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.
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Cited References:
Haley, RW, Billecke, S, & La Du, BN (1999). Association of low PON1 type Q (type A) arylesterase activity with neurologic symptom complexes in Gulf War veterans. Toxicology and Applied Pharmacology 157(3):227-33.
McKeown-Eyssen, G, Baines, C, Cole, D, Riley, N, Tyndale, R, Marshall, L, & Jazmaji, V (2004). Case-control studies of genotypes in multiple chemical sensitivity: CYP2D, NAT1, NAT2, PON1, PON2 and MTHFR. International Journal of Epidemiology 33, 1-8.
Schnakenberg, E, Karl-Rainer, F, Stanulla, M, Strobl, N, Lustig, M, Fabig, N, & Schloot, W (2007). A cross-sectional study of self-reported chemical-related sensitivity is associated with gene variants of drug-metabolizing enzymes. Environ Health. 2007 Feb 10;6:6.
