Interview with Dr. Boyd E. Haley: Biomarkers supporting mercury
toxicity as the major exacerbator of neurological illness, recent
evidence via the urinary porphyrin tests

Boyd E. Haley, PhD and Teri Small
Medical Veritas 3(2006) 1-14
Abstract
In the recent past, several biological finds have supported the
hypothesis that early exposure of infants to Thimerosal was the major exacerbation factor in the increase in autism-related disorders since the advent of the mandated vaccine program. These initially included the observations of a genetic susceptibility impairing the excretion of mercury and the increased retention of mercury by autistic children. This was followed by data indicating that autistics have low levels of the natural compound glutathione that is necessary for the bilary excretion of mercury, possibly explaining the genetic susceptibility. Other observations clearly point out that various biochemical processes are inhibited at exceptionally low nanomolar levels of Thimerosal, including the killing of neurons in culture, the inhibition of the enzyme that makes methyl-B12, the inhibition of phagocytosis (the first step in the innate and acquired immune system), the inhibition of nerve growth factor function at levels not cytotoxic, and the negative effect on brain dendritic cells. It is also now quite clear from primate studies that Thimerosal, or more correctly, the ethylmercury from Thimerosal delivers mercury to the brain, and causes brain inorganic mercury levels higher than equal levels of methylmercury.

Most recently, one study showed that 53% of autistic children had aberrant prophyrin profiles similar to mercury toxic individuals.
Treatment of these children with a mercury chelator brought these porphyrins back towards normal levels indicating mercury toxicity was the cause, not genetic impairment. Porphyrin profiles are one of the most sensitive methods of measuring toxic mercury exposures.

Recently, in a major advance it was shown that about 15% of
individuals in one population displayed a marked sensitivity to mercury exposure in their porphyrin physiology, again supporting the concept of a genetically susceptible population that is more sensitive to mercury than the general population.

This observation on porphyrin aberrancies brings into consideration other possible effects of mercury toxicity that are secondary to porphyrin depletion. Porphyrins are the precursors to heme synthesis. Heme is the oxygen binding prosthetic group in hemoglobin and depletion of heme would affect oxygen delivery to the mitochondria and decrease energy production. Also, heme is a component of the electron transport system of mitochondria and a prosthetic group in the P450 enzymes which are fundamental in the detox of the body from many organic toxicants including pesticides and PCBs. Just recently, a report was released implying that lack of heme was the major reason why ß-amyloid plaques build up in the brains of Alzheimer’s diseased subjects. It seems that heme attaches to ß-amyloid helping it remain soluble and excretable. Without adequate heme one of the major pathological diagnostic hallmarks of Alzheimer’s disease appears. It is well known that mercury rapidly disrupts the normal polymerization of tubulin into microtubulin in brain tissue and aberrant tubulin polymerization is a consistent factor observed in Alzheimer’s diseased brain. Therefore, it is the multiple inhibitions of mercury that can cause various neurological and systemic problems and many of these are secondary to the primary site of mercury binding.

 

OTHER RELATED INFO

Woods JS, Martin MD, Naleway CA & Echeverria D

Urinary porphyrin profiles as a biomarker of mercury exposure: studies on dentists with occupational exposure to mercury vapor.

J Toxicol Environ Health 40(2-3): 235-246 (1993)

ABSTRACT: “Porphyrins are formed as intermediates in the biosynthesis of heme. In humans and other mammals, porphyrins with eight, seven, six, five, and four carboxyl groups are excreted in the urine in a well-established pattern. Mercury selectively alters porphyrin metabolism in kidney proximal tubule cells, leading to an altered urinary porphyrin excretion pattern. Previous studies in rats have shown that changes in the urinary porphyrin profile during exposure to mercury as methylmercury hydroxide are uniquely characterized by highly elevated (20- to 30-fold) levels of four- and five-carboxyl porphyrins and by the excretion of an atypical porphyrin (“precoproporphyrin”), which elutes on high performance liquid chromatography (HPLC) approximately midway between penta- and coproporphyrins. Changes in the urinary porphyrin profile are highly correlated with the dose and duration of mercury exposure and persist for up to 20 wk following cessation of mercury treatment. In the present studies, the utility of urinary porphyrin profile changes as a biomarker of mercury exposure in human subjects was evaluated. Urinary porphyrin concentrations were measured in dentists participating in the Health Screening Programs conducted during the 1991 and 1992 annual meetings of the American Dental Association and compared with urinary mercury levels measured in the same subjects. Among dentists with no detectable urinary mercury, mean concentrations of urinary porphyrins were within the established normal ranges for male human subjects. In contrast, among dentists with urinary mercury in excess of 20 micrograms/L, mean urinary concentrations of four- and five-carboxyl porphyrins as well as of precoproporphyrin were elevated three to four times those of unexposed subjects. Significant differences in urinary porphyrin concentrations remained when porphyrin concentrations in spot urine samples were adjusted for creatinine levels. These findings suggest that urinary porphyrin profiles may serve as a useful biomarker of mercury exposure in clinical or epidemiologic studies of mercury-related human health risks.”

 

The www-address of this page is:
http://www.algonet.se/~leif/yrWOO93a.html

 

Mercury Impairs The Manufacture of Blood
A study by Dr. James Woods published in the Journal of Toxicology 1993 REFERENCE #5 showed that mercury can inactivate the liver enzymes that are used in the manufacture of a precursor to blood called HEME, and this disrupts one’s ability to generate energy. More specifically he showed that mercury can disrupt the Coproporphyrin III Porphyrin step. In our example case, George’s Coproporphyrin III level was out of range, as shown here. There are very few things that cause this abnormal range yet do not affect other porphyrins (there are a total of 9 of them); therefore, this test is sometimes viewed as a biomarker for mercury. In other words, one an run this test and see if mercury had been in the body in the past, to the extent that it was able to disrupt this enzyme. If so, it probably did other deeds as well. For more information on how mercury can affect the blood, search “woods AND mercury” or “Aposhian AND mercury” at www.infotrieve.com/freemedline

 

Porphyrin Analysis

Test Summary This test looks a the manufacture of HEME by special enzymes. Heme is used to make blood. This is a 9 step process, and if any of the enzymes are missing for one of these steps, the chemical that goes into the step does not get converted to the chemical for the next step, and it spills into the urine. It has been found by Dr James Woods that mercury molecules (from fish or amalgam) can inactivate the Coprophyrin III step.
Test Details
Interpretation These results showed the Coprophyrin III step as being inactivated. There are not many thing that can do this, however one of them is mercury molecules binding with the enzymes used in the copro III step.
10/98 Test

Result Page 1

The above is from:   http://www.beatcfsandfms.org/html/HgRootCause.html  How Mercury can cause CFS/FMS

 

Re: Porphyrin test for mercury: worthwhile or not?

Posted by: “Stephanie” sage@isle.org   stevie_94306

Fri Oct 27, 2006 6:56 pm (PST)

— In Autism-Mercury@yahoogroups.com, “walescrimson” <williamsjm@…>
wrote:
>
> I’ve read many posts on this subject on this forum and elswhere and am
> worried about several negative features.
> 1. Andy Cutler’s file article on porphyrins refers to other metals and
> factors that can elevate porphyrin levels.

My impression is uroporphyrin and coproporphyrin are fairly
specific for mercury. Other porphyrins are elevated for other
metals. Try here:

http://home.earthlink.net/~moriam/ANDY_INDEX.html#fractionated_urine_p_tests

I think the bigger concern is handling of the sample.

> 2. Mandi refers to possible false negative results (any reports of
> false positives?)
> 3. Results for NT children can be elevated.
>
> In summary it is an indirect test which is not specific for mercury.
> However its attraction is that it is not invasive compared with a
> challenge test with a chelating agent.

Items 2 and 3 above also apply to challenge tests. In addition to
being meaningless, challenge tests can cause increased symptoms and
misery, sometimes of a permanent nature. This is completely
pointless and unnecessary.

A lot of people do hair tests. The hair test is cheap, safe, and
informative. If the test meets the counting rules, that indicates
a very high probability of mercury toxicity. If the test does not
meet the counting rules, other features can raise suspicion of
mercury.

A trial of chelation is always the ultimate test.   Posted on Autism mercury group by a family member of an autistic child

 

Testing for Toxic Metal- and Chemical-Induced Porphyrinuria

Carl P. Verdon, Ph.D., Terry A. Pollock, M.S. and J. Alexander Bralley, Ph.D., C.C.N.

Introduction

Toxic chemicals, at any level of chronic exposure, affect human biochemistry. Fortunately, the body has mechanisms for transforming, eliminating or compartmentalizing many toxic chemicals encountered over a lifetime. Nonetheless, these ‘safety’ mechanisms may be inadequate or even inappropriate in our modern industrialized society, especially for susceptible people such as the elderly, individuals with poor nutritional habits, and others who are physiologically stressed . One class of ‘textbook’ toxic chemicals capable of subtle yet insidious health effects that may mimic other disorders, especially in children, is that of the heavy metals. Lead, mercury, arsenic, aluminum, and cadmium are well-documented examples. Chronic exposure to these metals often results in organ-specific accumulation, which compromises the physiology of that organ. Similarly, chronic exposure to organic chemicals such as herbicides, pesticides, industrial and manufacturing byproducts can have deleterious impact on the body’s biochemistry, resulting in decline of cellular function .

Identifying offending chemical(s) can present a challenge for the clinician. Many chemicals exert their effect at such low concentrations that they escape detection except by very sophisticated laboratory methods. While measuring effects of toxicity by observing symptoms is a time-honored procedure, a preferred approach is to use corroborative laboratory methods that measure biomarkers that are specific indicators of the toxicant’s action.

Porphyrins measured in urine serve as such a biomarker. The presence or elevation of various urinary porphyrin species can flag a potentially toxic condition. Metals and other toxic chemicals with prooxidant reactivity can inactivate porphyrinogenic enzymes, deplete glutathione and other antioxidants and increase oxidant stress, all of which lead to damaged membranes, enzymes and other proteins in cells . In addition, porphyrinogens (precursors to porphyrins in the reduced state) themselves are easily nonenzymatically oxidized to porphyrins by toxic metals such as mercury (Figure 1). Thus, the distribution pattern of porphyrins in the urine serves as a functional ‘fingerprint’ of toxicity .

The utility of urinary porphyrins as a diagnostic tool is not new—its use has been documented in the literature since 1934. Specific diseases collectively known as the porphyrias, which can be inherited or acquired (e.g. acute intermittent porphryia, porphyria cutanea tarda, variegate porphyria), are often diagnosed with the aid of information regarding the distribution profile of individual porphyrin species in human urine.

Definitions

The different molecular species of porphyrins that occur in the urine of healthy individuals form a predictable, characteristic pattern. The alteration of the usual pattern of porphyrins caused by the elevation in one or more porphyrins is designated porphyrinuria. Porphyria, as a term, is reserved for primary conditions exhibiting specific clinical symptoms caused by an inherited defect in one or more of the heme biosynthetic enzymes. Porphyrinopathy is an umbrella term for any disorder in porphyrin metabolism.

The porphyrias have been classified in the literature in several different ways. Most commonly, porphyrias are presented in textbooks with specific biochemical reference to the principal enzyme deficiency (e.g. ALA dehydratase deficiency, etc.) and the site of the deficiency (i.e. hepatic, erythropoietic, or both). Other valid classifications arrange porphyrias according to symptomatology (neuropathic, dermatopathic or a mixed presentation of these symptoms) or by whether symptoms appear episodically (e.g., acute intermittent porphyria or chronically. It is also useful to organize porphyrias according to etiology (e.g., hereditary vs. acquired or toxicant-induced porphyria).

Background

Porphyrins are oxidized byproducts that have escaped from the heme biosynthetic pathway, an essential pathway occurring in all nucleated mammalian cells. Heme is the all-important iron-binding molecule essential for the proper function of many proteins, including hemoglobin (oxygen-transport), cytochrome c (energy production) and cytochrome P-450 (detoxification). Biosynthesis of heme involves eight enzymes (Figure 2), five of which produce intermediate molecules that are collectively called porphyrinogens. Some porphyrinogens escape the intracellular pathway to become oxidized to porphyrins by other cellular processes. Some porphyrins, in turn, are excreted in urine and feces. Inhibition of an enzyme for heme biosynthesis can result in the inappropriate accumulation of that enzyme’s substrate. The more severe the enzyme’s inhibition, the greater the tissue accumulation of porphyrins, sometimes becoming severe enough to cause clinical porphyria. The reader is encouraged to consult any standard medical textbook for a detailed description of classical inherited forms of porphyria.

Concepts

Elevations of the individual porphyrin species above the normal range have a number of causes, both inherited and environmental (see Table 1). The effect of chemicals on the porphyrin pathway has been the subject of many scientific reports. Lead, mercury or arsenic toxicity induces porphyrinuria , as well as polychlorinated phenyls (e.g. dioxin, PCB’s) , and many drugs (see Table 2). A study of practicing dentists reported correlations between elevated urinary 5-carboxyporphyrin, precoproporphyrin, coproporphyrin and behavioral changes that were related to urinary excretion of mercury . Together, elevations of these porphyrins served as biomarkers of mercury toxicity.

Upregulation of the heme biosynthetic pathway, with the concomitant increase in delta-aminolevulinic acid (ALA), is another mechanism by which porphyria can be precipitated. Increased ALA production is usually a normal physiological response to provide enough of this pre-porphyrin precursor to meet the body’s demand for heme. However, overproduction of ALA can overwhelm even a normally functioning heme biosynthetic pathway resulting in the inappropriate accumulation of ALA and/or the porphyrins . Commonly, active porphyria occurs when ALA overproduction coincides with inhibition of one or more of the porphyrinogenic enzymes. Very often, porphyria is the result of a chemical insult to a porphyrinogenic enzyme combined with an external stressor that provokes disregulation of the heme biosynthetic pathway. It is estimated that in cases of porphyrinogenic enzyme deficiency, as many as 90% of the patients are healthy throughout adulthood until their porphyria is triggered mid-life by toxic chemicals or drugs, an acute illness or worsening chronic condition, or a major dietary change .

Clinical

The clinical utility of a urinary porphyrin assay is maximized when urine samples are taken during the presentation of symptoms (see Table 3 and Table 4). Urine is best collected over a 24-hour period with 7 g of sodium carbonate added as a preservative. It may be useful with some patients to provoke their porphyria (a low carbohydrate diet for 2 days can be effective). Changes in the urinary porphyrins (i.e. porphyrinuria) coincident with provocation (e.g. fasting) or therapeutic intervention (e.g. medications, chelation therapy) is suggestive of some type of porphyrinopathy. If the patient’s response upon provocation can be duplicated, the possibility of a diagnosis of porphyria should be investigated. The twenty-four-hour output of any urinary porphyrin that is three or more times the upper-limit of the reference range may be indicating that organ accumulation of porphyrins is reaching pathological levels. In such cases, comprehensive porphyria workups are warranted. For out-of-range results that are lower than three times upper-limit, the rationale for further porphyria testing is predicated upon the availability of corroborating clinical or biochemical data such as complaints or family and patient medical history.

Use of porphyrin tests as biomarkers of chemical toxicity is reasonable when used in combination with other laboratory tests (e.g. hair analysis in cases of suspected metal toxicity). The clinician should realize that there are many conditions unrelated to primary or toxicant-induced porphyria that can cause porphyrinuria . When considering a urinary porphyrin result, the clinician should be mindful that the distribution of normal urinary porphyrins values representing healthy individuals overlaps significantly with those who have suffered from porphyria at one time or another.  

Conclusion

Any patients testing positive on the urinary porphyrins test should be subjected to follow up with more specific testing for a differential diagnosis. Tests that assay toxic metals directly in biological samples (i.e. blood, urine and hair) are essential for confirming whether the toxicity symptoms are caused by a metal. Identification of toxic organic chemicals by laboratory methods is also possible. Ruling out porphyria as the primary cause of porphyria-like symptoms requires tests for porphyrinogenic enzyme activities (e.g. uroporphyrinogen decarboxylase), as well as tests for blood, fecal and urine porphobilinogen (PBG) and delta-aminolevulinic acid (ALA).


FIGURE 1: Toxic Metals and Porphyria

Untitled1

Figure 1. Toxic metals induce porphyria and cell injury in that: 1) metals perturb cellular organelle function and promote an increase in reactive prooxidants, 2) metals complex with GSH thereby compromising antioxidant and thiol status, 3) metals impair enzymes and other proteins via SH-complexation, 4) the result of metal-induced oxidant stress is cell injury and the oxidation of porphyinogens to porphyrins that are excreted in the urine (porphyrinuria).

 


FIGURE 2:The Heme Biosynthetic Pathway

pic

The enzymes that drive the heme biosynthetic pathway are: (1) d-aminolevulinate (ALA) synthetase, (2) ALA dehydratase, (3) uroporphyrinogen I synthetase (PBG deaminase) and uroporphyrinogen III cosynthetase, two enzymes that work in concert, (4) uroporphyrinogen decarboxylase, (5) coproporphyrinogen oxidase, (6) protoporphyrinogen oxidase, and (7) ferrochelatase (heme synthetase). Spilled porphyrins derived from porphyrinogens with 8, 7, 6, 5, and 4-carboxyl groups are largely excreted in the urine while the less polar 2-carboxyporphyrin (protoporphyrin) is excreted exclusively in the feces. The physiologically relevant pathway leading to heme is that leading via uroporphyrinogen III, in which the propionyl and acetyl groups are “reversed” compared to those of the type I pathway, which “dead ends” with coprophyrinogen I. The physiological significance of the type I pathway remains unclear; however, coproporphyrin I is elevated in hepatobiliary diseases and arsenic toxicity.


TABLE 1. Various causes and
conditions related to porphyria
Intoxications
Alcoholism; foreign and environmental chemicals such as hexachlorobenzene, polyhalogenated biphenyls, dioxins (TCDD), vinyl chloride, carbon tetrachloride, benzene, chloroform; heavy metals such as lead, arsenic, mercury; drugs

Liver diseases
Cirrhosis, active chronic hepatitis, toxic and infectious hepatitis, fatty liver, alcoholic liver syndromes, drug injury, cholestasis, cholangitis, biliary cirrhosis

Adverse effect of drugs
Analgesics, sedatives, hypnotics, anesthetics, sex hormones, sulfa-drug antibiotics

Infectious diseases
Mononucleosis, acute poliomyelitis

Diabetes mellitus

Myocardial infarction

Hematologic diseases
Hemolytic, sideroachrestic, sideroblastic, aplastic anemias; ineffective erythropoiesis (intramedullary hemolysis); pernicious anemia; thalassemia; leukemia; erythroblastosis; iron deficiency anemia

Malignancies
Hepatocellular tumors, hepatic metastases, pancreatic carcinoma, lymphomatosis, other systemic diseases

Disturbance of iron metabolism
Hemosiderosis, idiopathic and secondary hemochromatosis

Hereditary hyperbilirubinemias
Dubin-Johnson syndrome
Rotor’s syndrome

Pregnancy

Carbohydrate fasting

Bronze baby syndrome

Erythrohepatic protoporphyria

   Hereditary tyrosinemia

 

TABLE 2. Drugs known to cause or
exacerbate porphyria1
     Antipyrine
Amidopyrine
Aminoglutethimide
Barbiturates
Carbamazepine
Carbromal
Chloropropramide
Chloral hydrate
Danazol
Dapsone
Diclofenac
Diphenylhydrantoin
Ergot preparations
Ethanol (acute)
Ethclorvynol
Ethinamate
Glutethimide
Griseofulvin
Isopropylmeprobamate
Mephenyltoin
Meprobamate
Methylprylon
N-butylscopolammaonium bromide
Nitrous oxide
Novobiocin
Phenylbutazone
Primadone
Pyrazolone preparations
Succinimides
Sulfonamide antibiotics
Sulfonthylmethane
Sulfonmethane
Synthetic estrogens, progestins
Tolazamide
Tolbutamide
Trimethadone
Valproic acid
1- Although this list includes many of the better known drugs that can exacerbate porphyria, it should not be considered complete.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 


 

TABLE 3. Symptomatology of the porphyrinopathies
Primary Complaints Associated symptoms Condition Exacerbated by
Neurologic Presentations
Abdominal pain; nausea;vomiting; constipation; seizures Headaches; difficulty in concentration; personality changes; weakness; muscle and joint aches; unsteady gait, poor coordination; numbness, tingling of arms and legs; fluid retention; rapid heart rate; high blood pressure; increased sweating; intermittent fever Low carbohydrate diets (skipped meals); intake of alcoholic beverages; medications, including sulfa drug antibiotics, barbiturates, estrogen, birth control pills; exposure to toxic chemicals
Cutaneous Presentations
Changes in skin pigmentation; changes in facial hair; fragile skin; rashes; blistering Dark-colored urine (esp. after its exposure to sunlight), and above symptoms may be present. Above factors, and skin symptoms made worse by exposure to sunlight. Copper or brass jewelry exacerbates reaction.

TABLE 4. Interpretation of abnormal urinary porphyrin test results: Relationship to heme pathway defects and possible causes (with emphasis to toxic metals)
Abnormal Test Result1 Heme Pathway Defect2 Possible Environmental Cause3
Uroporphyrin and
7-Carboxyporphyrin (sometimes)
Uroporphyrinogen decarboxylase Arsenic (high levels; see References 8).
Certain organic chemicals.
5-carboxyporphyrin and
Coproporphyrin6-carboxyporphyrin (sometimes)
Uroporphyrinogen decarboxylase
Coproporphyrinogen oxidase
Mercury (see Reference 5)
Certain organic chemicals.
Precoproporphyrin4 (almost always accompanied by elevated coproporphyrin III) Uroporphyrinogen decarboxylase (possibly) Mercury (see Reference 5)
Coproporphyrin III
Coproporphyrin I (sometimes)
Coproporphyrinogen oxidase Lead or Mercury (see Reference 2)
Certain organic chemicals.
Coproporphyrin I: Coproporphyrin III
Ratio > 1
Hepatobiliary dysfunction (Reference 3)
PBG deaminase
Arsenic (see References 8)

NOTES

1Reference ranges vary depending upon the calibration standards of the laboratory doing the analysis. The following reference range (in units of nanomoles/24 hr) was set to accentuate sensitivity (i.e. more patients with true porphyrinuria being detected at the risk of an increased false-positive rate). A multiplication factor to convert values to micrograms/24 hr are shown in parentheses: uroporphyrin, 41 (0.830); 7-carboxyporphyrin, 14 (0.787); 6-carboxyporphyrin, 6 (0.743); 5- carboxyporphyrin, 5 (0.699); coproporphyrin I, 40 (0.654); coproporphyrin III, 79 (0.654). The reference range for the particular laboratory conducting the analysis should be used.

2Inherited disorders in the enzymes of heme biosynthesis are relatively rare but such a possibility should be considered if urinary porphyrins are greatly elevated. Please consult a specialist in inherited disorders if such a disorder is suspected.

3When evaluating urinary porphyrin results to arrive at a diagnosis of metal or chemical toxicity, the following should be ruled out: use of ethanol, estrogens, oral contraceptives, antibiotics, sedatives, analgesics, dietary brewer’s yeast; also rule out pregnancy, liver disease, malignancies, hematologic diseases such as pernicious or iron deficiency anemias. See Table 3 for a more complete list.

4The detection of precoproporphyrin is specifically diagnostic for mercury toxicity (see reference 5).


TOP


References 

  1. Rowland I, ed., Nutrition, toxicity, and cancer. Boca Raton, FL: CRC Press, 1991.
  2. Baker S., Detoxification and healing. New Canaan, CT: Keats Publishing Inc., 1997.
  3. Chang L, Magos L, Suzuki T, eds., Toxicology of metals. Boca Raton, FL: CRC Press, 1996.
  4. Fowler BA, Oskarsson A, Woods JS., Metal- and metalloid-induced porphyrinurias. Relationships to cell injury. Ann N Y Acad Sci 1987;514:172-82.
  5. Woods JS, Bowers MA, Davis HA., Urinary porphyrin profiles as biomarkers of trace metal exposure and toxicity: studies on urinary porphyrin excretion patterns in rats during prolonged exposure to methyl mercury. Toxicol Appl Pharmacol 1991;110:464-76.
  6. Kappas A, Sassa S, Galbraith RA, Nordmann Y., The porphyrias. In: Scriver CR, Beaudet AL, Sly WS, Valle D, eds. The Metabolic and Molecular Bases of Inherited Disease, Seventh Edition. New York: McGraw-Hill, 1995:2103-2159.
  7. Woods JS., Porphyrin metabolism as indicator of metal exposure and toxicity. In: Goyer RA, Cherian MG, eds. Handbook of Experimental Pharmacology. Berlin: Springer-Verlag, 1995:19-52.
  8. Garcia-Vargas GG, Del Razo LM, Cebrian ME, et al., Altered urinary porphyrin excretion in a human population chronically exposed to arsenic in Mexico. Hum Exp Toxicol 1994;13:839-47.
  9. Doss MO., Porphyrinurias and occupational disease. In: Silbergeld E, Fowler B, eds. Mechanisms of Chemical-Induced Porphyrinopathies, 1987:204-218.
  10. Moore MR, Disler PB., Drug-induction of the acute porphyrias [Review]. Adv Drug React Ac Pois Rev 1983;2:149-189.
  11. Woods JS, Martin MD, Naleway CA, Echeverria D., Urinary porphyrin profiles as a biomarker of mercury exposure: Studies on dentists with occupational exposure to mercury vapor. Journal of Toxicology and Environmental Health 1993;40:235-246.
  12. Woods JS., Altered porphyrin metabolism as a biomarker of mercury exposure and toxicity. Canadian Journal of Physiology and Pharmacology 1996;74:210-215.
  13. Donnay A, Ziem G., Porphyria protocol packet (on evaluating disorders of porphyrin metabolism in chemically-sensitive patients). MCS Referral and Resources, Inc., Baltimore, MD1995.

 

http://www.metametrix.com/Publications/Toxic%20Metals/

 

 

Go down this page and listen to Dr. Nataf, all 3 segments.

 

http://www.autismmedia.org/media4.html

 

I found Dr. Buttar to be inspiring also!

 

Mary

 

Begin forwarded message:

 

From: Mary Ludwig <mludwig@interrupt9.com>

Date: October 27, 2006 8:16:33 AM EDT

Subject: precoproporphyrin

 

Janet,

Actually, there is a fairly simple urine test–the urinary porphyrins
test–that measures body burden of mercury.

This test will show you if you are mercury toxic and how much so. If
you aren’t doing biomedical treatments and don’t have a DAN! doctor,
it’s not a problem. You do not need a doctor’s prescription to run
this test. You can request that the test results be emailed/mailed to
you directly.

The Lab had a booth at Autism One and Dr. Nataf (from France) gave a
Power Point Presentation about this. You can download it from the
AutismOne website.

http://www.autismone.org/uploads/Nataf%20Robert.ppt

AutismOne Radio had a broadcast regarding this. July 4, 2006, 10:00 am
- 12:00 ET, Teri Small : Autism: Help, Hope, and Healing, Guest: Dr.
James Woods, Topic: Urinary porphyrin profiles and mercury.

Email Laboratoire Philippe Auguste in France and request a porphyrin
test kit.

Laboratoire Philippe Auguste
119 Avenue Philippe Auguste
75011 Paris France
e-mail: contact@labbio.net
Tel: 0033143721398

It costs around 120 USD. First morning urine is the best. What sets
the porphryin tests from the Lab in France apart from the porphryin
tests that are performed in the U.S. is that they can test for a
specific porphyrin called precoproporphyrin. This specific biomarker
indicates mercury toxicity.