Multiple Chemical Sensitivity - Clinical Trials

Clinical Trials

There have been both trials that support and don't support the claim that the symptoms of multiple chemical sensitivity are caused by chemicals.

A double-blind inhalant challenge in 1991 concluded, "The conclusion of the study is that in these patients, chemical sensitivity clearly does exist (pulse rate differences between positive responses and placebo - p .001)"

A 1991 controlled comparison of symptoms and chemical intolerances reported by Gulf War veterans, implant recipients and persons with multiple chemical sensitivity suggests that "some patients with antecedent chemical exposures, whether exogenous (chemical spill, pesticide application, indoor air contaminants) or endogenous (implant), develop new chemical, food, and drug intolerances."

A 1993 double-blind study suggested that MCS subjects could not discriminate between their chemical triggers and clean air when an olfactory masker was introduced that eliminated the ability to discriminate on the basis of odor.

In a 2008 double-blind study, a variety of responses, including the subjective perception of being exposed to solvents, increases in blood pressure or heart rate, or increased symptom severity, were measured following the double-blind exposure to several solvents. People with an MCS diagnosis showed no differences in these parameters when they were exposed to clean air or to solvents at a concentration too low to smell. The trial did not support the hypothesis that MCS is directly related to the effects of chemical exposures. Since MCS sufferers seem to have symptoms only when they perceive exposure to chemicals, the syndrome is proposed to be a result of odor hypersensitivity in which individuals have an exaggerated response to scents, or psychological factors.

A 2010 Italian study that genotyped patients diagnosed with MCS, with suspected MCS, and healthy controls suggested inhibition of expression and activity of metabolizing and antioxidant enzymes in MCS, accelerated lipid oxidation, increased nitric oxide production and glutathione depletion and increased plasma inflammatory cytokines.