This topic is important to me, but also extremely difficult to write about due to my own experience and anxieties. I have this persistent urge to ask questions and gather information, but then wonder what the heck to do with what I have gathered when it becomes overwhelming. I’ll probably split this topic up into various blog posts instead of trying to fit everything into one. Maybe give some background on my experience and then delve into some of the information that I found. Rather than present everything in the disoriented fragmented fashion in which it happened, or how I found it. I’ll try to provide earlier research first and move forward toward more recent topics or references in later posts. I have a lot to share about mercury and porphyrins. It might end up being my autobiography in the end, but maybe that is what I am supposed to do. I just wish there was a purpose for all that I have been though. Here goes…
When I was eighteen years old I was diagnosed with a rare genetic disease called “acute porphyria” after a severe illness that completely changed my entire life (this is a gross understatement). However, even though I had told myself long ago that nothing I would ever endure in the future could ever be as bad as the first illness and original diagnosis was, I was dead wrong.
I just had some recent DNA studies completed and apparently I was misdiagnosed, well partially (genetic porphyria/likely wrong, acquired porphyrinuria/missed completely). For over fifteen years I have believed that I had a fatal, genetic illness that could cause mental illness and a whole strain of other lovelies. I also made life decisions based upon porphyria being genetic and autosomal dominant (50% chance of passing it on, not to mention an all around horrid illness you don’t want to pass on). However, porphyria or porphyrinurias can also be acquired through environmental exposure.
How could so many different physicians overlook my work environment? These are questions I will never be able to answer. I won’t go into too many details of my own medical case/records/symptoms etc. (interested verifiable physicians email me) except to note two things that might have provided a clue that genetic porphyria was not the answer, even though I was excreting abnormal amounts of porphyrins.
1) Elevated porphyrins were found in my urine and fecal samples. However, no PBG (porphobilinogen) testing was done during the time that I was urinating “strawberry”/”amber” urine in the hospital, which would have helped IMMENSELY when ruling out acute porphyria for sure. The initial porphyria tests were ran four months after the initial illness with discolored urine, vomiting, etc. The proud physician saw the elevated porphyrins and called it porphyria. Because proper testing was not performed while I was in the hospital (porphyrins and PBG during symptoms), and the initial porphyria tests were non-conclusive for a specific TYPE of porphyria, this “gray area” provoked me to ask questions for YEARS.
2) The reason I was kept overnight at the hospital to begin with was an initial urine test showing severe proteinuria (aside from the fact that I was peeing strawberries, puking myself inside out and felt like death) and some other abnormal test results (super high WBC count, high SGOT, rashes, etc.). It was noted in my records that I was a full time dental assistant (I had just started full time that year, after graduating from high school). Since the porphyrin testing was not done until four months after the initial hospital visit, they just called it a “virus” until then, apparently ignoring the proteinuria, other abnormal lab results and symptoms that might have led to what I now know, half my life later.
It was mercury. Not the planet, the Hg kind of mercury. It seems simple to me now, but why did it take so long to figure this out? I could be wrong, but I think it is because I am not the one with the PhD, yet I asked all the questions, did all the research, learned, and basically irritated a thousand different medical “professionals” by persisting they order further tests. If it were not for my persistence and bugging them to know exactly what type of porphyria I had, I would still think I had a horrid genetic disease!
What I was told: Elevated porphyrins = porphyria. Don’t drink, don’t go in the sun and watch the movie, “Madness of King George”. Oh yeah, we call this the “vampire disease”. Oh that’s freaking great! Anything else that may destroy me completely? That was it.
What I learned: Porphyrins are part of the heme biosynthetic pathway/porphyrin metabolism. If this pathway is disturbed, illness can occur. Naturally, I learned only about the porphyrias and how disturbances in the pathway caused porphyria. But I was not aware of the other things that could disturb this pathway causing illnesses that were similar to porphyria, but instead of being genetic, they are acquired.
Porphyrins LOVE binding to metals and they necessary for life, but in excess they can cause damage. Maybe I’ll delve into porphyrins in another post one fine day, but I just want to outline that they are IMPORTANT.
porphyrin + magnesium = chlorophyll in plants
porphyrin + iron = heme in humans
Here are some articles from various medical or dental journals. Some are available in free full text online, others can be ordered through PubMed.
Fatal mercury intoxication in a dental surgery assistant.
Authors: TA Cook, PO Yates
Publication: The British Dental Surgery Assistant, 1969 Dec 16;127(12):553-5.
See also, British Dental Journal 1970 Apr;28(9):167
In the article, a 42 year old woman (dental surgery assistant) with approximately 20 years of work exposure to mercury died as a result of that exposure. The high levels of mercury in her kidneys resulted in fatal nephrotic syndrome.
This woman’s symptoms mirror what I experienced while I was dental assisting and became ill, only I did not have nearly the long term exposure that she did. According to the case report the woman became,
“suddenly ill with vomiting, pain the the right lumbar region of the abdomen, adema of the face and legs, and the passing of dark urine.”
WOW, no way, me too! I was lucky though, she ended up going into renal failure, convulsions, cardiac arrest and then passed away. The report concludes with,
“Little doubt can remain that the rapidly fatal renal failure in this case was the result of mercury intoxication.”
Systemic mercury levels caused by inhaling mist during high-speed amalgam grinding.
Authors: Cutright DE, Miller RA, Battistone GC, Milikan LJ.
Publication: Journal of Oral Medicine, 1973 Oct-Dec;28(4):100-4.
Within this article is a list of conclusions from a book titled, Mercury in the Environment (Lars Friberg and J.J. Vosral):
8. Data from studies in both the U.S. and U.S.S.R. indicate that exposure to metallic mercury may give rise to effects at considerably lower concentrations than have been recognized before.
9. Despite the fact that exposure to, for example, metallic mercury has occurred for very long times; the biological half-life and accumulation risk in human beings in different organs are not known in any detail.
10. It is obvious that mercury compounds have various effects on the genetic material. Apparently all compounds are active as c-mitotic agents.
At the time this article was published (1973) there were apparently no references or previous studies to refer to regarding the mist created by high speed amalgam removal. This study used rats and exposed them to amalgam mist, concluding the following:
1. The dust [amalgam dust from removal] is almost immediately absorbed into the bloodstream as shown by immediate increases detected by measuring the blood mercury content.
2. The heart receives extremely high levels of mercury within minutes after exposure. Eighty-one times higher than the control level.
3. The brain and liver reach their very highest levels of mercury at 16 hours post exposure. Both these levels were approximately 7 times higher than controls.
4. The heart, liver, brain and kidney concentrate mercury from the blood.
“The authors cannot at this time state how much is absorbed by a patient under varying conditions or positively state that this rat study is comparable to humans. However, the authors wish to point out the possible dangers of exposure to mercury even in minute quantities that might occur in the dental practice.
U.S. Army Institute of Dental Research
Walter Reed Army-Medical Center
Embedded Sentinels of Toxicity.
Author: Janet Raloff
Publication: Science News, 1987 Feb 21;131(8):123-125.
This article jumped out at me while performing a search during a college course and using their “EBSCO” system for retrieving published articles. There are numerous important points made in this article, so I recommend reading the full article above.
Apparently researchers have KNOWN that porphyrins can be used as biomarkers for toxic exposure since 1987! (maybe one day I will explain why this comes as such a shock). For example, one quote states,
…enzymes that convert one porphyrin into the next during the synthesis of heme “are quite sensitive, as a group, to chemically induced disturbances,” explains toxicologist Bruce Fowler of the National Institute of Environmental Health Sciences…As soon as the action of one enzyme in the process is blocked, the porphyrin on which it was to have acted begins accumulating in the urine or blood…Identifying a relative excess of one or more porphyrins and a shortage of succeeding ones in the heme-building process “sort of points the finger at which enzymes are being inhibited by a toxic chemical,” Fowler says.
Additionally, a well known incident that occurred in Turkey in the late 1950’s was discussed in which three to four thousand people developed a porphyria after eating wheat that had been treated with hexachlorobenzene (HCB). This is one of the earliest examples of the use of porphyrins as a biomarker for a toxic chemical exposure. Until this huge porphyria epidemic, it was believed that all of the porphyrias were genetic.
Porphyrinurias and occupational disease
Authors: MO Doss
Publication: Annals of the New York Academy of Sciences, 1987;514:204-18.
The author cites a Goldberg and Rimington report from 1962,
In the past the term ‘porphyria’ was reserved for those diseases of porphyrin metabolism caused by an “inborn error of metabolism,” that is, a genetic defect. “Porphyrinuria” was the term used to describe minor disorders of porphyrin metabolism induced by other diseases, or certain drugs or chemicals….The term “porphyrinuria” should be confined to those minor disorders or porphyrin metabolism caused by another disease, or certain drugs or chemicals, in which the clinical features are not directly attributable to the porphyrin abnormality.
This article came out the same year as the article above it (1987). Both differentiate between the genetic and acquired porphyrias by calling the acquired or non-specific porphyrin abnormalities “porphyrinurias” or “porphyrinopathies”.
I have not even produced 99% of the resources I have compiled and I believe that anyone with an IQ could review my records from 1995, and determine mercury was the likely cause. However today, even from well known toxicologists in my area (rural), I am told that they are not sure what could have caused the porphyrin abnormalities and do not care to seek out what may have caused them or my current disability. However the irritating/conflicting things I have been told are for another day.
That wraps up Part 1 of this post. In my next part, I will provide more articles from PubMed moving later into further research (1990’s) where porphyrins are being used as biomarkers to detect occupational exposure to mercury in dentists and more.
I will always feel like I am forgetting something or that there is some detail that will help someone understand where I am coming from and what this means to me. All well. My emotions and feelings are here for everyone to see, errors and all.
 Goldberg, A. & C. Rimington. 1962. Diseases of Porphyrin Metabolism. C.C. Thomas. Springfield, IL. BACK