Neurogenic Inflammation: With Additional Discussion of Central and Perceptual Integration of Nonneurogenic Inflammation
Rebecca Bascom,1 William J. Meggs,2 Mark Frampton,3 Kenneth Hudnell,4 Kaye Killburn,5 Gerd Kobal,6 Michelle Medinsky,7 and William Rea8
1 Environmental and Airway Diseases Research Facility, University of Maryland School of Medicine, Baltimore, Maryland
2 Department of Emergency Medicine, East Carolina University, Greenville, North Carolina
3 Department of Pulmonary and Critical Care, University of Rochester School of Medicine, Rochester, New York
4 U. S. Environmental Protection Agency, Research Triangle Park, North Carolina
5 University of Southern California, Los Angeles, California
6 Department of Pharmacology and Toxicology, University of Erlangen-Nuremberg, Erlangen, Germany
7 Chemical Industry Institute of Technology, Research Triangle Park, North Carolina
8 Environmental Health Center, Dallas, Texas
Abstract
The Working Group on Neurogenic Inflammation proposed 11 testable hypotheses in the three domains of neurogenic inflammation, perceptual and central integration, and nonneurogenic inflammation. The working group selected the term people reporting chemical sensitivity (PRCS) to identify the primary subject group. In the domain of neurogenic inflammation, testable hypotheses included: PRCS have an increased density of c-fiber neurons in symptomatic tissues; PRCS produce greater quantities of neuropeptides and prostanoids than nonsensitive subjects in response to exposure to low-level capsaicin or irritant chemicals; PRCS have an increased and prolonged response to exogenously administered c-fiber activators such as capsaicin; PRCS demonstrate augmentation of central autonomic reflexes following exposure to agents that produce c-fiber stimulation; PRCS have decreased quantities of neutral endopeptidase in their mucosa; exogenous neuropeptide challenge reproduces symptoms of PRCS. In the domain of perceptual and central integration, testable hypotheses included: PRCS have alterations in adaptation, habituation, cortical representation, perception, cognition, and hedonics compared to controls; the qualitative and quantitative interactions between trigeminal and olfactory systems are altered in PRCS; higher integration of sensory inputs is altered in PRCS. In the domain of nonneurogenic inflammation, testable hypotheses included: increased inflammation is present in PRCS in symptomatic tissues and is associated with a heightened neurosensory response; PRCS show an augmented inflammatory response to chemical exposure. The working group recommended that studies be initiated in these areas. -- Environ Health Perspect 105(Suppl 2):531-537 (1997)
Key words: neurogenic inflammation, perceptual and central integration, inflammation, chemical sensitivity
This manuscript has been reviewed by the U.S. Environmental Protection Agency and approved for publication. Mention of trade names and commercial products does not constitute endorsement or recommendation for use.This paper is based on a work group discussion at the Conference on Experimental Approaches to Chemical Sensitivity held 20-22 September 1995 in Princeton, New Jersey. Manuscript received at EHP 14 August 1996; manuscript accepted 24 January 1997.
Address correspondence to Dr. R. Bascom, 10 S. Pine Street. Room 800, Baltimore, MD 21201. Telephone: (410) 706-2169. Fax: (410) 706-8162. E-mail: bascom@umabnet.umd.ab.edu
Abbreviations used: Ach, acetylcholine; CGRP, calcitonin gene related peptide; CO2, carbon dioxide; MCS, multiple chemical sensitivity; NKA, neurokinin A; Nor, norepinepherine; NPY, neuropeptide Y; PRCS, people reporting chemical sensitivity; sub P, substance P; VIP, vasoactive intestinal peptide.
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Last Update: March 24, 1997