On the Recognition of Multiple Chemical Sensitivity in Medical Literature and Government Policy

Abstract

The history of chemical sensitivity in America is reviewed from the first description published by Edgar Allan Poe in 1839, to its first medical definition as a symptom of neurasthenia in 1869, its rediscovery as allergic toxemia in 1945, its redefinition in 1987 as multiple chemical sensitivity (MCS), and its overlap in the 1990s with chronic fatigue syndrome, fibromyalgia syndrome, and Gulf War syndrome (GWS). More than half of the over 500 peer-reviewed articles on MCS support an organic basis for MCS, whereas less than one-quarter support a psychiatric basis. The same 2:1 difference is seen in the numbers of MCS researchers writing these articles and the number of journals publishing them. A psychogenic interpretation of MCS also is specifically rejected in the latest formal position statement on the subject, a 1994 consensus of the American Lung Association, American Medical Association (AMA), U.S. Environmental Protection Agency (US EPA), and U.S. Consumer Product Safety Commission (US CPSC) (U.S. Government Printing Office 1994–523–217/81322). This and other government recognition of MCS in policy, research, and scientific conferences are summarized. Dozens of federal, state, and local authorities accept MCS as a legitimate disease and/or disability that deserves reasonable accommodation in housing, employment, and public facilities. Official recognition is expected later in 1999 when the U.S. Centers for Disease Control and Prevention (CDC) announces a formal definition of MCS and the federal Interagency Workgroup on MCS releases its long-awaited final report, 4 years in the making. Given that epidemiological data from three states puts the prevalence of chemical sensitivity at 16 to 33% of the general population, 2 to 6% of whom have already been diagnosed with MCS, this truly is a hidden epidemic that deserves the priority attention of public health researchers and policy makers. Industrial toxicologists are encouraged to work on reducing and eliminating the use of synthetic fragrances, chemical sensitizers, and other irritants in consumer products and occupational settings.

NMDA sensitization and stimulation by peroxynitrite, nitric oxide, and organic solvents as the mechanism of chemical sensitivity in multiple chemical sensitivity

“…Exposure to carbon monoxide may help explain cases where there is no identifiable initiating exposure. Carbon monoxide has been proposed by Donnay (105, 106) to be a possible initiating chemical in MCS; because it is odorless and tasteless, carbon monoxide exposure may not be apparent to its victims. Carbon monoxide exposure can lead to chronic sequelae (29), with symptoms similar to those in CFS and MCS, and carbon monoxide is reported to induce excessive production of the two precursors of peroxynitrite: super‐oxide and nitric oxide (29).…”

Exploratory Investigation of a Brief Cognitive Behavioral Intervention and Transcranial Direct Current Stimulation on Odor Sensitivity

“…The diagnosis of MCS remains a controversial topic, in large part due to its unknown etiology. While numerous biological (19)(20)(21)(22)(23)(24) and psychological (25)(26)(27)(28)(29)(30)(31)(32) contributing factors have been considered, more recent work describes MCS as a disorder of central sensitization (13), a state in which sensory input becomes amplified by the central nervous system. Wherein past exposure of certain odors were benign, repeated exposures lead to a myriad of adverse reactions.…”

Multiple chemical sensitivity (MCS): women’s health issue

“…From this, it is clear that an alteration in the olfactory bulb or inside the limbic system triggers a neurovegetative response (Figure 1). Epidemiological observations suggest that MCS, even if underestimated, has a 2-3% prevalence in the general population and that women are more significantly at risk to develop the disturbance: about 80% of affected patients are in fact women aged 30-50 at time of diagnosis [21]. Is it therefore reasonable to include hormonal imbalance in the pathogenesis of MCS?…”