Imagine trying to lead your life while avoiding diesel exhaust, perfume, cleaning fluids, the myriad chemicals that give off gas from new cars, carpets, or treated woods and fabrics–and a whole lot of other things.

That’s exactly the case for the 10 million or so Americans who suffer from severe multiple chemical sensitivity (MCS). For them, sitting at a stoplight next to a bus or walking into a department store might be all it takes to bring on immediate and severe headaches, joint pain, muscle fatigue, dizziness, and brain fog.

And then, when they go to a physician for help, the doctor might just tell them it’s all in their head.

Martin Pall, professor of biochemistry and basic medical sciences at Washington State University, says that one reason many believe MCS is “all in the head” is that there has been no plausible mechanism proposed that explains how MCS happens and how people with MCS can be so exquisitely sensitive to such a wide variety of chemicals. Because there has not been a plausible explanation, there’s also little money available to study the disease–though that didn’t stop Pall from taking the time to research and develop a theory that may well provide the missing mechanism.

Pall’s theory is a fusion of two previously proposed theories, neither of which can completely explain the disease. The first, proposed by Iris Bell of the University of Arizona, suggests that MCS is due to nerve sensitization via mechanisms similar to those involved in learning and memory. The second, developed by Pall, suggests that abnormally high levels of two chemicals, nitric oxide and peroxynitrite, are responsible for the disease.

Learning and memory involve the reinforcement of specific pathways in the central nervous system. The pathways are established between nerve cells when a chemical neurotransmitter is released by one and travels to another. The second nerve cell responds, because it has a protein receptor on its surface that specifically recognizes the neurotransmitter. The pathway between the two cells becomes reinforced when the junction between them becomes hypersensitive. That might happen because more neurotransmitter is released or because the receptor becomes more sensitive to it.

In MCS, it appears that pathways over a large region of the brain become activated and reinforced. Pall’s theory explains how that might take place. He believes that high levels of nitric oxide and peroxynitrite are produced during the chemical exposure that is usually the initiating event in MCS. These compounds are known to stimulate nerve cells to release excess neurotransmitter and to make the receptors on many receiving cells hypersensitive. In addition, peroxynitrite may provide the means by which the chemicals gain access to the brain, for it is known to compromise the blood-brain barrier that normally protects the brain from drugs, chemicals, and other potentially harmful substances.

The idea to put Bell’s and his own theories together came to Pall as he was trying to determine how his initial theory might explain the many puzzling features of MCS. During that research, he found many observations that implicated a particular type of neurotransmitter receptor, one that previously had been shown to be involved in nerve sensitization. When that receptor is stimulated, it is known that more nitric and peroxynitrate are produced in the brain.

Pall’s theory is receiving increasing attention from the scientific community. It has been published in the Journal of the Federation of American Societies of Experimental Biology, and was extensively discussed at a recent meeting of the committee that advises the U.S. government on Gulf War syndrome. In addition, he has accepted invitations to speak at major meetings in London and Washington, D.C. Perhaps this attention will produce the critical mass of research and money needed if progress is to be made in determining the mechanism of the disorder, whether that mechanism is his or another as yet to be proposed.

“These things never go as fast as you want,” he says.

Pall believes that the mechanism he proposes for MCS also may explain several other “mystery” diseases: chronic fatigue syndrome, Gulf War syndrome, post traumatic stress syndrome and fibromyalgia. As with MCS, none have plausible mechanisms that explain the whole pattern of reported properties. It’s of interest that, for Gulf War Syndrome, published data suggest a correlation of the neurological symptoms with a gene that has a role in metabolism of a pesticide-like compound to which many Gulf War vets were exposed.