CENTER ON BEHAVIORAL MEDICINE
ADDITIONAL MATERIALRELATED PAPERS
by the author to reproduce this paper:
Into Thin Air: Exploring Cases and Causes of Phantom Fumes
Jerimy G. Blowers
The strange events
Mattoon, Illinois in the mid 1940s presents an enigma persisting into
times. However, the mystery surrounding seemingly random and
attacks by “Mad Gassers” is illuminated through the lens of
medicine paradigm. This paper explores the environmental constituents,
most likely pesticides, which induced hysterical reaction in a
SECTION I: Overview of Phantom Illness and Potential Contributing Factors
The year is 1944 and the war-weary United States is nearing the end of a long and costly world conflict. The loss of many brave servicemen and women paint a picture that the world is far from safe; fears of a distant enemy fall like shadows upon the minds of many. The once welcoming countryside now slips under a blanket of darkness as pondering the unknown fate of nations weighs heavy on restless thoughts. Perhaps this backdrop provided a perfect stage for one of the greatest drama-mysteries of the past century. The sudden appearance of “Mad Gassers,” as history now knows them, offers an interesting glimpse into a very strange and intriguing set of events.
One of the most prominent phantom attacker cases unfolded in the town of Mattoon, Illinois. According to author Jerome Clark (1999), whose name is associated with the investigation of many unexplained puzzles, Mattoon ranked as a relatively “small east-central Illinois town,” recording nearly 16,000 people in 1940 (p. 446). The attacks themselves, starting with the first, fit an identifiable pattern involving an unknown assailant(s) assaulting residents with the use of an unidentified gaseous substance. Assassins, armed with toxic vapors, used the cloak of darkness in selecting residences for potential attack. These perpetrators then used unidentified means in forcing the gas into designated homes, only to be seen disappearing into the night. A previous event, occurring in 1933, carried a parallel etiology of events (Clark, 1999); the author dismisses the latter incident’s influence on Mattoon, although the happenings are strikingly similar. Both cases described a distinctive odor often accompanying the attacks. Those seemingly preyed upon experienced “nausea, paralysis, facial swelling and unconsciousness” (p. 450) subsequent to the actual gassing incident. Physical illness and attack frequency would logically yield eventual clues to this string of brash and poignant strikes. Alas, only a few bits of information exist in offering any explanation.
Very few tangible clues remain in solving one of the most mysterious enigmas of the recent past. Aside from a woman’s footprints, lipstick tube, and a piece of cloth, little data exists suggesting the deliberate coordination of such wide spread incidents. Probably the most helpful bit of physical evidence consists of an oily substance found at one alleged crime scene consisting of “sulfur, arsenic, and mineral oil” (Clark, 1999, p.450). Such ingredients remain consistent, the author contends, with pesticides.
A second offering involves the presence of a nearby chemical factory in Mattoon, which produced the pesticide carbon tetrachloride. Clark (1999) contends that no satisfactory explanation is ever given for the industrial unit’s failure in impacting “Mattoon residents prior to August 31,” the premier gassing event (p. 449). However, this man-made material is extremely volatile and carries many of the same exposure symptoms as that experienced by phantom gas victims (Agency for Toxic Substances and Disease Registry, 1995). This very fact provides some tantalizing questions that demand answers utilizing the modern knowledge of a body-mind paradigm.
The premise of this paper rests with the contention that attacks suffered by the residents of Mattoon and related incidents are real. Certainly, individuals succumbed to an unseen foe that crept silently into one’s room, bringing illness and fear. This enemy, however, represents neither ghost nor flesh and blood attacker; the real culprit is much more complex in nature. Sifting through the limited evidence armed with the knowledge of body-mind interaction reveals the most plausible explanation. Victims of ‘Mad Gassers’ fell prey to the influence of noxious chemicals upon one’s own physiological and psychological being; solving the obscurity requires a more rational analysis of existing facts. The extraction of these truths requires a closer examination of toxic substances and relative impact on the human organism.
Found in the previous cases, all victims experienced a distinct smell accompanied by feelings of sickness, muscular paralysis and loss of consciousness. Sightings of the culprit(s) also ensued, yet despite circumstantial evidence (i.e. footprints); the offenders remained elusive (Clark, 1999). This fact suggests that sufferers also succumbed to visual hallucinations in the progression of this event. Several studies point to a similar set of symptoms, all centering on the exposure to poisonous agents. For example, contact with hydrogen cyanamide, used in aiding vegetation growth, produces many negative consequences. Sickness, breathing distress, sedation, sensory disruption and diffuse mental clarity all manifest with chemical contact (Morbidity and Mortality Weekly Report, 2005). Bradberry, Proudfoot and Vale (2004) contend that herbicides produce distinct consequences as well; visual disturbances and paralysis result from this chemical classification. Basic sequencing of a toxic response in each case involves an individual coming in contact with the agent followed by a discrete set of consequences on multiple body symptoms. Agricultural compounds represent only one possibility; many other agents exist, promoting a wide array of effects on the human body.
Establishing the definitive impact of herbicides and growth enhancement products, exploring alternative environmental causes is also important. One contemporary theme is that of ‘sick building syndrome.’ This malady is defined as “non-specific complaints, including upper respiratory irritative symptoms, headaches, fatigue, and rash which are usually associated with a particular building by their temporal pattern of occurrence and clustering among colleagues of inhabitants” (Redlich, Sparer & Cullen, 1997, p. 1013). The contributing environmental factors to this phenomenon commonly reflect the presence of mold and fungi sources (Scheel, Rosing & Farone, 2001; Kilburn, 2003; Straus, Cooley, Wong & Jumper, 2003; Laumbach & Kipen, 2005). Even building materials (Lundholm, Lavrell & Mathiasson, 1990) and interior conditions appear as dismantling occupant health status (Li, Hsu & Tai, 1997; Reinikainen & Jaakkola, 2001). Aside from sick building constituents, other substances in one’s surroundings contribute toward physical and psychological illness.
Research into the immense damage caused by heavy metals and related elements remains plentiful; examples of contemporary concern are mercury (Trasande, Landrigan, Schechter, 2005; Zahir, Rizwi, Haq & Khan, In Press), lead (Alkondon, Costa, Radhakrishnan, Aronstam & Albuquerque, 1990), thallium (Peter & Viraraghavan, 2004), Cadmium, and Nickel among others (Pulido & Parrish, 2003). The influences of these metals possess great potential in producing physiological problems as well as psychological abnormalities. Mercury provides an excellent illustration; its poisoning is sometimes characterized by Erethism, a condition mimicking symptoms of psychosis through erratic and anomalous behaviors (Volz, Weaver & Shooltz, 1997). This interface between environment, physiology, and mind urges a more detailed examination of psychological states.
Understanding that mental state constitutes both a preceding factor and result of present toxic stimuli (Bauer, Greve, Besch, Schramke, Crouch, Hicks, Ware & Lyles, 1992), examining this premise remains important in establishing a link between human poisons and psychiatric expression. Individuals themselves may possess a predisposition toward outcomes after chemical exposure, as demonstrated by Hudnell, Otto, House & Molva (1992). Taken in context, the interaction of all factors may illuminate the mysteries of phantom illness; isolating potential components now requires placing each element in its proper place in solving the mystery at hand.
Section II: Exposing the Phantom: Specific Contributions to ‘Mad Gasser’
Information presented in
section outlines the development of ‘Mad
Gasser’ events as
recounted by Clark (1999). Also previously suggested, such happenings
not represent solitary, isolated events. Similar attacks and unknown
smatter both past and present times, creating a wave of hysteria among
the populous (Knight, Friedman, Sulianti, 1965; Stahl & Lebedun,
Pesticides are known for being very effective in eliminating unwanted insect populations, but remain equally notorious for incidental human poisonings. Reviewing the properties and types of industrial repellants (Weiss, Amler & Amler, 2004), many produce symptoms consistent with those reported by allegedly gassed victims. For example, toxins inhibiting acetylcholine esterase function may induce paralysis (Weinbroum, 2005); chloroform, once utilized as an anesthetic, initiates unconsciousness (Occupational Safety and Health Administration, n.d.). However, the strongest pesticide examples paralleling ‘Mad Gasser’ syndrome are carbon tetrachloride and chloroform (Environmental Defense, 2004; Occupational Safety and Health Administration, n.d.). A comparative review of the known evidence gathered from Mattoon ‘Mad Gasser’ reports as well as facts regarding carbon tetrachloride and chloroform is displayed in Table 1.
Mechanism of Action
Dissecting the mechanisms of action between the two suspect toxins, tetra hydrochloride and chloroform command a basic understanding of an insecticide’s main ingredients. Weinbroum (2005) asserts that the main action of highly potent pest control chemicals centers on nicotinic and muscarinic systems. The action or inhibition of these acetylcholine receptors plays an expansive role in the central nervous system; the timulation or blocking of receptors increases synapse firing or, in some cases, induces muscle paralysis (Carlson, 2001). Action on the muscarinic receptor sites by a receptor antagonist “are considered second tier agents for the treatment of symptoms of parkinsonism,” arresting the excess movement of muscles in the disease’s characteristic tremors (Julien, 2005). Examples of humans being impacted by organophosphates, which operate on these same receptor sites is not uncommon. The case of a young person affected through a low –dose pesticide poisoning exhibited manifestations including disrupted cardiovascular, respiratory, and neurological disruptions. Also noted are loss of muscle control and unconsciousness (Mattingly, Sullivan, Spiller & Bosse (2003). Taking all of the facts presented thus far, the incidental intake of pesticides appears as a plausible explanation for Mattoon victim’s physiological symptoms. Nausea, paralysis, and unconsciousness experiences all fit with the toxicity of strong insecticide agents. The presence and type of hallucinations invite further questioning regarding individual mind states.
All physical evidence supports the introduction of toxic environmental compounds whereas the advent of hallucinogenic phenomenon appears as yet another unknown. Contrarily, production of phantasms in this case meshes precisely with presented data when examining the interface of body-mind elements. hemical-induced mental illusions are witnessed through a variety of examples; many substances acting in complex ways upon select receptors and neurotransmitters is well established (Bradbury, 2004; Julien, 2005). Likewise, researchers such as Dalton (1999), suggest that mental variables play a significant part in a human being’s reaction to environmental stimuli. Particularly, investigators confirmed this premise in uncovering diverse individual tolerances for olfactory stimuli stating that “the observed differences in suprathreshold perceived odor and irritation…are reflective of a cognitive or affective appraisal of the odor rather than a change in sensitivity” (p. 585). Bauer et al. (1992) support this contention, reinforcing the exploration of psychological factors when studying the impact of outside agents.
Application of this logical progression to the enigma in Mattoon, experienced hallucinations reflect two important points. First, the perception of ambiguous invaders, gassing hapless victims is consistent with the time period’s psychological mindset. War is a frightening prospect during any era, and the consistent, looming threat of an invading force certainly taxes the psyche in unfathomable ways. Fears of being assaulted under the cover of darkness became a theme woven into toxin provoked illusions. The advent of night assault implicates vulnerability and the heavy, summer evening air most likely allowed chemicals from the nearby plant in settling closer to ground level. Therefore, town occupants possessed a much greater opportunity in breathing these poisons. A second consideration is the fact that only a select grouping of residents experienced the confrontations. This is best explained through the individual sensitivity, both corporal and mind, of the seemingly ‘chosen’ sufferers. Spreading the frequency of assaults from this point fell into the real of expanding hysteria, a happening not isolated to war-time (Knight et al, 1965; Stahl et al., 1974). One may also speculate that the use of gas as a known and abhorred combat weapon paired the real-life vapor exposure with that of an imagined, but robust, threat. Chasing the ghosts of Mattoon through the utilization of a body-mind paradigm establishes that the happenings constituted neither hoax nor assault by an unknown enemy. Instead, the intriguing interaction of environment, body, and mind produced one of the country’s greatest obscurities.
Testing for the presence of heavy metals and other poisons did not attain the sophistication, in the 1940s, as experienced in contemporary times. Superimposing modernized evaluative procedures on the resident of Mattoon potentially involve the utilization of three analytic methods: body fluid, hair, and electromagnetic imaging studies. Each procedure supplies a piece to this complex puzzle and used together, guide the detection, prognosis, and treatment of insecticide poisoning. Ruling out a plethora of physical and psychological conditions is always a valid premiere step in determining the presence of any ailment. Drawing upon the facts of the Mattoon case, structural interviews regarding mental health status and medical history are warranted. Investigation in this way lessens the potential for psychiatric illness and non-related physical conditions in confounding true diagnoses. Once this is accomplished, a testing of body fluids for the existence of harmful compounds is prudent. Dependent on the suspect chemical classification, blood, urine and other exams remain appropriate (Pagana & Pagana 2002).
Hair testing is a procedure gaining recognition in detecting a variety of influences on psychological state. Since the presence of carbon tetrachloride is depleted rapidly in the body (Agency for Toxic Substances and Disease Registry, 1995), hair analysis represents a logistical examination choice. Zakrzewski (1993) presents a compelling case for the use of this tool, citing its ability in uncovering a variety of corporal pollutants. Thus, securing an inspection of Mattoon victim’s hair significantly increases the chances for discovering the offending environmental agents over an extended period of time.
Finally, the development of electronic, neurological imaging establishes a tool intricately exploring physiological micro-environments. Magnetic Resonance Imaging (MRI) and Positron Emission Tomography (PET) enable the observance of respective physical damage and neural activities in the brain (Carlson, 2001). These tests are potentially helpful, coordinating with the other mentioned investigative methods, in determining both presence and scope of toxin-induced neurological damage. Localizing and predicting the impact of chemical exposure is very challenging with many of the long term outcomes existing as unknowns (Claudio, Kwa, Russell & Wallinga, 2000). However, more physical and psychological markers gathered through testing procedures directly translate into increasingly effective treatment strategies.
Immediate intervention in addressing the impact of pesticide poisoning involves the reversal of neurological activity promoting harmful symptoms. Activity at the nicotinic and muscarinic receptor sites requires intervention at the synaptic level (Weinbroum, 2005). Introduction of pharmacological agents such as atropine (Mattingly et al., 2003) appear in mediating site reactions. Atropine itself is a substance “that blocks muscarinic acetylcholine receptors” (Carlson, 2001, p. 113), in other terms, an antagonistic agent. Blocking these locations prevents the unpleasant and even deadly effects of immediate chemical exposure. An investigation by Balali-Mood and Shariat (1998) demonstrated that another drug recommencing the function of acetyl cholinesterase, an integral enzyme, produced effective and safe treatment outcomes. When aralysis occurs as a part of exposure, medicines resuming or unblocking nicotinic receptor function is warranted as the inhibition of muscle activity is associated with the inhibition of nicotinic function. This decision, of course is made within the context of suspect chemicals, presenting symptoms, and other important factors.
Taurine, “the most abundant amino acid in mammalian tissues” may prove an effective and inexpensive treatment for pesticide exposure, particularly in the case of carbon tetrachloride poisoning (Miyazaki, Karube, Matsuzaki, Ikegami, Doy, Tanaka & Bouscarel, In Press, p. 1). Administering this substance to rat subjects diminished the damage induced through chemical intoxication and led the researcher’s conclusion that “the administration of taurine may be an optional therapeutic and preventative measure against oxidative stress-induced liver injury and hepatic fibrosis” following pesticide introduction (p. 7). Perhaps research in other areas will uncover other amino acid profiles with toxicological applicability and related ease of delivery.
Extended outcomes involving pesticide-related illness remain largely unknown. Mattingly et al. (2003) clearly show that acute treatment of insecticide poisoning is a grave challenge, conceding that the presence of linical features and treatment is a process not entirely understood. Knowing this, a scheduled and continuous monitoring of the patient is paramount. Symptoms of neurotoxin exposure potentially manifest over a ignificant time span (Claudio et al., 2000) and require appropriate, coordinated responses. This model requires the use of all discoursed analytical tools and research into new methods and drugs aimed at intervening in this serious medical event. Professional health practitioners remaining current in research findings, retaining an understanding of pesticide profiles, and utilizing the most contemporary intervention methods offer the greatest opportunity for client healing. Reducing one of the nation’s most puzzling occurrences to its logical conclusions does not detract from its intrigue. Acceptance of the most probable elements, carbon tetrachloride and chloroform, in distressing the populous of 1944 Mattoon, is more interesting than any phantom menace. The interaction of body-mind elements behind this hysteria offers that collective learning of how and why these events occur is ongoing. No longer can maladies be reduced to simplistic biological or psychological components. Accordingly, this understanding also invites the use of novel assessment and treatment modalities meant in addressing the patient holistically. Seemingly unsolved mysteries akin to Mattoon are far from over, but with the expanding knowledge of behavioral health, practitioners certainly become better detectives. This case, it appears, is closed.
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