Ask the Canary

Posted on Jul 08, 2010 by Susie Collins in Blog, MCS, Research, Susie Collins

Does Multiple Chemical Sensitivity have anything to do with the sense of smell?

What role does the sense of smell play in MCS?

What role does our sense of smell and the olfactory system play in Multiple Chemical Sensitivity? Do people with MCS have a heightened sense of smell?

Thank you,
A Nosy Canary

Aloha Nosy!

I am often asked these questions. The first point I always clarify is that MCS does not center on our sense of smell or an olfactory response. To understand this better, let’s review the cause of MCS.

Current research shows that MCS is initiated by a previous toxic chemical exposure from one or more of seven classes of chemicals, notably organic solvents (volatile organic compounds or VOCs), three classes of pesticides, mercury, and/or carbon monoxide. Toxic mold exposure also is reported to initiate MCS, and we find this cause most often in people with MCS who have lived or worked in “sick buildings” that have a toxic mold infestation (Pall, 2009).

So the first thing to understand is that despite many descriptions of MCS that you may find on the Web and elsewhere saying that the olfactory system has a central role in MCS, there is no evidence supporting that claim and in fact, there is considerable evidence against such a role. There are cases of MCS in people with no sense of smell– in fact we have several members of our community who have no sense of smell and also have severe cases of MCS.

Many people with MCS report symptoms of a chemical exposure without any chemical odor. I personally have had this happen: while sitting in my livingroom one day I was overcome with feeling ill, dizzy with loss of cognitive ability, only to discover the neighbor was spraying some sort of herbicide that had no odor.

There are three studies of MCS patients where a nose clip was used to block off access of odors and the MCS patients still reacted to toxic chemicals (Joffres et al, 2005; Millqvist and Lowhagan, 1996; Millqvist et al, 1999).

This is not to say that the olfactory system is never impacted in people with MCS, but rather that it does not play a central role in cause.

To explain this, I’d like to refer to the work of MCS researcher Martin Pall, professor emeritus of biochemistry and basic medical sciences at Washington State University. Pall’s research on MCS is widely published in books and articles, the most recent of which is a chapter in the authoritative international reference manual for professional toxicologists, General and Applied Toxicology, 3rd Edition, 2009.

Pall’s review of the literature and other research he’s conducted over the past eleven years show the probable cause of MCS is a biochemical mechanism involving nitric oxide (NO) and peroxynitrite (ONOO-), what Pall calls the NO/ONOO- cycle. Pall describes MCS, also known as chemical sensitivity and toxicant-induced loss of tolerance (TILT), as a disease initiated by toxic chemical exposure, leading to brain injury that produces high level sensitivity to the same set of chemicals that cause the disease. To get a little deeper into the science: all seven classes of chemicals mentioned at the top of my answer are thought to act indirectly to increase the activity of NMDA receptors, which are glutamate receptors for controlling synaptic plasticity and memory function. This activity, in turn, leads to rapid increases in intracellular calcium (Ca2+), nitric oxide, and peroxynitrite (ONOO-), acting to greatly stimulate the NO/ONOO- cycle. That cycle is what causes our myriad symptoms.

So how does this impact our olfactory system? Do people with MCS have a heightened sense of smell? Let’s ask Martin Pall.

“MCS is not primarily a defect in the olfactory system,” Pall says. “But when the olfactory system is impacted by the NO/ONOO- cycle it will impact the sense of smell. This is because both the NMDA receptors and nitric oxide have roles in the olfactory mechanism. However what impact the cycle has, varies from person to person, possibly depending on the severity of the cycle in that region of the body. Some people report being much more sensitive to odors but others are anosmic, completely devoid of the sense of smell.”

Aloha,
Susie

Photo credit.

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Tags: Air, Chemicals, Indoor Pollution, MCS, Mold, Multiple Chemical Sensitivity, Research

13 Responses to “Ask the Canary”

maria

08. Jul, 2010

In my case the impact has been HUUUUUUUUUUGE! I usually explain it to people saying that it’s like someone who goes blind at an adult age and develop better hearing or sense of tact, to help them find their way around. So developing a more sensitive olfatory system is our brain’s way of protecting us from what’s harming us by saying “can’t you feel you must leave this place at once or else you’ll end up being very ill?”… among other things. Like the immflamatory response of the mucosae etc. Just ways of alerting us that something’s wrong with the environment that surround us and trying to establish barriers against the harming agents.

Reply to this comment
- Susie Collins
  
  08. Jul, 2010
  
  Isn’t it interesting, Maria? It’s not black and white. MCS is not caused by olfactory defect, but a person’s sense of smell can be affected (heightened or deadened) after MCS is initiated depending on various physiological factors. For those who have a deadened sense of smell, life with MCS is especially horrific because there is no warning system at all for exposure to toxic chemicals that have an odor (like fragrance). And all of us are at the mercy of the toxic chemicals that have no odor at all. Not a static illness by any means! Susie
  
  Reply to this comment
maría

08. Jul, 2010

That’s why I get so hysterical when an allergic reacion or a cold don ‘t let me breathe, because I feel trapped.

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Roslyn Rodgers

08. Jul, 2010

When we learn to read our bodies it makes no difference if there is an odour or not because our reactions/symptoms will tell us when there are toxic chemicals around us.
Saying that, my sense of smell is extremely heightened when I am overloaded and diminishes when the toxic load becomes lower.

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Lisa

09. Jul, 2010

Has anyone improved using the Pall protocol of supplements?

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Catherine Hollingsworth

09. Jul, 2010

I completely agree with Susie here….there is much evidence to show that smell has little to do with MCS other than become an early-warning system.

I have noticed that my sense of smell is better now that I have eliminated more of the fragrances around my area. It is easier to smell something you are not sensitized to. This can be explained further by understanding why people feel they must use more and then more of their favorite fragrance….they can’t smell it when they become used to it.

My doctor told me that he has noted in MCS patients that a mucos plug normally found over the olfactory receptor is not present in them…..why is not clear, but it may be from chemical exposures. This allows chemicals to get access to the brain much faster than “normals”.

To the point that Lisa asked, I have been on the Pall protocol, and I have gotten much, much better in 18 months.

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Lourdes Salvador

09. Jul, 2010

Lisa, I’m on a variation of the Pall protocol and the improvement has been huge for me! Night and day! The change was subtle at first… a gradual improvement that diminished quickly when I accidentally ran out of protocol components. The longer I’ve been on it, the greater the improvement and less backslide I’ve had if I run out. I’ve actually halved the amount I take with no negative effects. I’ve heard others say the same thing… that there reaches a point where taking less becomes better as they heal.

Reply to this comment
Susie Collins

14. Jul, 2010

Some comments were lost from this post when we changed web hosts yesterday. It was not done intentionally. I’ll try to retrieve them tomorrow. Susie

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Sandra Lee

16. Jul, 2010

Congratulations on changing webhosts!

My sense of smell is heightened without question. I often read that a heightened sense of smell can be one of the first clues of MCS. That does mean its central to MCS, but it does appear to be an indicator in one segement of MCS sufferers.

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Amelia Black

21. Jul, 2010

I’m curious why there is the need to separate MCS from the chemical reception of smelling? When you describe the contact with VOCs and or pesticide exposure as a cause of MCS, what type of contact are you describing?

The human sense of smell (olfaction as well as retronasal olfaction) makes up the strongest source of chemoreception in the human body and occurs both through conscious contact as well as subconscious. And correct me if I’m wrong but most volatile and organic solvents that cause MCS have an odor whether our bodies detect them or not.

Reply to this comment
- Susie Collins
  
  21. Jul, 2010
  
  Amelia, as I wrote in the post, I’m not saying that the olfactory system is never impacted in people with Multiple Chemical Sensitivity, but rather that it does not play a central role in the cause of MCS. Contact with VOCs and pesticides that result in initiating MCS are not limited to breathing through the nose, the contact can also occur through skin or ingestion for example. By the way, there are in fact toxic chemicals with no odor that can initiate MCS; carbon monoxide is one.
  
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HEIRS Research

04. Aug, 2010

Unfortunately, the studies on MCS do not address neutrotrophin regulation such as BDNF which does have an association with the olfactory system as well as the nerves that regulate it. BDNF dysfunctions has been found to be important in CFS and PTSD as well as other mental health conditions. The methylation of this protein and other proteins is totally ignored by most studying MCS. I just do not understand why when epigenetic factors provide a reasonable explanation for why EI runs in families and can develop after certain biological events.

Also why is it that the proteins such as PGC-1a and Nrf2 that control the antioxidant regulation and the master regulator for detoxification of xenobiotics, increased by exercise and decreases with age and as a consequence of dietary factors is ignored as a potential factor in MCS. This is true even though these proteins have tremendous influence on immune and neural regulation and redox and cellular control of metabolism. In addition, the proteins that regulate the antioxidant system are found in the olfactory system and can also be dramatically influenced by methylation as well as have an influence on other organ systems that may reflect symptoms in MCS. Also, the inflammatory cytokines produced in the intestinal tract and the liver promote neuroinflammation in the brain, as well as, gene changes that can reflect behavior changes that are consistent with MCS without NO even though NO may be secondary.

The problem with MCS is few want to be part of the “real” solution — and even fewer that actually study it are without inherent bias in their research. Hopefully, PANDORA will have a much better and unbiased and holistic approach to studying these conditions as their program in NJ develops. In addition, a recent statement paper suggests that mold is really just chronic inflammation disease (CID)by another name which is treatable. In addition, this supports another claim that chronic intestinal conditions are very similar to CID and some suggest that chronic inflammation in the intestinal tract (or respiratory tract) may lead to MCS through a loss of tolerance and certain types of T cells. Again one never hears this about MCS even though this has been noted in reference with autism where chemical sensitivity is almost always a co-factor and also autoimmune diseases. Curiously and from an adaptive perspective MCS presents more like an autoimmune-type loss of tolerance condition than anything else.

Again, there is little research in reference to MCS to issues like these even thought there is lots of studies that deal with them with other environmental illnesses like IBD and asthma. Worth noting here is many with MCS complain the most severe symptoms began with an infection or illness. Endotoxin which is a component of bacteria has the ability to excite the inflammatory process including NF-kappaB cascade. In addition, endotoxin has been demonstrated to promote depressive-like symptoms even before it stimulates cytokine production. I suggest that one of the problematic issues with MCS is the same as it is for CFS –a problem with labelling and also cultural bias. IN addition, a much broader emphasis and focus must be paid to the ever-increasing levels of greenhouse gases in the environment which by the way, have the ability to cause symptoms that are MCS. The question here is does this mean a patient has MCS — I would say no. For this point, I find it extremely discouraging that some expert endorse the use of devices that generate greenhouse gases….it just provides a glimpse of some of the poor education many of us get that have MCS. Another important consideration is how much attention has been brought to the greenhouse gases that are produced in our homes that we can are not aware of or by agriculture or the landscaping of our neighbors that contribute to our symptoms???

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Lou Cheese

19. Aug, 2010

Our nervous systems are so sensitive now that the level of toxin is so small that it can be far below the human ability to perceive odor and still have a negative impact on our health and functioning.

One time I was working for a couple of weeks in a client’s data center. The environment inside and the access to the room is tightly controlled. I was thinking for once I could take off my respirator and I did so. By the end of the week I was becoming extremely fatigued and I couldn’t figure out why-keep in mind this was early on and I wasn’t as aware of triggers like I am now. On Friday, a woman who worked on the far side of the room came by to ask me a question and my lungs almost exploded in an instantaneous, non-stop, and somewhat violent coughing fit that had me kneeling on the ground involuntarily and bent over in a matter of seconds.

It was her perfume. That was what was making me fatigued, and that was what caused the severe reaction. The difference was distance-as long as she remained on the far side of the room, I could not smell her perfume although I was still breathing minute portions of it. My body reacted to the smaller, imperceptible amount by creating fatigue. When it got a big dose it acted in accordance with the level of exposure. But it wasn’t until the smell of the perfume was above the ability to perceive it that I was mentally able to connect the cause and effect.

There has also been may times I got a sore throat, fatigue, or dizziness and was unable to determine the cause, probably because the level of toxin was so small.

And let’s be honest, with the hyper-sensitivity that the chemically injured often has, we could be lowering our tolerance to a certain toxin or smell by absorbing other toxins in ways besides respiration, like through the skin or in the diet. If unknowingly ingesting a toxin, our systems would be even more prone to a reaction via the respiratory channel.

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