Toxic
Exposure Induced Multiple Chemical Sensitivity (MCS)
Review,
B. Windham (Ed) {with emphasis on pesticide exposures}
Doctors are increasingly seeing a
unique pattern of illness involving chemically exposed groups in more than a
dozen countries, who subsequently report multisystem symptoms and new-onset
chemical, food, and drug intolerances at levels of exposure below that
affecting most other individuals [1-4]. The common pattern of development of
these intolerances is a compelling anomaly pointing to a new theory of disease,
one that has been referred to as "Toxicant-Induced Loss of Tolerance"
("TILT") or Multiple Chemical Intolerance(CI).
TILT or CI has the potential to explain certain cases of asthma, migraine
headaches, chronic fatigue, fibromyalgia, as well as other chronic conditions
including depression, alzheimer’s disease[12],
and "Gulf War syndrome". It appears to evolve in two stages: (1)
initiation, characterized by a profound breakdown in prior, natural tolerance
resulting from either acute or chronic exposure to chemicals (pesticides,
solvents, toxic metals[4], indoor air contaminants,
etc.), followed by (2) triggering of symptoms by small quantities of previously
tolerated chemicals (traffic exhaust, fragrances, gasoline), foods, drugs, and
food/drug combinations (alcohol, caffeine). Multiple mechanisms of chemical
injury that magnify response to exposures in chemically sensitive patients can
include neurogenic inflammation (respiratory,
gastrointestinal, genitourinary), kindling and time-dependent sensitization
(neurologic), impaired porphyrin metabolism (multiple
organs), and immune activation. Severe CI is a characteristic of 20-47% of
individuals with CFS
and/or fibromyalgia, all patients with multiple chemical sensitivity (MCS), and
approximately 4-6% of the general population. In the general population, 15-30%
report at least minor problems with CI[2]. The levels
of chemicals reported to trigger CI would normally be considered nontoxic or subtoxic. However, host factors--e.g., individual
differences in susceptibility to neurohormonal
sensitization (amplification) of endogenous responses--may contribute to
generating a disabling intensity to the resultant multisystem dysfunctions in
CI. One site for this amplification may be the limbic system of the brain,
which receives input from the olfactory pathways and sends efferents
to the hypothalamus and the mesolimbic dopaminergic [reward] pathway. Chemical, biologic, and
psychological stimuli can initiate and elicit sensitization. In turn,
subsequent activation of the sensitized limbic and mesolimbic
pathways can then facilitate dysregulation of
behavioral, autonomic, endocrine, and immune system functions. Research to date
has demonstrated the initiation of neurobehavioral sensitization by volatile
organic compounds, toxic metals, and pesticides, as well as sensitizability
of cardiovascular parameters, beta-endorphin levels, resting EEG alpha-wave
activity, and divided-attention task performance in persons with CI. Chronic pesticide
exposure has been found to be a common cause of MCS and related symptoms
such as CFS, Fibromyalgia, Migraine Headaches, Depression,[1-3,5-11] etc. as
well as Alzheimer’s Disease[12].
References:
(1) The compelling anomaly of chemical intolerance, Miller CS. Ann N Y Acad Sci. 2001 Mar;933:1-23; & Elevated nitric oxide/peroxynitrite mechanism for the common etiology of multiple chemical sensitivity, chronic fatigue syndrome, and posttraumatic stress disorder. Pall ML, Satterlee JD . Ann N Y Acad Sci. 2001 Mar;933:323-9.
(2)Illness from low levels of environmental chemicals: relevance to chronic fatigue syndrome and fibromyalgia. Bell IR, Baldwin CM, Schwartz GE. Am J Med. 1998 Sep 28;105(3A):74S-82S; & Chronic fatigue syndrome following a toxic exposure; Racciatti D, Vecchiet J, Ceccomancini A, Ricci F, Pizzigallo E. Sci Total Environ. 2001 Apr 10;270(1-3):27-31.
(3)Profile of patients with chemical injury and sensitivity; Ziem G, McTamney J. Environ Health Perspect. 1997 Mar;105 Suppl 2:417-36.
(4)Mechanisms
of mercury induced chemical sensitivity, chronic fatigue, fibromyalgia; B
Windham (Ed.), www.flcv.com/cfsfm.html
(6) The specificity of the CDC-1994 criteria for chronic fatigue syndrome: comparison of health status in three groups of patients who fulfill the criteria; Kennedy G, Abbot NC, Spence V, Underwood C, Belch JJ. Ann Epidemiol. 2004 Feb;14(2):95-100.
(7) Peripheral cholinergic function in humans with chronic fatigue syndrome, Gulf War syndrome and with illness following organophosphate exposure; Khan F, Kennedy G, Spence VA, Newton DJ, Belch JJ. Clin Sci (Lond). 2004 Feb;106(2):183-9.
(8) Association between human paraoxonase gene polymorphism and chronic symptoms in pesticide-exposed workers; Lee BW, London L, Paulauskis J, Myers J, Christiani DC. J Occup Environ Med. 2003 Feb;45(2):118-22.
(9) A genetic rat model of cholinergic hypersensitivity: implications for chemical intolerance, chronic fatigue, and asthma; Overstreet DH, Djuric V. Ann N Y Acad Sci. 2001 Mar;933:92-102.
