MCS 5 Research Letter

[michael edward badolato jr]

The research quoted is that of Bascom, Meggs, Veronesi, and Bonham. The three former (Bascom, Meggs, Veronesi) have formed a cornerstone pointing to airway epithelial defects as the cause of most MCS.

Rebecca Bascom. Environmental and Airway Diseases Research Facility, University of Maryland School of Medicine, Baltimore MD.

BASCOM ET AL. NEUROGENIC INFLAMMATION: WITH ADDITIONAL DISCUSSION OF CENTRAL AND PERCEPTUAL INTEGRATION OF NON-NEUROGENIC INFLAMMATION ENVIRON HEALTH PERSPECT 1997 105 (SUPPL 2): 531-37:

....The structure of the C-fiber system and function of the neuroinflammatory system is altered in people reporting chemical sensitivity....

William Meggs. Division of Toxicology, Department of Emergency Medicine, East Carolina University School of Medicine, Greenville NC.

MEGGS W.J. NEUROGENIC INFLAMMATION AND SENSITIVITY TO ENVIRONMENTAL CHEMICALS. ENVIRON HEALTH PERSPECT 1993 101 (3): 234-38:

....Neurogenic inflammation is now a well defined physiological mechanism by which mediators are directly released from sensory neurons to produce vasodilitation, edema, and other manifestations of inflammation. The nerve fibers have been identified as slow velocity C-fibers and the regulation of neurogenic inflammation has been studied...important regulators of inflammation, interleukin 1 and interleukin 2, suppress central nervous system activity....

MEGGS W.J. HYPOTHESIS FOR INDUCTION AND PROPAGATION OF CHEMICAL SENSITIVITY BASED ON BIOPSY STUDIES. ENVIRON HEALTH PERSPECT 1997 (SUPPL 2) 473-78:

"...There are defects in the tight junctions between respiratory epithelial cells, focal desquamation of the epithelial cells in places, hypertrophy of glandular structures, lymphocytic infiltrates, and proliferation of sensory nerve fibers..."

MEGGS W.J. ARCH ENV HEALTH 1999 54(5) 309-11:

"...The mechanism by which inflammatory conditions are provoked by chemicals is via chemoreceptors on sensory nerve C-fibers with the release of substance P and other mediators of neurogenic inflammation...progression of inflammation to organ damage is possible to those who continue to be exposed...".

Bellina Veronesi and Marga Oortgiesen. National Health Effects and Research Laboratory, Cellular and Molecular Branch, Neurotoxicology Division, US Environmental Protection Agency, Research Triangle Park, North Carolina. Cato Research LTD., Durham, North Carolina.

VERONESI B. & OORTGIESEN M. NEUROGENIC INFLAMMATION AND PARTICULATE MATTER (PM) AIR POLLUTANTS. NEUROTOXICOLOGY 2001 (22):795-810:

.....neurogenic inflammation. In this process, a cascade of cellular and sub-cellular events...the sensory nervous system and its peptidenergic transmitters (i.e. SP, CGRP, NKA) initiate and sustain this inflammation...Once released these pro-inflammatory peptides interact with a variety of immune (e.g. lymphocytes, neutrophils, macrophages, eosinophils) and non immune (e.g. smooth muscle, endothelial cells of the vasculature, epithelial cells that line the lumen of the airways and gut, keratinocytes of the skin) target cells...overt symptoms of inflammation (e.g. erythema, edema, vasodilitation, vasoconstriction, mucous secretion) through the phenomenon of the axon reflex... on involvement of the immune system, the initial symptoms of inflammation are exacerbated and perpetuated with resulting tissue damage...In normal physiological settings, the respiratory epithelial population and its sensory innervation act reciprocally to influence the growth, differentiation, and homeostasis of each other...These relationships are especially critical to the organism's inflammatory response...In all instances, sensory neurons release 10-200 fold higher levels of IL-6 (pro-inflammatory cytokine) relative to epithelial cells...conditions associated with chemical pollutants are characterized by damage to the epithelial barrier that lines the airways. Such damage not only results in the loss of critical neuropeptide deactivating enzymes (e.g. NEP) but allows the sensory fiber to physically extend closer to the airway lumen and in closer proximity to the inhaled PM particles...enhanced and prolonged inflammatory events...increased inflammatory response....

A.C. Bonham (a), C.Y. Chen (a), T. Mutoh (a,b,c), and J.P. Joad (b). (a) Departments of Internal Medicine and Pharmacology, (b) Department of Pediatrics, University of California, Davis CA. (c) Department of Anatomy and Brain Sciences, School of Medicine, Kobe University, Kobe, Japan.

BONHAM ET AL. ENVIRON HEALTH PERSPECT 2001 109 (SUPPL 4) 573-78:

....sensory nonmyelinated C-fibers innervating the lung...the responses evoked through the local axon reflex include bronchoconstriction, mucous secretion, and microvascular leak....

 

References

BASCOM ET AL. NEUROGENIC INFLAMMATION: WITH ADDITIONAL DISCUSSION OF CENTRAL AND PERCEPTUAL INTEGRATION OF NON-NEUROGENIC INFLAMMATION ENVIRON HEALTH PERSPECT  105 (SUPPL 2): 531-37 1997

BONHAM ET AL. ENVIRON HEALTH PERSPECT  109 (SUPPL 4) 573-78 2001

MEGGS W.J. ARCH ENV HEALTH 54(5) 309-11 1999

MEGGS W.J. HYPOTHESIS FOR INDUCTION AND PROPAGATION OF CHEMICAL SENSITIVITY BASED ON BIOPSY STUDIES. ENVIRON HEALTH PERSPECT  (SUPPL 2) 473-78 1997

MEGGS W.J. NEUROGENIC INFLAMMATION AND SENSITIVITY TO ENVIRONMENTAL CHEMICALS. ENVIRON HEALTH PERSPECT  101 (3): 234-38 1993

VERONESI B. & OORTGIESEN M. NEUROGENIC INFLAMMATION AND PARTICULATE MATTER (PM) AIR POLLUTANTS. NEUROTOXICOLOGY  (22):795-810 2001