
John Rossi (1996) reviewed the kindling research in a technical but very comprehensive and informative paper and made suggestions as to what type of kindling might be operating in MCS. Studies show that many areas of the brain can be sensitized, but that the limbic system kindles more easily than any other area. Although there are several types of chemical kindling, Rossi (1996) believes that IntraCerebral-Localized (ICL) kindling is the most probable model for MCS. In ICL kindling, a chemical is introduced into the brain of an animal through a narrow glass tube at frequent intervals until localized seizures result. Future chemical infusions cause seizures that are longer and more severe, occur farther away from where the chemical was introduced (causing other parts of the body to be affected), and eventually involve the whole organism. Thus Rossi found parallels to both the increasing severity of reactions and their tendency to spread to an increasing number of chemicals seen in MCS. Rossi suggests that because chemicals can stimulate the brain via the olfactory system, and olfactory bulbs are sensitive to chemical kindling, that repetitive inhaled exposure to low-dose chemicals may trigger responses in the brain’s limbic area. He suggested that although animal researchers have not directly investigated kindling and MCS, they easily could.
Rogers, Miller, and Bunegin (1999) tested male and female rats with acute high level (a one time exposure of 1600 parts per million for 6 hours), repeated low-level (20 weekdays of 80 ppm for 6 hours), sham, or no initiating exposures. On the first day after a 16-day rest period all rats were subjected to and measured on a learning task. Then for 18 weekdays rats were exposed to 1 hour of toluene at 10-ppm and again given the learning task. The rats that had been pre-exposed to either the acute or repeated low-level toluene took longer to learn the task even before the 10-ppm exposure (thus showing persistent effects of the sensitization). They also showed greater effects from the 10-ppm exposures, demonstrating sensitization effects of the pre-exposure. Even the rats without pre-exposure showed some effect from the 10-ppm toluene exposure in what is perhaps the first study to find effects at this low level. The authors think that this is significant given that “[t]he American Conference of Governmental Industrial Hygienists, the National Institute of Occupational Safety and Health, and the Occupational Safety and Health Administration all have occupational (8h/day, 5 days/week) exposure guidelines or limits for toluene of 100 ppm” (p. 366). There were differences in the way that male and female rats sensitized to the toluene as well, suggesting an underlying biological substrate for the apparent gender differences in the distribution of MCS.
Most recently, Martin Pall (2003) has extended the neural sensitization (kindling) hypothesis and postulated in a series of publications that MCS and other conditions including fibromyalgia (FM), chronic fatigue syndrome (CFS), and PTSD are the result of elevated peroxynitrite/nitric acid in biological enzymatic pathways. Pall believes that organic solvents activate N-methyl-D-aspartate (NMDA) receptors in the brain, that create a feedback loop in which both peroxynitrite and nitric oxide are elevated, NMDA receptors become more sensitive, cytochrome P450 then is inhibited by the nitric oxide, and the blood brain barrier made more permeable by the peroxynitrite. Pall sees organophosphate and carbamate pesticides and organic solvents as the primary sensitizers in MCS, and his suggestions are congruent with the self-reported sensitization histories of those with MCS. Pall points out that the inflammatory nature of the proposed feedback mechanism in his theory makes it congruent also with Meggs’ theory of neurogenic inflammation. To date, Pall’s theory is the most broad-based, and accounts for the largest number of characteristics of MCS of any theory.
Xenobiotic (chemical compounds foreign to living organisms) detoxification pathways are responsible for responding to toxicants that enter the body, but because of genetic or acquired variability their effectiveness differs from person to person. Sherry Rogers’ book, Tired or Toxic (1990), explains some of the workings of the detoxification system and reviews some of the problematic pathways specific to MCS. This book also makes suggestions for testing and for replacing nutrients and nutrient precursors (substances that your body uses to make nutrients). (See Appendix C for further reading.)
Toxicants that enter the body through breathing, eating/drinking, or are absorbed by the skin must be detoxified or biotransformed. This means that for excretion, chemicals must be able to be processed for elimination. If your detoxification system is damaged, the excretion process could be too slow with the resultant buildup of poisons; or it could be pathological, and you might actually manufacture compounds that are more—rather than less—toxic. Although many water-soluble compounds are excreted in the urine without metabolizing, fat-soluble compounds must be processed by the body. Rogers (1990) cites studies that show deficiencies in zinc, iron, and molybdenum are common. If you are deficient in one or more of these minerals and thus cannot process toxicants through your detoxification pathways, you may shunt to an alternative pathway to make chloral hydrate instead. This can contribute to your own continued poisoning, since another name for chloral hydrate is “Mickey Finn” or “knockout” drops. One problem is that the same pathways that detoxify environmental chemicals also metabolize alcohol, sugar, and endogenous hormones. So these substances may accumulate if these pathways are not working properly.
It is possible that people with MCS have inherited a genetic weakness in regard to metabolizing toxicants. McKeown-Eyssen et al. (2004) found that women with MCS showed a pattern of genetic differences from women without MCS in genes that control metabolism (detoxification) of toxic substances. The differences were statistically significant and may only scratch the surface of genetic research because the researchers only looked at a small number out of the myriad of possible genetic differences. Likewise Haley, Billecke, and La Du (1999) have cited a study that found a higher incidence of Parkinson’s disease in people who have the R allele of the paraoxonase/arylesterase (PON1) gene. Their own research found that ill Gulf War veterans also were more likely than well controls to have this form (or phenotype) of the PON1 gene that detoxifies organophosphates such as sarin and soman. More importantly, Haley et al. found that low levels of type Q arylesterase in blood plasma were associated with illness. Those vets who had become ill after taking pyridostigmine bromide had lower levels of the PON1 type Q arylesterase activity. The authors believe that these people may have been damaged by the pyridostigmine due to pre-existing genetically low levels of this enzyme. The 10% of veterans who reported a severe reaction to the pyridostigmine may have been demonstrating “a clinical marker for genetically low levels of type Q arylesterase activity” (p. 232). Perhaps most relevant for MCS, Haley et al. believe that some people have genetic polymorphisms that predispose them to organophosphate poisoning.
Inherited porphyria is a deficiency in the enzyme system that synthesizes heme, a component of hemoglobin that carries oxygen to all tissues. Porphyria can also be acquired, or caused by drugs, chemicals, infections (including hepatitis C), and malnutrition. Baker (1994) reported that about half of his chemically injured patients tested positive for porphyria.
Another example of an inherited deficiency is that of the enzyme G-6-PD (glucose-6-phosphate dehydrogenase). G-6-PD predisposes 16 percent of African-American men to greater risk from environmental oxidants, such as ozone and nitrogen dioxide (Rios, Poje, and Detels 1993), much as the sickle cell trait makes African-Americans more vulnerable to aromatic amino and nitro compounds, carbon monoxide, and cyanide than other racial groups.
Many chemicals are capable of inactivating or impairing enzymes, including enzymes that metabolize toxicants. In fact, pesticide manufacturers take advantage of this either by designing active ingredients to wreak havoc on the enzymes themselves, or by adding an “inert ingredient” that harms enzyme pathways and thus keeps the active ingredient in the body longer. Examples of the first strategy are found in organophosphate insecticides that knock out acetylcholinesterase (AcE). Normally, AcE breaks down the neurotransmitter acetylcholine so there is not too much stimulation at once at the nerve junction (the site where chemicals cross from one nerve to another and cause the receptive nerve to “fire”). When AcE is depleted, acetylcholine builds up at the nerve site and the targeted bugs die of convulsions after exposure to the pesticide. Since humans have the same neurotransmitters as bugs, these chemicals also affect us. People may experience a wide variety of symptoms from too much acetylcholine including convulsions, nervousness, excess salivation, nausea, vomiting, abdominal cramps, headache, weakness, tremors, noise sensitivity, and many others.
An example of the second strategy is seen in the addition of piperonol butoxide to the biological insecticide rotenone. By itself, rotenone is very toxic. With the addition of piperonol butoxide to knock out liver enzymes, the poison stays longer in the body, and is thus even more toxic.
The upshot of this is that there is a strong suggestion that people with MCS may have damaged detoxification pathways from environmental insults, but we don’t have much detail regarding which exposures are likely to knock out which pathways. There are studies that show some people are poor sulfate metabolizers and some do not metabolize through the pathway at all. Reduced sulfate metabolism has been found in Parkinson’s, Alzheimer’s, systemic lupus erythematosis, as well as in MCS. McFadden (1996) focuses on Phase II sulfation and points out that sulfation also metabolizes neurotransmitters such as adrenaline, noradrenaline, and dopamine; steroids; bile; progesterone; DHEA; and other drugs and chemicals. Thus, poor sulfation alone can impair many bodily functions and create the poorly understood collection of symptoms called MCS.
Some researchers believe that MCS is primarily the result of immunological damage (Meggs 1992a; 1992b). Many chemicals including formaldehyde, solvents, hydrocarbons, and organochlorines have been shown to suppress immune system functioning in humans (Thornton 1993; Vojdani, Ghoneum, and Brautbar 1992, cited in Duehring 1993a). Other researchers think that the immune problems may be secondary to neurological or other damage.
Helper and Suppressor Cells
The helper/suppressor ratio is often used as one index of immune system health. Helper cells fight pathogens or turn on an immune response, while suppressor cells turn off or prevent a response. Too few helper cells are present in conditions such as AIDS, while too many helper cells are present in autoimmune conditions, such as systemic lupus and multiple sclerosis. Immunological findings in MCS include elevated, normal, and depressed helper/suppressor ratios (Heuser, Wojdani, and Heuser 1992; Levin and Byers 1992). Although a few studies have found too high a ratio of helper/suppressor cells in MCS, more have found the opposite—a reduced ratio. Levin and Byers believe that this may be because immune profiles for those with MCS are unstable early on, but that the profiles stabilize to low helper/suppressor ratios as the disease progresses.
MCS patients may generate antibodies to chemicals, or even to their own tissues, which may activate an autoimmune response where the immune system acts against its own body. Levin and Byers report finding antithyroid and antismooth muscle antibodies in MCS patients, and some chemically sensitive patients may eventually develop full-blown autoimmune disease (Heuser et al. 1992; Levin and Byers 1992). Levin and Byers found that some of their patients developed cancer, lupus, multiple sclerosis, or adult onset diabetes. The authors say, “In our opinion, these patients have a genetic propensity to a specific illness, which was triggered by an insult from an environmental agent. The first symptoms of this triggering were MCS.”
Airway Inflammation and Neurogenic Inflammation
William Meggs (1995a; 1995b) believes that MCS may be mediated by neurogenic inflammation, and develop in a fashion similar to reactive airways dysfunction syndrome, where an airborne insult such as fumes or smoke initiates chronic asthma. In reactive upper-airways dysfunction syndrome, people experience rhinitis (inflammation of the mucous membrane of the nose) following a chemical exposure. Meggs and Cleveland (1993) found that patients with MCS do have nasal abnormalities including increased nasal resistance, cobblestone-like appearance of the pharynx and base of the tongue, swelling, abnormal mucus, and pale mucosa with prominent blood vessels.
Meggs explains that we know that chemicals cause receptors on sensory nerves to produce substance P and other chemicals that mediate neurogenic inflammation. Epithelial cells form the top layer of cells of the mucous membranes and protect the underlying nerve cells. But if the epithelial layer is damaged, nerve cells are more likely to suffer damage from contact with irritants such as chemicals.
We know that MCS also involves symptoms such as confusion and fatigue that are not directly connected with airways. Meggs proposes that these symptoms occur because impulses can travel from inflamed mucous membranes to the central nervous system, where they are rerouted to distant locations to produce neurogenic inflammation at the new site. He refers to this as “neurogenic switching.”
Millqvist, Ternesten-Hasséus, Ståhl, and Bende (2005) added to the evidence for airway problems in those with MCS, finding enhanced sensitivity to inhaled capsaicin (the irritant in hot pepper) in people with sensitivities to chemicals. This enhanced sensitivity included coughing and an increase in nerve growth factor (NGF) and demonstrates “a neurochemical imbalance of the respiratory system in patients with SHR [sensory hyperreactivity]” (p. 850).
With candidiasis, allergies and chemical sensitivities can be caused by an overgrowth of candida albicans and related yeasts that compete with healthy digestive bacteria for space in the gut. Pathological yeasts may become overpopulated in the digestive tract including the mouth and colon, in the vaginal tract (causing repeated yeast infections), and even eventually in internal organs. The yeast growth is seen as being caused by a high sugar diet; the use of antibiotics, steroids and birth control pills; and the elevated hormones that occur during pregnancy. The yeasts are problematic because they manufacture toxins, such as acetaldehyde, which may cause adverse reactions in any number of organs, and may also suppress immunity.
In their mycelium form, the yeasts may grow completely through the intestinal lining creating an opening for undigested food to enter the bloodstream (hence the term “leaky gut”). This presence of undigested food in the bloodstream is thought to trigger allergic reactions to foods. Yeasts are also said to cause headaches, depression, menstrual difficulties, and autoimmune problems. There are a number of tests for this condition, many of questionable accuracy. Often a sugar-free, yeast-free diet is prescribed along with the use of oral acidophilus to add beneficial bacteria to the gut. People with conditions unresponsive to these measures may be prescribed antifungal medications such as Nystatin that kill yeast in the gut, or Nizoral, Diflucan, or Sporanox, which are absorbed into the general system to eliminate yeast in blood and internal organs. The anticandida diet is summarized in chapter five, and suggestions are offered for further reading.
The yeast theory alone probably does not account for the phenomenon of MCS, but may be a component or a secondary effect of the systemic breakdown that occurs.
Undiagnosed Lyme Disease
There is a growing awareness that Lyme Disease can masquerade as other illnesses, is complicated to diagnose, and is resistant to treatment. With the increasing incidence of Lyme Disease, particularly in the Northeast U.S., some are hypothesizing that MCS is really undiagnosed Lyme. Some estimates are that over 18 million people in the U.S. may have Lyme. Some of the misconceptions about Lyme Disease include the beliefs that it is only spread by ticks and that the person must have the bulls-eye rash. The spirochete that causes Lyme (Borrelia burgdorferi) is now thought to spread not only through ticks, but through fleas, mosquitos, mites, sexual contact, food, and even through the placenta. The Spirochete has been found in a variety of human body fluids, in donated blood, and in dairy cattle (http://www.samento.com.ec/sciencelib/sarticles/thegreatimpostor.html). And the characteristic bulls-eye rash, thought to be a marker of possible Lyme infection, never develops in over half of people afflicted.
Because the organism lacks a cell wall and can change shape, it may hide in tissues and may not provoke an immune reaction from the host on a test such as the Western Blot test. Therefore, there are many false negatives on this test and diagnosis needs to be made on the basis of symptom picture (http://www.benabraham.com/html/what_makes_lyme_disease_tick_.html). See Chapter 6 for more discussion of Lyme Disease and its treatment.
Carbon Monoxide Poisoning
Albert Donnay (1999) of MCS Referral and Resources believes that carbon monoxide may be a causal factor in MCS, and has noted numerous descriptions of MCS-like symptoms dating back to Edgar Allen Poe. Donnay believes that illuminating gas poisoning may have caused historical cases of MCS. In fact, some physicians are now experimenting with oxygen treatment in order to clear the body of carbon monoxide.
A teenager named Dilnaz Panjwani has won honors for her research that identified an abnormal metabolite in people with CFS, FM, and MCS. This metabolite interferes with oxygen metabolism, thus starving cells for oxygen. The Environmental Illness Society of Canada has supported her work and there is speculation that the test may become a screening tool for these conditions.
Additional Brain Changes
Chemicals certainly affect brain activity, function, and even structure. Brain activity can be measured by an electroencephalogram (EEG) where electrodes are attached to the person’s head, and brain waves are measured either in the resting state, or when “evoked” by some stimulus (sound, chemical, etc.). People with MCS have demonstrated abnormal EEGs in the resting state and abnormal evoked potentials (purposefully elicited in the lab) during chemical exposure (Dudley 1993).
Those who believe that MCS is caused by changes in the brain often cite the research done with people who had large occupational solvent exposures. People exposed to solvents demonstrated slower brain waves (which means slower cognitive processing) (Morrow, Steinhauer, and Hodgson 1992); decreased activity on a positron-emission test (PET) scan (a measure of brain activity); problems with learning, memory, and attention; and indicators of psychological problems (Morrow, Ryan, Hodgson and Robin 1991). In one study, painters were shown to have more neurological problems in areas such as mood, concentration, sleep, and fatigue than did people in the study’s control group (Hooisma, Hanninen, Emmen, and Kulig 1994).
Tests that show how the brain is working, e.g., brain wave tests (EEG), measures of metabolism (PET scans), and of blood flow (Single Photon Emission Computed Tomography (SPECT) scans), can indicate problems even when tests that measure brain shape/structure (i.e., magnetic resonance imaging [MRI] and computerized tomography [CT] scans) do not. Therefore, a SPECT scan is more likely to provide evidence of brain damage/dysfunction in people with MCS than is an MRI or CT scan, although some people with MCS do show abnormal MRI results as well (Heuser et al. 1992).
There are researchers and writers who believe that MCS is a psychological illness, although they are in the minority and seem to lack a sophisticated understanding of what people with MCS experience. I have included these theories not because I believe they should be taken seriously, but because familiarity with them reduces the likelihood that they can be used against you effectively (forewarned is forearmed). (See chapter nine for a critique of these theories.)
Preexisting Psychological Vulnerability—Anxiety, Depression, and Panic Disorder
Donald Black (1996) has said:
. . . many individuals who receive a diagnosis of EI (environmental illness) suffer from common emotional disorders, such as depression, anxiety, and somatization, and that these illnesses are, in fact, responsible for the high level of symptoms of psychological distress that they exhibit; in these cases, a diagnosis of EI represents a misdiagnosis.
Bornschein, Hausteiner, Zilker, and Förstl (2002) interviewed 264 people with MCS and labeled three-quarters as having at least one psychiatric disorder with the most common disorders being somatoform disorder, affective (mood) and anxiety disorders, and substance problems.
Simon, Katon, and Sparks (1990) found that plastics workers who developed sensitivities tended to have a history of anxiety, depression, and unexplained physical symptoms, but no current psychological symptoms. They concluded that “development of environmental illness related more to an underlying trait of symptom amplification and prior psychological distress than to current psychiatric symptoms or diagnoses.” In other words, previous psychological distress, particularly depression or anxiety, is seen as predisposing people to develop MCS, which is considered to be a different manifestation of psychological illness.
Poonai et al. (2001) report that persons with ideopathic environmental intolerance (IEI) showed higher scores on measures of panic disorder, depression, and agoraphobia than controls. The authors admit that “Although IEI subjects appeared to differ from otherwise healthy controls on a number of psychological measures, it must be emphasized that these scores were all below what has been found for clinical patients with PD, depression, and agoraphobia on these measures” (p. 540). However, this does not stop the authors from musing that perhaps, 1) MCS participants underreported their pathology, or that alternatively, 2) these people are in between the normal population and a clinical sample in their “morbidity.” Translation: crazier than normal but not crazy enough to diagnose.
Part of the preexisting pathology for MCS is sometimes said to be symptom amplification. People are seen as amplifying (or exaggerating) any negative sensations or as being more disturbed than others by noxious odors. Simon (1994) says chemically sensitive patients may exaggerate symptoms from low-level exposure, or normal subtle sensory phenomena, and then attribute those sensations to chemical exposures.
People high in negative affectivity experience more negative moods and emotions, such as anxiety, dissatisfaction, and pessimism. They are more introspective and focus more on negative aspects in regard to themselves and other people. Regardless of health status, people with high negative affectivity report more symptoms than those with low negative affectivity. They pay more attention to their bodies, worry more about symptoms and, because of this, are seen as being at risk for MCS (Pennebaker 1994).
Personality disorders are a category of mental illness and are seen as being long-term exaggerated personality styles. They are not generally understood as intermittent, like acute bouts of anxiety and depression, but are said to appear in late adolescence and to continue throughout life. Personality disorders are seen as being difficult to treat and requiring long-term psychological care. Black (1996) labeled three-quarters of a sample of twenty-three people with MCS as having at least one personality disorder.
Another viewpoint is that people with MCS are somaticizers, that is, people who project their psychological problems onto their bodies and experience them as physical symptoms. The idea of somatization has its roots in Freud’s work. He coined the term “somatic compliance” (cooperation from the body) and said that people who had somatic compliance could place their mental symptoms and conflicts onto the body and then develop hysteria rather than an alternate mental illness.
People who are diagnosed as having somatization disorder are said to have a number of complaints for which no physical cause can be found. Complaints begin before age thirty, persist long term, and impair functioning. At some time during the course of the disturbance, the person must have four pain symptoms, two gastrointestinal symptoms, one sexual symptom, and one pseudoneurological symptom, according to the Diagnostic and Statistical Manual of the American Psychiatric Association (DSM IV). Diagnosticians are ten times more likely to give this diagnosis to women than to men, and four times more likely to give it to African-Americans than to Caucasians (Nevid, Rathus, and Greene 1997).
In a culture that generally discounts women and denies decent health care to minority people, there may be all sorts of biases operating here. Donnay (1997) has cited studies that show that MCS symptoms have only slight overlap with somatization disorder criteria.
Even the psychoanalytic folks (Freudian orientation) are now weighing in with descriptions of how somatic compliance manifests in people with MCS. Henningsson and Sundbom (2000) describe persons with MCS as showing poorer reality testing than healthy persons and avoiding anxiety-provoking stimuli through “blocking maneuvers.” The authors then invoke the French psychoanalytic tradition to describe how these consciously-ignored stimuli then create psychosomatic illness: “Instinctual energy, bypassing the psyche, thus affects the soma directly, with catastrophic results” (p. 816).
Another writer, J. C. Selner (1988), believes that symptoms in response to odors are “traceable to identifiable psycho trauma frequently experienced in childhood, but often continuing into adult life.” Selner says that psycho trauma affects more women than men and that the coping mechanisms that were developed for keeping the trauma at bay tend to deteriorate between the ages of thirty and fifty. Hence, the large numbers of middle-aged women who are diagnosed with MCS. But this is incongruent with population studies that have found MCS to cross gender, race, and age categories.
Selner and Staudenmayer (1992) also subscribe to the child abuse schema and describe “universal reactors” as fragile personalities who feel unsafe in the world due to early childhood trauma. People are seen as having repressed (unknowingly buried) or suppressed (consciously placed out of awareness) memories of childhood abuse. As adults, these individuals are left with depression, anxiety, and poor coping skills; they project the trauma onto external factors, such as chemicals.
Psychological and Behavioral Conditioning
MCS patients are sometimes said to blame chemicals for the angst of modern civilization as well as for their illness. Brodsky (1983) believes that media attention to toxins contributes to patients’ heightened health concerns or “ecofear.” He says, for example:
[U]ncertainty about the presence of toxic substances in the workplace makes intoxication in the workplace a likely projective target for those who feel unwell and in whom physical illness cannot be diagnosed. It is an explanation that places the cause and the responsibility in the environment and avoids the stigma of mental illness that they fear (p. 463).
In some cases, avoidance of chemicals is seen as leading to agoraphobia since people are advised by doctors to avoid crowds, malls, and other places where they would encounter perfumes and chemical vapors. Black (1996) describes a patient who developed reactions that included anxiety, fear, shortness of breath, and dizziness in places such as malls, which would remit soon after she left. This patient is seen by Black as having behaviorally conditioned herself to avoid malls. In other words, she came to believe that she was sensitive to odors, avoided these, and thus conditioned herself to have a more and more restricted life. Black suggests that treatment should include desensitization where “the patient is gradually given increasing exposure to odors and fumes in typical home and work situations.”
Odor conditioning is related to behavioral conditioning, but it is able to actually train physiological responses. To understand odor conditioning, you must understand classical conditioning in psychology. As an example, if I gave you an avocado, and every time you tried to eat it, I whacked you upside the head, you would eventually get nervous when you tried to eat an avocado. Why? The avocado did not cause the knock on the head. I did. But the avocado would become associated with the knock on the head. A fear of avocados would be a conditioned response to being hit whenever you tried to eat one.
Simon (1994) points out that animal studies show that physical processes, such as immune response, can be classically conditioned. The proponents of odor conditioning believe that people with MCS may have had one experience that caused true symptoms in response to a chemical, but that future reactions to the low levels of the same chemical are a conditioned (learned) response to the odor of the chemical and not to any harmful properties of the substance. When repeated encounters with the odor provoke symptoms, and the response has become strengthened, the person has been classically conditioned to experience symptoms when exposed to the odor. Generalization occurs when the conditioned response takes place to stimuli that are similar to, but not identical with the original stimulus. One common example of this is seen when assault victims come to fear people who resemble their attackers. The same model applied to chemical sensitivity posits that someone who has an initial reaction to diesel fuel eventually will come to react to all petrochemicals. Proponents of the odor conditioning theory, such as Bolla-Wilson, Wilson, and Bleecker (1988), believe that this explains why people with MCS respond to more and more chemicals over time.
Van den Bergh, Winters, Devriese and Diest (2002) review the learning/classical conditioning research and conclude that their work and that of others shows that people can be conditioned to react with CO2 (carbon dioxide) symptoms to an odor previously paired with CO2. Thoughts of being stuck in an elevator or sauna and forced to breathe CO2 can then replace the odor and also bring on the symptoms. (So even a person’s thoughts are said to be able to trigger MCS-like reactions.) The effects of this learning are said to persist at least a week, and to be able to spread to other odors if those odors are foul smelling. This learning paradigm holds only for “negative affective valence” stimuli, not for positive or neutral unless the researchers create a negative expectation in the minds of the participants. They do this by contextualizing the exposure as negative through perhaps having the persons read about MCS and environmental dangers beforehand. In this condition, they report being able to condition the person to have symptoms even to a neutral or positive odor. They proceed to warn that environmental education and campaigns may actually “promote the development of MCS as a side effect to beneficial effects for the environment” (p. 150). This odor conditioning is said to be more likely to occur in those with high “negative affectivity.”
The premiere issue of the Journal of Health Psychology published an article on MCS that said that all of the cognitions/thoughts of people with MCS revolve around chemicals (Gomez, Schvaneveldt, and Staudenmayer 1996):
“Psychologically, EI/MCS patients differ from normal patients in personality, attitudes, affect and, most relevant to this research, strength of belief about toxicogenic attribution. We hypothesized that if psychosomatic illness is mediated by belief, then methods for representing beliefs should show systematic differences between psychosomatic patients and other populations” (p. 119).
There were many sophisticated schematics, but the bottom line was that the thought processes of people with MCS have erroneously placed chemicals in a more central position than they belong or than they have in the schemas of “normal people.”
Controversy Affects Treatment Protocols
There is tremendous controversy around the nature of MCS, which ends up as vehement disagreement regarding its treatment. Practitioners who treat MCS as a physiological disorder prescribe chemical avoidance to prevent further deterioration in their patients’ health. Those treating MCS as a psychological disorder advise treating the underlying psychological problem, discouraging chemical avoidance, and altering patients’ beliefs that toxicants are making them ill. These practitioners have been criticized on ethical grounds by physicians who treat MCS as a physiological problem (Levin and Byers 1992; Ross 1992; Ziem 1992). Ziem (1992) reported that several of her patients followed advice not to worry about chemical exposures and were made worse. Practitioners who believe that MCS is psychological in nature criticize avoidance for worsening social isolation and reducing mobility and productivity in people with MCS.
Levin and Byers (1992) believe that MCS has a psychological “overlay” that can distract health providers from the physical nature of the condition. We also know that chemical injury can cause psychological symptoms. For example, Morrow, Ryan, Goldstein, et al. (1989) showed personality disturbances in solvent-exposed workers, and Dager, Holland, Cowley, et al. (1987) describe panic disorder resulting from exposure to organic solvents. Heuser et al. (1992) note that patients with systemic lupus erythematosus often exhibit psychiatric symptoms; they believe that any psychiatric symptoms exhibited in MCS may be neurologically based. In an attempt to separate physiological from psychological indicators, Bell, Peterson, and Schwartz (1995) examined self-reported illness from chemical odors in a nonclinical population and found that people who became ill from chemicals tended to have close family members who had physiological—but not psychological—illnesses. (See chapter nine for more information on the psychological symptoms as well as criticisms of the psychological research.)
A New Generation of “Are They Crazy?” Studies
There are some newer studies that attempt to tease out psychological variables in comparing MCS patients to both normal populations and persons with other health conditions. Kai Österberg and colleagues have done a series of studies of this sort. Österberg, Ørbaek and Karlson (2002) question how persons with MCS can have “neurotoxicologically induced brain dysfunction” when their previous exposures are “as a rule, found to be very faint or nonneurotoxic” (p. 140). The authors gave persons with MCS and matched controls a battery of neuropsychological tests and found differences on only one: a complex reaction time test. They then conclude that “Obviously, neurotoxic brain impairment in the traditional sense is an untenable explanation for the smell intolerance in MCS because of the absence of previous exposure of neurotoxic significance in most cases” (p. 145). (Apparently the authors classify pesticides, solvents, anesthesias, and other sensitizers and “nonneurotoxic,” which seems to fly in the face of the toxicology data.)
In another study published in that same year, Österberg, Karlson, and Ørbaek (2002) compared persons with MCS, patients with toxic encephalopathy (TE), and controls on risk perception, the Karolinska Scales of Personality (KSP), and the Symptom Checklist 90 (SCL-90). There were no differences in risk perception between any of the groups (meaning that persons with MCS did not exaggerate risks). On the Karolinska Scales persons with MCS were elevated on only one of sixteen variables: psychasthenia. On the SCL-90 people with MCS scored higher than controls on Somatization, Depression, and Interpersonal Sensitivity scales, and on the Global Severity Index, a sum total of all of the scales. But the elevations for those with MCS were “moderate” compared with those with TE. The authors then explain that the elevation on the SCL 90 for TE shows that
“responses in inventories to both mental distress and personality traits may be affected even by very slight neurotoxic brain impairment. In the present context, this suggests that it might be completely misleading to view elevated scores on self-rating scales of mental distress and personality as evidence of primary psychiatric disease in MCS cases” (p. 173).
So it seems that in this study, the researchers move toward admitting to neurological effects in MCS. They go further and give their “impression of MCS cases as a basically non-psychiatric group” (p. 173). But they backslide a bit when they say that people with MCS may have “a somewhat more asthenic personality than most people and . . . more sensitive in social relations, more bothered with bodily perceptions, and more prone to depressive reactions” (p. 173). Clearly having trouble pigeonholing this population, they finally conclude: “The MCS syndrome does not fit into either a somato-immunological or a traditional psychiatric explanation model” (p. 174).
The group gets down to the nitty-gritty in 2003 by using an exposure chamber to expose both women with MCS and control women to n-butyl acetate or toluene. Women with MCS showed more mucous membrane irritation and fatigue (physical indicators), but not greater expectancy effects (psychological indicators). The women with MCS also showed poorer (slower) initial reaction times as well as more deterioration in reaction times than controls and did not show learning on an eye-hand coordination task like the control group did (neurological effects) (Österberg, Ørbaek, Karlson, Åkesson, and Bergendor, 2003). Although the authors are not completely able to renounce the somatization possibility in this study, they state in the abstract “The results offer the most support to an irritative basis for multiple chemical sensitivity” (p. 40).
Where Does This Leave Us?
You can see that people are not finished arguing over the causes of MCS. Although I am all for constructive research into etiologies, I believe that we could do two things that would give us much more insight into MCS than comparing people with MCS to “normals” on psychological tests. First, we could listen to people with the condition, as they often have tremendous insight into exactly what happens to them when they suffer exposures. Second, we could invest research money into following populations that are accidentally exposed to poisons to understand the ensuing physiological changes. Gulf War veterans, persons exposed to the chemical cocktail at the World Trade Center bombing, victims of chemical spills, and others could be followed for a better understanding of how the body accommodates to these exposures over time. However, even though the present “are they crazy?” format for research seems to waste valuable time and resources, it may be necessary in order to convince a critical mass of people that MCS is real.