In researching my triggering agent for MCS (phenoxyethanol), I've come across some interesting connections with MCS in office workers. A significant find, as not only are the vast majority of MCS sufferers female; 80% according to Gibson et al. l996 (see my \"Delegitimization\" post/article by Pamela Gibson, Ph.D in the General EI thread). But also there is a substantial statistical spike of MCS in office workers. This is normally attributed to tight/sick building syndrome, but there is another possibility.

When I think of office workers, I find lots of makeup, and all too often entirely too much perfume are a commonly shared trait (along with lots of dry cleaned clothes!). In googling around on phenoxyethanol, I find, not only is this chemical one of the most common preservatives in cosmetics/makeup, but a very common fixative/agent in perfume. Phenoxyethanol is also a common ingredient in ballpoint pen ink.

Hard to believe phenoxyethanol evaporating off ink on paper could be a substantial factor, but I had a flare up of my MCS while taking notes sitting on a jury a couple of months ago. One particular brand of pen I hadn't seen in a while was supplied by the court, and after a couple of days taking many pages of notes, I noticed my note pad was starting to get stinky and my head was spinning. When I got home, I googled the brand of pen I was using and Phenoxyethanol, and sure enough, this pen was full of phenoxyethanol!

I also found an Industrial Hygiene web site with an article stating phenoxyethanol had been attributed to a case of sick building syndrome at airborne levels of LESS THAN 2 PARTS PER BILLION! Here's the site: www.enviro-net.com/main.asp?page=story&a...ga&year=1999 And the story:

\"A chemical pollutant case study

At a government building in the Washington, D.C. area, the presence of an irritating, pungent odor forced the evacuation of more than 400 employees. Initial air quality studies failed to identify the offending agent. Review of this study showed that the initial investigator had sampled the air using a standard NIOSH, charcoal tube method that could only measure limited organic compounds present at very high levels (greater than 1 mg/m3). When the appropriate technique was used, the offending chemical was identified as 2-phenoxyethanol and traced to a floor leveling material applied to the concrete sub-flooring prior to installation. Studies showed that this compound was present in the air at concentrations less than 10 ug/m3 (2 ppb). This VOC has a low odor threshold and can be objectionable in building air. Once the source was identified, remediation plans were made, and employees could be assured they weren't being exposed to a harmful substance\".

An entire building evacuated due to phenoxyethanol at less than 2 ppb!

More googling came up with this PubMed citation on: \"Redox cycling of phenol induces oxidative stress in human epidermal keratinocytes\" Here's the link: www.ncbi.nlm.nih.gov/pubmed/10651998

Here's what it says:

A variety of phenolic compounds are utilized for industrial production of phenol-formaldehyde resins, paints, lacquers, cosmetics, and pharmaceuticals. Skin exposure to industrial phenolics is known to cause skin rash, dermal inflammation, contact dermatitis, leucoderma, and cancer promotion. The biochemical mechanisms of cytotoxicity of phenolic compounds are not well understood. We hypothesized that enzymatic one-electron oxidation of phenolic compounds resulting in the generation of phenoxyl radicals may be an important contributor to the cytotoxic effects. Phenoxyl radicals are readily reduced by thiols, ascorbate, and other intracellular reductants (e.g., NADH, NADPH) regenerating the parent phenolic compound. Hence, phenolic compounds may undergo enzymatically driven redox-cycling thus causing oxidative stress. To test the hypothesis, we analyzed endogenous thiols, lipid peroxidation, and total antioxidant reserves in normal human keratinocytes exposed to phenol. Using a newly developed cis-parinaric acid-based procedure to assay site-specific oxidative stress in membrane phospholipids, we found that phenol at subtoxic concentrations (50 microM) caused oxidation of phosphatidylcholine and phosphatidylethanolamine (but not of phosphatidylserine) in keratinocytes. Phenol did not induce peroxidation of phospholipids in liposomes prepared from keratinocyte lipids labeled by cis-parinaric acid. Measurements with ThioGlo-1 showed that phenol depleted glutathione but did not produce thiyl radicals as evidenced by our high-performance liquid chromatography measurements of GS.-5, 5-dimethyl1pyrroline N-oxide nitrone. Additionally, phenol caused a significant decrease of protein SH groups. Luminol-enhanced chemiluminescence assay demonstrated a significant decrease in total antioxidant reserves of keratinocytes exposed to phenol. Incubation of ascorbate-preloaded keratinocytes with phenol produced an electron paramagnetic resonance-detectable signal of ascorbate radicals, suggesting that redox-cycling of one-electron oxidation products of phenol, its phenoxyl radicals, is involved in the oxidative effects. As no cytotoxicity was observed in keratinocytes exposed to 50 microM or 500 microM phenol, we conclude that phenol at subtoxic concentrations causes significant oxidative stress.

PMID: 10651998 [PubMed - indexed for MEDLINE]

I may be biased, as it was phenoxyethanol that triggered my MCS (in an industrial exposure at work), but I really think this one chemical may be the cause of a lot of cases of MCS. After daily exposure to this chemical for many months, I developed a remarkable cross sensitivity to petroleum solvents that took years to get under control. My 20 year career with the same group of doctors is in shambles, I've got lesions in my brain, and an ipsative drop in IQ.

I can't get any doctor interested in this matter thus far, so I simply cast this information out on the web in hopes someone will see this and connect the dots, so we can get a cause and effect for MCS established.

Hi Bill,

Great post as always.

I have no doubt that phenoxyethanol could be the cause of many cases of MCS, particularly in office workers, since it is so ubquitous. Obviously enclosed spaces such as offices only amplify exposures.

From my reading on multiple chemical sensitivity by authors such as Martin Pall, Sherry Rogers, Claudia Miller and others, it seems to me that the condition results from a sensitization of the brain (and/or immune system) which can be initiated by any number of chemicals. This sensitization however is not specific so that the individual suffers symptoms when exposed to a wide range of substances....which all of us MCS sufferers know is the case.

I put my own MCS down to chronic ethanol/acetaldehyde poisoning from intestinal Candida overgrowth. After being diagnosed with chronic fatigue syndrome I was left with a weakened immune system which made me susceptible to such infection. It's entirely plausible to me that years of low level exposure to ethanol and acetaldehyde being absorbed through my intestines could initiate MCS in the same way chronically inhaling phenoxyethanol could. It doesn't matter which route these chemicals take to reach the bloodstream. Clearly ethanol, acetaldehyde and phenoxyethanol are chemically related compounds which could be expected to result in the same damage to sensitive tissues.