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Researchers Clear the Confusion: Allergies, Non-Immune Contact Reactions and Chemical Sensitivity





by Lourdes Salvador


One of the frequent misunderstandings about multiple chemical sensitivity (MCS) is confusing it with an allergic response due to IgE (immunoglobulin E). MCS is not an allergic reaction. Rather, it appears to be a reaction to the toxic properties of the incitants due to a genetically damaged detoxification system. Thus far, science is still searching for the existence of biomarkers to diagnose the condition.

Researchers conducted a study involving non-immune immediate contact reactions (NIICR), which are defined as “non-immunoglobulin E (IgE)- mediated skin responses that occur without previous sensitization” (Harth et all, 2007). NIICR's exhibit the same symptoms without the presence of an IgE allergy. NIICR has been observed from contact with benzoic acid, trans-cinnamic acid and methyl nicotinate as well as cinnamic aldehyde of fragrance mix. Antihistamine treatment in these cases has been ineffective because the reaction is non-immune or NIICR. The best treatment is removal of the inciting agent.

Researches examined a case report of a subject with workplace related reactions to perfumes. The subject presented delayed reactions to a mixture of odorous substances in patch testing. A bronchial challenge with perfume was performed and yielded and immediate asthmatic reaction with a diagnosis of occupational allergy to perfumes.

The researches then tested a 47 year old female gardener who complained of shortness of breath and headaches when exposed to any and all odors (volatile organic compounds) since 2000. The patient experienced the symptoms at home and work, though they were more pronounced at work. The diagnosis of idiopathic environmental intolerance (IEI) was the most likely diagnosis, though the researchers decided to perform further tests.

For the first time, the researchers applied an NIICR inducing component of fragrance mix in a bronchial challenge test which showed an asthmatic reaction. The symptoms were determined to not be due to hyperosmia. It was determined that the negative results for asthma favored the diagnoses of the accidental coincidence of IEI and NIICR. Though the researchers did not find a cause for IEI, the did determine that cinnamic aldehyde has effects of the lower airways of the patient and that bronchial effects and clinical relevance of NIICR need to be further examined.

This study reinforces the fact that environmental illness is not allergy mediated or asthma related, yet there may be co-occurring allergy or asthma in some patients. In simple terms, three recent studies show that a genetic variant makes sufferers of multiple chemical sensitivity (MCS) more likely to develop the condition. In 2004, McKeown-Eyssen studied 203 MCS sufferers and 162 controls and found that genetic differences relating to detoxification processes were present more often in those with MCS than those without. The study concluded that "a genetic predisposition for MCS may involve altered biotransformation of environmental chemicals. Haley found similar, confirmatory results in a 1999 study with the PON1 gene in Gulf War syndrome veterans.

A new study by Schnakenberg et al (2006) confirmed the genetic variation previously found by McKeown-Eyssen and Haley. A total of 521 unrelated individuals participated in the study. Genetic variants of four genes were analyzed: NAT2, GSTM1, GSTT1, and GSTP1. The researchers concluded that individuals who are NAT2 slow acetylators and those with homozygously deleted GSTM1 and GSTT1 genes are significantly more likely to develop chemical sensitivity.

According to the study the glutathione S-transferases act to inactivate chemicals so people without these GSTM1 and GSTT1 genes are less able to metabolize environmental chemicals. If a person cannot metabolize chemicals they build up in the body and cause disturbances in normal body function. Schnakenberg and fellow researchers explain that "glutathione S-transferases play an important role in the detoxification of chemicals... the deletion of this gene may be an important step in the early onset of diseases" which is a critical discovery that provides a biological basis behind the etiology of multiple chemical sensitivity. The researchers also noted that diseases such as non-Hodgkin's lymphoma, hepatocellular and prostate carcinoma, and Alzheimer's disease have been associated with the common chemicals metabolized by GSTP1. The deletion of the GSTP1 gene leaves individuals more susceptible to developing these diseases, as lack of these genes means a loss of protection from oxidative stress.

This discovery is crucial to being able to diagnose and treat those who suffer from multiple chemical sensitivity and other toxic injuries. It is the first step toward understanding and explaining the cause of chemical injury and resulting sensitivities so that treatments can be developed.

View the very BEST Environmental Illness Videos!

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About the Author

Lourdes Salvador is a writer and social advocate based in Hawaii. She is a passionate advocate for the homeless, having worked with her local governor to open new shelters and provide services to the homeless in a new approach to end homelessness. That passion soon turned to advocacy and activism for victims of multiple chemical sensitivity. Since 2006, she has been the president of MCS America and a featured monthly writer for MCS America News. She co-founded MCS Awareness in 2005. She also serves as Partner, Environmental Education Week and Partner, Collaborative on Health and the Environment (CHE). For more information about Lourdes and her advocacy work, please visit:,, and

Copyrighted © 2007 Lourdes Salvador




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