Sitting at a table in his home in Snowflake, Arizona, Steen reads a book encased in a clear, plastic box. The front of the box is fitted with two holes to which latex gloves have been attached. Steen inserts his hands into these gloves and demonstrates how he turns the book’s pages using wooden pencils inside the box. When asked why he reads books this way, Steen explains: “The fumes from the ink is a problem for me, and paper itself is, too. You know, I wouldn’t even be able to read a couple of pages before the ink would get to me. Just the ink fumes.”
Steen is a participant in a 2016 short film by The Guardianthat documents the lives of people suffering from what is commonly referred to as ‘multiple chemical sensitivity’ (MCS). Individuals living with MCS experience a range of symptoms – neurological, gastrointestinal, and respiratory – from exposure to what are usually considered safe levels of chemicals present in the environment. These chemicals are found in common products such as pesticides, solvents, paint, fragrances and cleaners. People with MCS typically describe the onset of symptoms as coinciding with an accidental exposure to a specific chemical, or occurring after long-term exposure to one or more chemicals in an occupational setting. Once someone has developed MCS, very low doses of many unrelated chemicals may precipitate their symptoms, severely impacting their daily functioning and overall quality of life.
However, as the Guardian film reveals, those who suffer the symptoms associated with MCS are often dismissed by the mainstream medical establishment; and the validity of the diagnosis as a “real” illness has been repeatedly contested by medical professional associations and societies. Thus, whilst people with MCS maintain that their symptoms are physiological in nature and caused by chemical agents producing biological effects, certain medical entities, in concert with insurance companies and worker compensation organisations, have argued that the condition has purely psychogenic origins (Kroll-Smith & Ladd, 1993; Staudenmayer, 1999). At the heart of these debates is the theme of etiology; what are the causes of MCS symptoms, and on what side of the individual-environment binary do they lie? Etiological explanations of MCS have significant political ramifications, and a number of commentators suggest that the ‘deligitimisation’ of MCS by ‘mainstream’ medicine has been motivated by specific interests (Kroll-Smith & Ladd, 1993; Gibson, 1997).
Today, MCS is variously referred to as universal allergy, 20th century disease, chemical hypersensitivity syndrome, total allergy syndrome, and cerebral allergy. As these names suggest, the experiences of people with MCS point to a deeper epistemological and ontological conflict at the centre of chemical sensitivity. This conflict revolves around who gets to know and what counts as knowledge. More specifically, what kinds of evidence count as ‘real’ in contemporary society, and how does illness and its causes come to be verified?
For instance, chief amongst the arguments of medical professional societies against the validity of MCS are that no clear cause and effect relationships can be identified between specific chemicals and reported symptoms, and that apparent effects occurred at levels of chemicals often orders of magnitudes lower than established ‘toxic’ levels (AAAAI, 1999). On the other hand, those experiencing MCS exhibit an embodied response to what they argue is a toxic world. The implications of these opposing epistemological regimes (embodied, situated etc vs. biomedical, objective etc.) are relevant for all of us, and can perhaps be captured by the question of whether the apparently banal environment of late capitalist consumer culture, with its ubiquitous plasticisers, pesticides and off-gassing materials, is actually dangerous for human health. If MCS is a real condition, and is really caused by low levels of environmental chemicals, then we are all at risk of developing such responses to the environment.
Emerging Patterns of Disease
In Mad Travelers: Reflections on the Reality of Transient Mental Illnesses (1998), philosopher of science Ian Hacking develops a model to understand how new diseases arise at particular times and places. According to Hacking, certain illnesses “thrive” in what he terms particular “ecological niches.” A niche is formed at the convergence of specific historical, social, technical and institutional conditions, and, when these conditions mutate, the illness recedes. Hacking’s model was developed specifically with reference to what he terms ‘transient mental illnesses’; “an illness that appears at a time, in a place, and later fades away…[it may] reappear from time to time” (1998: 2).
Some historical accounts of MCS have argued for a hypothetical continuity between 19th and early 20th century ‘hysterical’ disorders and modern chemical sensitivities, claiming that these ‘new’ diseases are in fact new iterations of old diseases. For instance, historian of medicine Edward Shorter (1997) argues that chemical sensitivity is merely a mass hysteria, identical in form to previous cases, but merely attributed to the presence of new chemicals in the environment. One concern with these accounts is that the diagnosis of ‘hysterical’ conceals more than it reveals; hysteria has often been used as a catch-all diagnosis for any set of physical symptoms with unknown organic causes. Moreover, despite its professed historical grounding, this interpretation of chemical sensitivity is in fact a deeply ahistorical way of explaining the illness. Shorter’s analysis neglects several components of the historicity of newly described diseases; MCS is able to emerge only under the correct conditions (its “niche”); the question therefore is not whether an “illness called MCS/hysteria has or has not always existed but had different names” but rather “under what conditions can/does MCS emerge?” Because MCS emerges under particular institutional conditions it then exercises its own causal efficacy as a category, and it is in this way that any hypothetical continuity between ‘hysteria’ and MCS is disrupted.
Shorter further argues that chemical causes for chemical sensitivity are historically implausible, stating that “the world has been awash for a hundred years in chemicals supposedly responsible for this ‘new’ disease” (1997: 39). According to these arguments, the role of chemicals in chemical sensitivity is of symbolic or psychological relevance only, allowing sufferers to construct an internally consistent ‘belief system’ that validates the reality and organic nature of their physiological symptoms. However, the second half of the 20th century has seen the creation of (tens of) thousands of new synthetic chemicals (and counting), along with thorough reorganisations of built environments and work patterns. All of this has produced a radically transformed chemosphere to which people are now exposed (Miller and Ashford, 1998; see also Murphy, 2006). Claudia Miller, a Texas based physician and researcher who began her career in occupational health, puts these socio-historical considerations into a biological context, stating on her website that:
After World War II, people began using a broad range of synthetic organic chemicals in their homes and work. From cleaning fluids and fragrances, to construction materials and pesticides, many of these chemicals are novel – having been ‘invented’ in the last 70 years. Over this time our genes have not changed. This means our bodies’ elaborate detoxification systems are not equipped to effectively deal with these new substances.
Such substances include the organochloride and organophosphate pesticides, as well as a host of plastic-technologies, pharmaceuticals and other petrochemical derivatives. Through remaining intellectually sensitive to the profound shifts in chemical composition of the built environments and consumer cultures of post World War II, Miller suggests that chemical illness realises an uncoupling between human biology and its modern environment, realised as a result of the contradiction between humanity’s inventive capacities (of synthetic chemicals) and its biological limitations.
Miller’s thesis is that the conjunction of the newly transformed chemosphere with human biology is manifesting in disease processes not encountered before. As a physician, Miller has synthesised her clinical observations of chemically sensitive individuals into a new theory of disease that she terms “Toxicant Induced Loss of Tolerance” or TILT (Miller 1997; 1999). In developing and relaying this model, she repeatedly places emphasis on the importance of taking detailed histories and clinical information from patients suffering from chemical sensitivities. Indeed, through being sensitive to such accounts, the TILT model formalises the internal structure and form of chemical illness and MCS; according to which “sensitivity to chemicals appears to be the consequence of a two-step process: loss of tolerance in susceptible persons following exposure to various toxicants, and subsequent triggering of symptoms by extremely small quantities of previously tolerated chemicals” (Miller 1997). In Miller’s model, large or repeated exposures to chemicals exceed the bodies’ ability to adapt and its homeostatic mechanisms break down. Subsequent exposures are then able to induce symptoms at successively lower doses (Miller 1997; 1999).
In one of Miller’s articles about the TILT model of chemical sensitivity, through drawing reference to the germ and immune theories of disease, the author states that “historically, new theories of disease arose when physicians observed patterns of illness that did not fit accepted explanations for disease at that time” (Miller 1997). She argues that we are currently in such a time and that MCS is such a pattern of illness. Miller’s project, therefore, is the development of a new theory of disease, a theory of chronic diseases specific to late industrial society as triggered by chemical contaminants. Chemical illness presents itself as a new pattern of disease emerging in the interstices of increased environmental chemicals, changing scientific knowledge and medical practice and various socio-cultural factors. It is in this context that the TILT model aims at a thorough overhaul of standard toxicological theory, contributing to ‘scientific debate concerning the origins of disease’ (Miller 1997).
The epistemological shift prompted by MCS reflects the limitations of current models of disease origin in explaining its symptoms. Such a shift can be thought of productively inside Hacking’s ecological niche theory; the constellation of factors surrounding the emergence of chemical illness extends beyond a world ‘awash in chemicals…for hundreds of years’; rather, it is a vast network of visibilities and invisibilities enabled through various medical and social practices. Miller’s formulation of the TILT model contributes to the construction of this illness’ niche, as she is creating “a larger framework of diagnosis, a taxonomy of illness” (Hacking 1998: 2) and it is only within this habitat that MCS can “thrive.”
The Vicissitudes of Biomedicine
By design the TILT model remains neutral with respect to specific biological mechanisms at play in MCS. This is because TILT describes a pattern of illness, one that cannot be captured by a singular biological mechanism but by many potentially overlapping pathways. In her book Chemical Exposures: low levels and high stakes (1998), co-authored with Nicholas Ashford, however, Miller does offer some potential immuno and neuro-mediated mechanisms that might contribute to chemical sensitivity. Another chemical sensitivity researcher, William Meggs, who approaches chemical illness less as a clinician and more as a toxicologist, points out that neurogenic inflammation, identified as early as 1910, is a potential mechanism mediating physical symptoms in response to chemical exposure. In neurogenic inflammation, chemicals activate chemoreceptors on peripheral nerve endings leading to the release of inflammatory mediators. This produces symptoms such as local irritation, coughing, burning etc. Moreover, neuronal signals initiated at chemo-receptors by environmental chemicals may be routed through the spinal and central nervous systems to efferent neurons terminating in tissues distal to the insult site. Inflammatory processes may then be set up at these distal sites, resulting in pain, itching etc. This process, referred to as ‘neurogenic switching’ helps to explain the multi-organ system symptoms of chemical sensitivity and exemplifies objective processes that may underlie ‘unexplained’ symptoms in response to environmental chemicals (Meggs, 1995; 2017). Meggs also draws our attention to the ‘common chemical sense’ that renders the human organism exquisitely sensitive to chemicals present in the environment and provides a potential physio-anatomical substrate for chemical sensitivity (Meggs, 1993). The mucous membranes of the nose and throat, as well as the epithelial cells of the eyes and airways are densely innervated with chemo-receptive neurons. Activation and over-activation of these neuronal pathways by environmental chemicals results in their remodelling, leading them to become super-sensitive to future exposures.
More recently, mechanisms involving chemo-reception and neuronal sensitisation have been subsumed into psychobiosocial models of MCS (Bell et al. 1996; 2001; Nordin, 2020). This research, often coming out of psychology and psychiatry departments, culminates in notions of ‘allostatic load’ which distribute the causes of chemical illness amongst many different (social, biological, genetic) factors and events dispersed in time and space, with no true initiating ‘cause.’ In these analyses, which build on basic biological mechanisms and pathways to (re)-render chemical illness a misinterpretation by the body that the environment is dangerous, chemical exposure becomes just one factor in the calculus of disease. This hypothesis, which stands in contrast to Miller’s two-step TILT model, also relies on a psycho-biographical situatedness of the subject to explain chemical sensitivity, and tends toward locating illness in individual idiosyncrasy rather than environmental exposure.
As the above examples make clear, biomedicine has had a fraught relationship with MCS, and seems to paint the picture of a case in which the experimental paradigm, the test performed, and the expert knowledge deployed embodies the very assumptions being assessed.
Regimes of Perceptibility
Different approaches to the study of MCS, both within and outside of biomedicine, constitute what Michelle Murphy terms “regimes of perceptibility.” It is through the specific practices of scientists, toxicologists, psychologists, lawmakers, etc. that certain aspects of chemical illness are rendered legible or illegible. Biomedicine’s job is therefore not to unearth the ‘essence’ of chemical illness, but to ‘illuminate’ certain facets of it, whilst at the same time (intentionally or not) interacting with its object of study. As Murphy writes in the introduction to Sick Building Syndrome and the Problem of Uncertainty: Environmental Politics, Technoscience, and Women Workers (2006), “the ‘very terms’ of the question of ‘is it real or not…can be understood as an effect of historical processes” (18). Biomedicine has played a central, if equivocal, role in such processes.
Thinking about MCS in the context of “regimes of perceptibility’” therefore challenges the authority of one specific discourse and knowledge system in accessing and representing the ‘true’ ‘nature’ of chemical illness. This perspective also allows for a different perspective on the contested nature of chemical illness, as well as some of its political implications.
In one sense, a parallel may be drawn between Freud’s 18th/19th century ‘hysterics’ and the chemically sensitive individuals of today. This parallel, however, is not between the ‘essences’ or ‘true natures’ of the illnesses, but between how both of the illnesses have been contested over time and provided fertile ground for development of feminist epistemologies.
Freud’s ‘hysterics’ were predominantly women subjects who exhibited many ‘mysterious’ physical symptoms that were, similarly to MCS today, unexplainable by recourse to organic or physiological knowledge available at that time. Using his method of psychoanalysis, Freud argued that these women ‘somatised’ or physically manifested mental traumas, which he invariably ascribed to sexual incidents. For instance, Freud remarked of Dora, his most famous hysteric, that her cough and aphonia were expressions of her (repressed) desire for oral sex with her father. In response to Freud’s interpretations, many commentators have since located the origin of the hysterics’ trauma within patriarchal oppression, arguing that the hysterics’ body registered the oppressive forces against which it contended (Hunter, 1983; Moi, 1981, Ramas, 1980).
These shifting understandings of hysteria were afforded not by the illnesses’ niche, but by an intellectual or ‘scholarly niche.’ In the case of hysteria, there was a temporal gap between its descriptions and interpretations by Frued (1890s – 1900s) and its reclamation within feminist psychoanalysis (1980s – 1990s) whereas with MCS today, its delegitimisation is synchronous with its contestation. The parallel between MCS and hysteria is that both conditions are contested, being understood differently by people in different positions using different frameworks of understanding.
These different understandings are not relative, however. And although one may be no more ‘true’ than another, they each prescribe vastly different courses of political and ethical action. A good question to ask is why is mainstream medicine or ‘society’ hesitant to take the bodily symptoms of chemical illness literally, that is, as the effects of chemicals present in the environment? Some scholars argue it is because they do not want to hear the message of the environmentally unwell and chemically sensitive person (Hosey, 2011; Gibson, 1997). The chemically sensitive person’s body knows something that consumer and petrochemical culture is ‘aggressively uninterested in’ (Hosey, 2011) precisely because it is an accusation of the unsustainability and toxicity of that very culture.
Thus, whilst reading hysteria as a symbolic and metaphorical disease could be co-opted within a psychoanalytical framework that reclaimed it for feminist ends, viewing chemical illness as metaphorical risks “shift[ing] attention away from the toxic chemicals and consumer practices that might result in illness? (Hosey 2011). Some feminist critiques argue that what renderings of chemical illness require is not a shift internal to the psychoanalytic and metaphorical tradition that focuses on the immaterial and socially constructed causes of disease, but a shift from this tradition to a material understanding of toxic chemicals and their impacts on bodily health.
Within such situated feminist epistemologies, the body is conceived of as being coextensive with its environment and ever porous to it. This ‘transcorporeal’ nature of the body means it acts as a truthful, meaningful and relevant registration of the environment’s health, despite the claims of an ‘objective’ biomedicine. This is evident in Stacey Alaimo’s (2010) encouragement for us to interpret the bodily symptoms of MCS metonymically. She argues that the deterioration of bodily functions in chemical illness participates in a ‘chain of material significations in which environmental illness extends the body outward into a trans-corporal space’ (2010: 115). In other words, Alaimo argues that a toxic and unwell body implicates a toxic and unwell environment. As the biomedical research reviewed above makes clear, however, these ways of knowing the world are not squarely opposed. A number of the disease models and physiological mechanisms reviewed above are part of a line of research that can be seen as both ‘scientific/objective’ and ‘situated/embodied’ and can participate productively in critical and feminist projects.
The need for ongoing evaluation of our epistemologies to reflect the changing social and material aspects of existence is underscored well by MCS, as are the political implications of our favoured epistemological regimes. From this perspective, which is relevant for us all, the focus of chemical sensitivity research must extend beyond the unwell individual and onto society, its material practices of chemical production, usage, circulation and contamination, and must continue to be addressed from a number of interdisciplinary and critical perspectives.
Aaron Bradshaw is currently a postdoctoral researcher working at University College London (UCL). Bradshaw’s lab-based work focuses on modelling the biology of neurodegenerative disease in cell culture models. Bradshaw has recently begun focusing more closely on the sociology and philosophy of science, and, in theoretical research, attempting to draw links between the ‘natural’ and the ‘social’ sciences to gain new perspectives on both. Bradshaw has a BSc in Pharmacology from the University of Leeds, a PhD in Cellular Neuroscience from UCL and a Graduate Certificate in Psychosocial Studies from Birkbeck College, University of London.
 Snowflake, Arizona: where the residents are allergic to life. Available at: https://www.youtube.com/watch?v=sMzEmvv48pE&t=86s
 These ‘regimes’ are neither entirely opposed nor completely stable. One question is whether or not they are incommensurable. I address this towards the end of this essay.
 From “TILT – A New Class of Diseases: How Exposures to Chemicals are Undermining Our Mental and Physical Health,” available at http://new.drclaudiamiller.com/
 ‘Allostatic load is defined as ‘the cost of chronic exposure to elevated or fluctuating endocrine or neural responses resulting from chronic or repeated challenges that the individual experiences as stressful’ – from Sciencedirect.
 It is important to note that these models (especially Bell et al. 2001) are also explicitly gendered in their explanations of chemical illness. Bell et al. (2001) comment on how females, by virtue of their biology, are more prone to neuronal sensitisation than males. This aspect doesn’t invoke individual idiosyncrasy to explain chemical sensitivity, but constructs sensitivity as an intrinsic feature of female biology. A number of publications deal explicitly with chemical illness from a feminist perspective. See, for example, Gibson, 1997; Hose, 2011; and Murphy, 2006 chapter 3 especially.
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