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From the Townsend Letter
November 2016

Potential Proof of Chemical Sensitivities
by Laurie Dennison Busby, B.Ed.
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Xenobiotic-metabolizing enzymes (XMEs) are found in the olfactory epithelia, bronchiolar epithelium, and skin.45  "In addition to protecting against inhaled toxic compounds, these enzymes could also metabolize odorant molecules, and thus modify their stimulating properties or inactivate them."45  Inhibitors of these enzymes, increased the electro-olfactogram (EOG) response, "… likely due to enhanced olfactory sensory neuron activation in response to odorant accumulation."45

For several compounds tested, the rate of olfactory mucosa metabolism from parent compound to subsequent compound was 3 to 65-fold higher than hepatic.45  If the body has a greater need for xenobiotic metabolizing enzyme activity in the olfactory mucosa, possibly as a first line of defense from airborne chemicals that might enter the CNS, then lower levels or activity of these enzymes in olfactory mucosa may expose patients to higher levels or longer effects of airborne chemicals. 

In MCS, CFS, and FM, some enzymes involved in xenobiotic metabolism have been found to have polymorphisms or lower levels or activity: cytochrome P450 (CYP2C9 and CYP2D6),  glutathione S transferases (GSTM1 and GSTT1), N-acetyltransferases (NAT), and/or paraoxonase (PON).46,47

Lower activity of PON, which breaks down some organophosphate pesticides, has been found in FM; Hashimoto's thyroiditis/hypothyroidism, which is often a comorbidity in CFS and MCS; and Graves disease/hyperthyroidism.13,48-50 

Some patients with CFS and an infectious trigger were found to have crimson crescents on their pharyngeal pillars, which were, " … most closely associated with elevated HHV-6 titers …"14  Whether the crimson crescents in CFS are related to the red streaks in the lateral recesses of the oropharynx in acute sinusitis is unknown.51  Nevertheless, in patients with CFS, who continue to have them, the crimson crescents are a visible sign that a permanent change has occurred. 

Patients, with the most severe cases of self-reported airborne sensitivity, also had significant non-allergic cutaneous reactions to patch testing, "Our results suggest that individuals with self-reported chemical sensitivity show increased non-allergic cutaneous reactions … "2

The popliteal lymph node assay (PLNA) has been proposed as a potential test for predicting reactions (allergic and autoimmunergic) to chemicals including medications and environmental pollutants.52  "The most simple, primary PLNA measures popliteal lymph node hyperplasia after subcutaneous injection of a chemical into the footpad of the hindpaw of a mouse or rat."52  This may help explain my lymph node hyperplasia. 

At one point, CFS and FM research stood at a crossroads; while patients desperately waited for answers, a lot of time was wasted debating the validity of those illnesses.  However, in CFS and FM, research has since made vast strides in finding some of the potential underlying mechanisms in those illnesses.

Over two decades ago, Meggs theorized neurogenic inflammation might play a role in MCS.  Over 15 years ago, Millqvist found patients with MCS and asthma-like symptoms were more sensitive to inhaled capsaicin and responded to lidocaine indicating MCS may, "originate in the sensory nervous system."32 

Yet, MCS is still at a crossroads.  Patients deserve better.  Hopefully, this paper has provided enough "potential proof" researchers will stop debating the issue and instead finally move on to finding answers.  (Thank you to the researchers who have been tirelessly looking for answers all along.)

Notes .pdf

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©2016 Laurie Dennison Busby, B.Ed.

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