Environmental Medicine: Excerpts from Articles on Current Toxicity, Solvents, Pesticides and Heavy Metals

by Walter J. Crinnion ND

Originally published as multi-part review article in Alternative Medicine Review, Volume 5, 2000. P.O. Box 25, Dover, Idaho 83825 USA.

Abstract: Chemical compounds ubiquitous in our food, air and water are now found in every person. The bioaccumulation of these compounds in some individuals can lead to a variety of metabolic and systemic dysfunctions and in some cases, outright disease states. The primary classes of the most common toxic offenders are solvents, pesticides and heavy metals. Of heavy metals, mercury is the one most individuals are burdened by. The systems most affected by these xenobiotic compounds include the immune, neurological and endocrine systems.

Environmental Toxic Load

The 20th Century with its promise of “Better Living Through Chemistry” has brought a host of chemical toxin related illnesses (referred to here as “Environmental Illnesses”). Recent articles in the medical literature have shown that the rate of cancers not associated with smoking are higher for those born after 1940 than before, and that this increase of cancer is due to environmental factors other than smoking_.1 We are also experiencing the new medical diagnoses of Sick (Closed) Building Syndrome,2,3 and Multiple Chemical Sensitivity (MCS)_,4-6 both of which are known to be related to overexposure to environmental contaminants. The primary action of the major pesticide classes is to disrupt neurological function_.7 The primary action of the solvents is neurotoxicity8_ as well. In addition to being neurotoxic these compounds are profoundly immunotoxic9-11 _ _and are often toxic to the endocrine system as well. The adverse health effects are not limited to those systems only as these compounds can also cause a variety of dermatological, gastrointestinal, genitourinary, respiratory, musculoskeletal, and cardiological problems.12

Our environment is currently flooded with chemicals that fill our air, our water, our food and our bodies. Since 1976 the Environmental Protection Agency (EPA) has been running the National Human Adipose Tissue Survey (NHATS).13 NHATS is an annual program to collect and chemically analyze a nationwide sample of adipose tissue specimens for the presence of toxic compounds. The objective of the program is to detect and quantify the prevalence of toxic compounds in the general population. The specimens are collected from autopsied cadavers and elective surgeries from all regions of the country. In 1982 they expanded beyond their normal list to look for the presence of 54 different environmental chemical toxins. Their results were astounding. Five of these chemicals: OCDD (a dioxin) and four solvents: styrene, 1,4-Dichlorobenzene, xylene, and ethylphenol were found in 100% of all samples. The ranges of these five compounds found in every sample were also alarming. OCDD levels ranged from19-3,700ng per gram of fat, styrene 8-350 ng/g, 1,4-Dichlorobenzene from 12-500 ng/g, xylene from 18-1,400 ng/g and ethylphenol from 0.4-400ng/g. These alone would give each person a total toxic burden ranging between 57.4-6,350 ng of toxins per gram of fat!

Another nine chemicals were found in between 91-98% of all samples, including such toxins as: Benzene, toluene, chlorobenzene, ethylbenzene, DDE*, three dioxins and one furan. In addition, PCBs were found in 83% of all samples and beta-BHC in 87%. These along with a few more gave a total of 20 toxic compounds found in 76% or more of all samples. This would provide a range of toxic compounds in 76% of individuals that would go up to 25,704 ng of these twenty toxins per gram of fat (not total load)! Additional studies have shown the same startling facts. A CDC study of 5994 persons aged 12-74 found that 99.5% had p,p-DDE at serum levels equal to or greater that 1 ppb, in a range of 1-379 ppb.14 A study of adipose levels taken from autopsies from older subjects who had lived in Texas showed the presence of p,p-DDE, Dieldrin, Oxychlordane, Heptachlor epoxide and para-BHC in 100% of all samples.15 A study of four-year old children in Michigan revealed the presence of DDT in over 70%, PCB in over 50% and PBB in over 21%.16 It was found that nursing was the primary source of exposure for these individuals. These ongoing assessments have shown quite clearly that it is not a question of if we are carrying a burden of toxic xenobiotic compounds, it is a question of how much and how do they affect our health. This multiple chemical load comes from daily exposures to chemical compounds in our air, food and water.

Indoor Air – Home

In 1985 the TEAM study (Total Exposure Assessment Methodology) by the Environmental Protection Agency (EPA) changed the way we viewed our indoor air quality. This study showed that the greatest personal exposure to levels of volatile organic compounds (VOCs) occurred from air in the home and not from outside air as had previously been thought.17,18_ These studies looked for the presence of 20 VOCs also known as ‘solvents’ in indoor air, outdoor air, breath and “personal air” in a total of 780 persons. Their “personal air” was sampled by attaching sampling cartridges on their clothing. Personal air samples revealed very high exposure levels to eleven VOCs (see Table 1), in levels much higher than would have been predicted by outdoor air levels. The biggest source of these “personal exposures” came from indoor air, which showed much higher levels of VOCs, especially at night, than what was measurable in the back yard of the same home in the same time frame.

Table 1. The Volatile Organic Compounds Found Consistently in Breath Samples in the TEAM Study:




Carbon Tetrachloride








The compounds found most commonly were: paradichlorobenzene (from mothballs, and room deodorizers), styrene (plastics, foam rubber, and insulation), tetrachloroethylene (dry cleaning), vinylidene chloride (plastics), and xylene (paints), as well as benzene and ethylbenzene from gasoline. Higher levels were found in the breath of smokers than in non-smokers, confirming earlier work that showed smoking increased alveolar retention of inhaled chemicals. They also reported higher levels of benzene, xylene and tetrachloroethylene in personal sample cartridges after the individual visited a gas station or a dry cleaning establishment. Individuals working in dry cleaning businesses obviously have much higher exposures than their patrons. However, the dry cleaners also bring the tetrachloroethylene (also known as perchloroethylene) home with them, presumably on their clothing, hair and in their lungs. Significantly higher levels of tetrachlorethylene are found in the indoor air of the homes of dry cleaners than in selected control homes, leading to increased exposure for their families as well.19

Studies done previously and reviewed in the TEAM study showed fairly consistent results in more than 800 homes. All reported that every one of the 40 or more VOCs studied were found in higher levels indoors than outdoor, often 10 times higher. The sources for these compounds were numerous and included: building materials, furnishings, dry-cleaned clothes, cigarettes, gasoline, cleansers, moth crystals, hot showers and printed materials. They also found that the ranges of concentration were great, often with two or more orders of magnitude difference. Not only have repeated studies shown the amount of solvents that all are exposed to – they have also shown that those who are exposed must pass them through their bodies. As mentioned earlier dichlorobenzene, from moth balls and room deodorizers, was one of the solvents found high in indoor air. The metabolite of dichlorobenzene has been found in the urine of 96% of all children in Arkansas and in 98% of 1,000 selected adults from across the United States_.20

The elevated levels of these compounds in home air can be attributed to two major factors. First, as a result of the “oil shortage” in the 1970’s, building techniques were changed to emphasize airtight “energy efficient” homes. The new building methods emphasized a reduction in incidental exchange of inside and outside air so that the internal home climate would not diffuse, and therefore less energy would be needed to maintain its temperature. As a consequence of reducing the inside air exchange, these homes retain the off-gassed VOCs in higher levels than less airtight homes.

Second, during the same time frame a tremendous increase in the use of VOC-containing compounds in building materials, fabrics, and home furnishings began. The use of standard plywood gave way to using less-costly chipboard with higher formaldehyde and VOC content. Plywood laminate beams with higher formaldehyde content have replaced solid wood beams. Flooring has gone from hardwood to plywood with pad and carpeting, all of which off-gas VOCs. The 1970s also saw changes in home-furnishing materials that put VOCs into the indoor air. Polyurethane foam and polyester fiberfill replaced traditional upholstery fillers in sofas and chairs, and synthetic fabrics replaced cotton, rayon, and silk in draperies and upholstery. The upholstery fabrics themselves have formaldehyde in them to prevent them from getting wrinkled. Plastic items, off-gassing phthalates, are now found throughout the home. The presence of many “home offices” with computers, fax machines and copiers has increased the amount of ozone, plastic fumes and VOCs present in the homes as well. These items, in addition to paints, glues, gas heating, gas appliances, attached garages, storage of paints, paint thinner, gasoline, pesticides, herbicides, as well as biological contaminants of molds and bacteria all contribute to a very toxic home environment. Table 2 lists the categories of indoor air pollutants.

Table 2. Categories of Indoor Air Pollutants

1. Combustion by-products

2. Volatile organic compounds

3. Respirable dusts and particulates: Molds, Cigarette smoke, Infectious agents, Animal dander

4. Bioaerosols

5. Contaminants generated by human activity

The unfortunate truth is that wherever we go, outdoors or indoors, at work or at home, we are breathing in solvents. The worst places with high solvent content in the air are the homes where people usually spend at least half of their day, and their workplace, where they spend at least eight hours.

Indoor Air - The Workplace

In office buildings the operational costs of ventilation were given higher priority than ventilation rates. This brought about more recycling of air, rather than a greater exchange with outdoor air. Throughout the 1980’s and still into the 1990’s there have been many instances of poorly conceived and poorly operated heating, ventilation and air conditioning (HVAC) systems. HVAC systems have condensers that can provide a fertile place for the proliferation of biological agents that contaminate the air. This was first noted in the Legionnaire’s disease outbreak, when 221 attendees at the 1976 American Legion conference became ill from an airborne biological agent (later named Legionella pneumophilia). The office buildings of two of my patients had the fresh air intake in direct line with the exhaust for the heater system in one and the underground garage in another, thus putting high levels of polycyclic aromatic hydrocarbons directly into the HVAC system. With the new modular/cubicle office landscapes containing carpeted floors and partitions, along with new laminated pressboard furniture, computers, fax machines and copiers, the level of formaldehyde, ozone and VOCs is high in many buildings. Often the levels of these compounds are within the ‘threshold’ values that industry has set for itself, but these levels continue to cause problems for certain individuals

New or newly remodeled buildings have a high amount of chemical off-gassing and can easily become “sick buildings” with many workers getting “sick building syndrome” (SBS)_.21,22 The most common presenting symptoms of SBS are: headache, eye, nose and throat irritation, dizziness, disorientation, difficulty concentrating and fatigue.23 When complaints of SBS first surfaced, the complaining workers were often treated poorly. Upon repeated complaints, the building owners would often hire an air quality consultant who would test for the presence of a single compound, such as carbon monoxide. Quite often these individual compounds would be well within the standards for air quality set by the EPA. In fact, this happened in the EPA itself after completion of a new headquarters building in Washington DC in 1988. Many of the workers began to complain of adverse health symptoms, the air was tested, and no single agent was found to be out of range. However when 71 ill employees evacuated the building due to health problems (that went away when they were not in the building) and began picketing, the EPA realized there was a real issue here. This awakening on the part of the EPA resulted in the EPA booklet entitled: The Inside Story, A Guide to Indoor Air Quality (September 1988, EPA/400/1-88/004).

Food Pollution

Testing for chemical residues on food has routinely been done throughout the world, which consistently find multiple contaminants. The most comprehensive for the United States is the ongoing FDA Total Diet Survey.24 While the Total Diet Survey looked for the presence of many different chemicals, by looking at their findings of chlorinated pesticides we see alarming information. DDE was found in 100% of the samples of raisins, spinach (fresh and frozen), chili con carne (beef and bean), and beef. It was found in 93% of the samples of American processed cheese, hamburger, hot-dogs, bologna, collards, chicken, turkey and ice cream sandwiches. It was found in 87% of the samples of lamb chops, salami, canned spinach, meatloaf and butter. It was found in 81% of the samples of cheddar cheese, pork sausage, quarter-pounders, white sauce, and creamed spinach. Of all items sampled, 42 had DDE in 63% or more of all samples. The foods with the highest concentrations of DDE were: fresh or frozen spinach (mean concentration of 0.0234 ppm), then butter (mean concentration 0.0195 ppm), followed by collards (0.0126 ppm), pork sausage (0.0124 ppm), lamb chops (0.0113 ppm) and then canned spinach (0.0109 ppm). Since DDT and DDE have been banned for use in this country since 1972, it is likely that some of this contamination is from produce imported from other countries where it is still used.

Unfortunately, since toxic chemicals are so ubiquitously used in the world, they move easily around the globe on the winds. Unless these pesticides get trapped in the soil, tree bark, or other stable materials, persistent volatile pesticides, including DDT and toxaphene, begin a wind-driven leapfrogging around the globe.

The more volatile the chemical, the faster it hops and the less readily it enters the structure of any plant or animal it contacts. Volatile chemicals applied in tropical regions evaporate into the atmosphere and then condense in cooler climates. As the ambient temperature falls, the compound becomes less volatile, so the periods between when a compound hops from one place to another tend to lengthen. So, if two forests were exposed to identical amounts of a volatile pesticide, trees in the colder one would become more heavily contaminated.

DDT is less volatile and doesn’t leapfrog as well so it tends to get stuck where it lands and may be there for a year before jumping again. This global leapfrogging can account for one alarming study of diet of arctic indigenous women. The diets of two groups of women (from both the eastern and western Canadian arctic) were found to be very high in organochlorine compounds (OCC). The primary sources of these compounds were the meat and blubber of ringed seal, walrus, mattak and narwhal as well as caribou, whitefish, inconnu, trout and duck_. Since these OCCs were transported in the air, they landed in the arctic, but due to the low temperature were unable to volatilize again and leapfrog away.

Adverse Health Effects of Solvents

Solvents can have a variety of adverse health effects. Previously I reviewed the EPA National Human Adipose Tissue survey that showed that four solvents were present in 100% of samples tested across the country. These four were xylene, dichlorobenzene, ethylphenol and styrene (listed in decreasing order).26 For them to be in the adipose tissue of every US citizen that was tested that year would confirm that US residents have been regularly exposed over long periods of time to VOCs and that these compounds are being stored in our adipose tissue.

The VOCs primarily act in the body as both peripheral and central nervous system neurotoxins.27,28 When the central nervous system is primarily affected the symptoms can include diminished cognition, memory, reaction time, hand-eye and foot-eye coordination, balance and gait disturbances. It can also lead to mood disorders, with depression, irritability and fatigue being common symptoms. Peripheral neurotoxicity usually results in paresthesias, tremors, and diminished fine and gross motor movements.

VOCs have been implicated in kidney damage.16-18,29-31 _ _ They have been associated with immunological problems including increased cancer rates and immunotoxicity.32 Solvents have been found to lower testosterone, LH33_ and increase insulin and sex hormone binding globulin.34,35 They have been associated with infertility,36 decreased sperm count,37 increased rates of spontaneous abortions38_ and increased rates of fetal malformations.39 They have also been associated with hematological disorders40 and increased rates of cardiovascular deaths.41 Indoor air levels of solvents and formaldehyde are closely associated with increased rates of asthma and chronic bronchitis, especially in children.42 The typical presentation of low-dose formaldehyde exposure includes upper respiratory irritations (rhinitis, sinusitis, pharyngitis), lower respiratory symptoms of wheezing in certain cases and frequently, a feeling of having a flu-like illness that persists.

Elemental Mercury

Silver “amalgam” dental fillings typically weigh between 1.5-2.0g with approximately 50% of the material being elemental mercury. Persons with such fillings on their occlusal surfaces have been found to have levels of mercury vapor in their oral cavity nine times greater than persons without amalgams when no chewing has occurred (unstimulated). When chewing stimulation occurs, those same individuals had a six-fold increase in elemental mercury levels. This gave those amalgam-bearing individuals 54 times greater levels of mercury vapor in their oral cavities during chewing than persons without amalgams.43 Serial measurements of these individuals found that mercury concentrations remained elevated during 30 minutes of continuous chewing and declined slowly over 90 minutes after cessation of chewing.44 Based upon their small trial (35 subjects) the researchers concluded that persons with one to four occlusal amalgams would be exposed to an average daily dose of 8ug elemental mercury. Those with twelve or more occlusal amalgams were estimated to receive 29ug per day. They placed the average of all the 35 subjects at 20ug per day. Individual cases have been published showing urinary mercury excretion to be 23-60ug/Hg/day (25-54ug/g creatinine) indicating a daily intake as high as 100ug.45 In these individuals bruxism and gum chewing were noted as the probable causes of the high mercury output, which fell back to “normal” levels with amalgam removal. Greater levels of mercury release from dental amalgams have also been found with tooth brushing46 _ and after consuming hot drinks.47

Mercury vapor released in these instances is highly lipid-soluble and enters the blood from both the lungs and oral mucus membranes, traverses cell membranes (including the blood-brain and placental barriers), rapidly partitions between plasma and red blood cells and becomes widely distributed. Up to 40% of the mercury vapor is excreted through the feces.48 Once in the cells Hg gets oxidized by catalase-hydrogen peroxide and becomes divalent Hg2+, a reactive species. This combines covalently with nearby sulfhydryl groups such as hemoglobin, reduced glutathione and protein cysteine groups. Those with mercury exposure have been found to have lower levels of reduced glutathione.49

Blood mercury concentrations have been positively correlated with the number and surface area of amalgam restorations and are significantly higher in those with amalgams than those without.50 Amalgams are also associated with higher urinary output51_ as well as high levels in breast milk but not hair.52 When examining association with mercury presence in breast milk it was found that total and inorganic mercury levels in blood and milk were correlated with the number of amalgam fillings. In this study where seafood was not the main dietary staple there was no association found between dietary methylmercury intake and milk levels. Exposure of the breastfeeding infant to mercury was calculated at a range of up to 0.3ug/kg (one half of the tolerable daily intake for adults recommended by the World Health Organization).

Animal models have demonstrated that mercury from dental amalgams will migrate to, and concentrate in the kidney, liver, gastrointestinal tract, and jaw.53,54 The choroid plexus, an important part of the blood-brain barrier, acts as a sink for mercury and other heavy metals.55 It has also been shown that mercury is selectively concentrated in human brains in the medial basal nucleus, amygdala and hippocampus regions, all of which are involved with memory function, the granule cells in the granular layer of the cerebellum and the sensory neurons of the dorsal root ganglia. It has also been shown to be taken up by the retina,56 the granule cells of layer IV in the visual cortex of the brain, and to cause an reversible impairment of color perception.57

Cellular and Nutritional Alterations

Mercury has the ability to cause changes on the cellular level including in platelets and erythrocytes. These cells were used as surrogate markers for mercury damage of neurological tissue. It was found that the addition of methylmercury to whole blood caused a dramatic dissolution of microtubules in platelets and red blood cells. This effect was more pronounced in erythrocytes than platelets, which was consistent with the known sequestration of methylmercury in erythrocytes.58 This effect on microtubules has also been found in the brain59 and results in the disruption of the cell cycle. This disruption has been shown to lead to apoptosis in both neuronal and non-neuronal cells.60

Mercury has also been found to cause apoptosis in monocytes and to decrease phagocytic activity.61 The percentage of cells undergoing apoptosis was dependent upon the mercury content of the medium, regardless of the form of mercury. Methylmercury chloride was also shown in the same study to cause a decrease in the mitochondrial transmembrane potential within one hour of exposure. Methylmercury has also been shown to cause increased rates of lymphocyte apoptosis. The mechanism for this includes a depletion of glutathione (GSH) content, predisposing the cell to oxidative damage while activating death-signaling pathways.62 These researchers also found that mercury led to altered mitochondrial function. When synovial joint tissue was looked at it was found that mercury (as well as cadmium and lead) caused a decrease in DNA content and an increase in collagenase-resistant protein formation.63

Mercury is bound by selenium in the body, which can actually counteract mercuric chloride and methylmercury toxicity.64,65 While this does not result in a decrease in the amount of mercury, it does result in a decrease in the toxicity of mercury. However, it appears to lead to a reduced amount of available selenium which compounds the oxidative burden on the body. It was previously mentioned that mercury reduces the level of GSH in the body, which is accomplished by several mechanisms. Mercury will bind irreversibly to GSH causing the loss up to two GSH molecules through the bile into the feces. Part of the irreversible loss of GSH is due to the inhibition of GSH reductase by mercury,66 which is used to “recycle” oxidized GSH and return GSH to the pool of available antioxidants. At the same time, mercury also inhibits GSH synthetase so that less new GSH can be made. This is compounded by the mercury-reduced selenium content that would normally stimulate more GSH production. Since mercury promotes formation of hydrogen peroxide, lipid peroxides and hydroxyl radicals at the same time, it is clear that mercury sets up a scenario for a serious imbalance in the oxidative/antioxidant ratio of the body.67 The heavy oxidative toll on the body by mercury has been postulated to be a cause of increased rates of fatal myocardial infarctions and other forms of cardiovascular disease.68 All of these interactions show the clear need for increased levels of Selenium, and Vitamin E, which has also been shown to reduce methylmercury toxicity.69

Mercury-Induced Neurotoxicity

Mercury in both organic and inorganic forms is neurotoxic. Methylmercury accumulates in the brain and becomes associated with mitochondria, endoplasmic reticulum, golgi complex, nuclear envelopes, and lysosomes. In nerve fibers methylmercury is localized primarily in myelin sheaths where it leads to demyelination and in the mitochondria.70 Pathologic examination of patients with methylmercury poisoning indicates that the cerebellar cortex is prominently affected with granule cells being more susceptible than Purkinje cells. Typically, glial cells are spared direct damage, although reactive gliosis may occur. Toxicity from mercury probably does not result from action on a single target. Instead, because of its highly reactive nature, a complex series of many unrelated (and some interrelated) effects may occur more or less simultaneously, initiating a sequence of additional events that ultimately lead to cell death. Some of these events include the following:

The adverse effect of mercury on GSH has secondary effects on the levels of Na+, K+ and Mg++ ATPases, all of which are –SH dependent. These enzymes are all found to be reduced by various mercurial compounds71_ and are critical for the proper functioning of nervous and other tissues. Injections of GSH in animals exposed to methylmercury fortunately resulted in the recovery of N+, K+, and Mg++ ATPases.72 In the absence of nutrients to counteract this action, the reduction of these ATPases results in the neurotoxic swelling and destruction of astrocytes.73 Astrocytes are the primary cells responsible for the homeostatic control of synaptic pH, Na/K and glutamate. Mercury is also known to inhibit the uptake of dopamine,74 serotonin,75 and norepinephrine76_ at synaptic sites. For serotonin-binding sites the mercury apparently has a higher binding affinity. Mercury has also been reported to cause an increase in evoked acetylcholine release followed by a sudden and complete blockade.77 Prolonged exposure to methylmercury results in an up-regulation of muscarinic cholinergic receptors in the hippocampus and cerebellum and on circulating lymphocytes.78 It also affects the release of neurotransmitters from presynaptic nerve terminals. This may be due to its ability to change the intracellular concentration of Ca2+ by disrupting regulation of Ca2+ from intracellular pools and increasing the permeability of plasma membranes to Ca2+.79 While there is undoubtedly much more to learn about the specific mechanisms of mercury-neurotoxicity, its symptoms are fairly clear.

The widespread pollution of Minamata bay by methylmercury in the 1950s has provided researchers with a clear picture of methylmercury-induced neurotoxicity as a great cost to the inhabitants of the area. Known as Minamata Disease (MD), the neurotoxic signs include ataxia, speech impairment, constriction of visual fields, hypoesthesia, dysarthria, hearing impairment and sensory disturbances. These neurological problems persisted and were found in other areas of Japan as the mercury contamination spread.80 Follow-up studies in the Minamata area almost 40 years after the spill and almost 30 years since a fishing ban was enacted for the area, showed continued problems. Residents in fishing villages in the area in 1995 reported significantly higher prevalences than “town-resident-controls” in males for the following complaints: stiffness, dysesthesia, hand tremor, dizziness, loss of pain sensation, cramping, atrophy of the upper arm musculature, arthralgia, insomnia and lumbago. Female residents of the fishing villages had significantly higher incidents of complaints of leg tremor, tinnitus, loss of touch sensation, leg muscular atrophy and muscular weakness.81 Amazonian children exposed to methylmercury from local gold mining have also been studied for the neurotoxic effect of methylmercury. In the villages studied, more than 80% of the children had hair mercury levels above 10ug/g (a level above which adverse effects on brain development are likely to occur). Neuropsychological tests of motor function, attention, and visuospatial performance in these children showed decrements associated with hair mercury concentrations.82

Neurotoxicity is not related only to methylmercury as a study of 98 dentists with 54 non-dentist controls revealed. The dentists, with an average of 5.5 years of exposure to amalgams, performed significantly worse on all of the following neurobehavioral tests: motor speed (finger tapping), visual scanning (trail making), visuomotor coordination and concentration (digit symbol), verbal memory, visual memory and visuomotor coordination speed.83 The dentists’ performance on each of these tests diminished as their total exposure increased (amount of daily exposure and years of exposure).

Mercury is also being implicated in Alzheimer’s disease and other chronic neurological complaints. In 1988, it was reported from Alzheimer cadaver studies that mercury was found in much higher levels in the nucleus basalis of Meynert than in controls (40ppb vs. 10ppb).84 Subsequent studies have shown elevated mercury throughout the brain in persons with Alzheimer’s.85 Further, when rats were exposed to elemental mercury vapor at the same levels as have been documented in the oral cavity of humans with amalgams, lesions similar to those seen in Alzheimer’s disease have occurred.86 The same lesions have been demonstrated when rat brains were exposed to EDTA-mercury complex.87 While ALS has been associated in some instances with possible Cadmium exposure, a published case history revealed a diagnosed case of ALS recovering after amalgam removal. The individual in question had 34 amalgam fillings. After the first removal her ALS symptoms were exacerbated, but noted improvement fairly soon after all were removed. Five months later upon returning to the neurology clinic, she was found to have no evidence of motor neuron disorder.88

Mental health symptoms are also quite common with mercury toxicity. Evidence linking mercury exposure to psychological disorders has been accumulating for the past 60 years. The recognized psychological symptoms of mercury include: irritability, excitability, temper outburst, quarreling, fearfulness, restlessness, depression and in some cases insomnia. In a study of individuals with amalgam filling who had them removed, the majority noted psychological improvements. The greatest improvements were found in anger outbursts, depression, irritability and fatigue.89 None of these manifestations being too surprising when related to the effect of mercury on reducing serotonin effect. The association of mercury to depression has stimulated some interesting questions as to whether mercury toxicity was to blame for Sir Isaac Newton’s health problems of 1692-93.90 One would also wonder if it might have contributed to the depression and apparent suicide of Meriwether Lewis.

Renal Toxicity of Mercury

Kidney injury is a characteristic consequence of acute poisoning from inorganic mercury. Albuminuria is a classic sequelae, and may be of either glomerular or tubular origin. In rabbits, rats and mice, multiple exposures to inorganic mercury induce the production of antibodies against the glomerular basement membrane, deposition of immune complexes in the mesangium and glomerular basement membrane, and glomerular nephritis.91-94 Further studies have shown that mercury induces a nephropathy that at the lowest effective doses is restricted primarily to the S3 segment of the proximal tubule. With greater doses of mercury the lesions move to include the S2 and S1 segments as well.95 This nephropathy is apparently due to a selective induction of apoptosis of the renal proximal tubular cells,96 presumably by the same method of apoptosis previously mentioned regarding other cell lines. Studies in sheep have identified renal tubular reabsorption of inulin to be impaired following amalgam placement.97 In a small human study no increased albuminuria was found in healthy male students with amalgams,98 but a study of natural gas workers exposed to mercury vapor revealed minor kidney changes without the presence of neurological changes.99 Mercury has also been associated in potassium-wasting nephropathy100; including one case in the author’s own practice.101

Immunotoxicity of Mercury

As mentioned earlier, mercury increases apoptosis of both monocytes and lymphocytes and reduces phagocytic ability of the monocytes. It has been demonstrated that workers occupationally exposed to mercury vapor exhibited diminished capacity to produce both TNFalpha and IL-1.102 A number of investigators have reported that mercurials are capable of immune activation leading to autoimmunity while simultaneously reducing the cellular immune response leading to increased infection,103-106 which is the classic appearance of immunotoxicity.107 Simultaneously with the immune alterations are changes in the hypothalamic-pituitary-adrenal axis as exhibited by increased levels of ACTH and corticosterone.108 The increase in corticosterone levels could add to the immunosuppresiveness that is already present. Not only will the mercury cause abherent responses in both the cellular and humoral immune systems but also it may cause bacteria to become resistant to antibiotics. Studies done on monkeys has shown that within five weeks of getting amalgam fillings, the intestinal bacteria of the primates became resistant to penicillin, streptomycin, kanamycin, chloramphenicol and tetracycline.109

Adverse Immune Effects of Other Environmental Pollutants (Immunotoxicity)

Environmental chemicals have a wide range of effects on the function of the immune system. They range from decreased cell mediated immunity (with a decrease in infection and tumor fighting) to increased sensitivity (allergy) and increased autoimmunity.110-112 Among the organochlorine compounds (OCCs), DDT has been found to have the following effects on the immune system: reduced killing capacity of polymorphs, reduced number of plasma responder cells, increased degranulation of mast cells, leukopenia, decreased phagocytic ability, changes in the spleen, thymus, and lymph glands, variation in complement, and disturbances in fetal and perinatal immune regulation. Similar effects have also been found from exposure to Hexachlorobenzene (HCB)2 and the chlordanes3_ (also OCCs). Studies of thousands of patients at the Environmental Health Center-Dallas have shown that persons with two or more OCCs present in their serum have some form of immunotoxicity.113_

The chemicals produced by combustion, the polycyclic aromatic hydrocarbons (PAH), have been shown to have similar depressing effects on the immune system including: decreased T-cell dependent antibody response, decreased splenic activity, diminished T cell effector functions, suppression of T-cytotoxic induction, lower Natural Killer cell activity, as well as being highly carcinogenic.114 The organophosphate pesticides (OPs), which are not as biologically persistent as the OCCs are also toxic to the immune system. They have been found to cause: decreased percentages of CD4 and CD5 cells, increased number and percentages of CD26 cells, increased incidence of atopy and antibiotic sensitivity, and high rates of autoimmunity. This elevation in autoimmunity is reflected by high levels of antibodies to smooth muscle, parietal cells, brush border, thyroid, myelin and elevated ANA_.115 Similar immunosuppression is also found for the organotins and for the heavy metals.

The mode of exposure to the pesticide appears to have an effect on the persistence of immunotoxicity as demonstrated by two Polybrominated Biphenyl (PBB) “spills.” One exposure took place in Taiwan when rice bran cooking oil was contaminated with PBBs. This oil was used for cooking and the persons who used it were found to have immune abnormalities. One year after exposure, they were found to have decreased concentration of IgM and IgA (with normal IgG), low T suppresser cells, low B cells and suppression of delayed hypersensitivity to recall antigens. When rechecked two years after exposure, the above indices had returned to normal. This was not the case in Michigan, where a massive PPB “spill” occurred in the 1973/4. During that time period a PBB-containing flame retardant called “Firemaster” was inadvertently sold as an animal feed called “Nutrimaster.” This mistake was devastating to both the livestock and those that raised them and consumed their products. Exposed individuals were found to have lower levels of circulating T lymphocytes and reduced lymphoproliferation response, resulting in reduced cell-mediated immunity (CMI). These individuals also had a high prevalence of persistent skin, neurological and musculoskeletal symptoms.116_ These changes have persisted on all subsequent studies. This seems to indicate that when these toxins are concentrated in the food chain before reaching humans, their effect can be longer lasting.

The development of autoimmunity has been linked with chemical exposure as well. The notion of chemically induced autoimmune states is, or course, not new since many chemicals are known to induce the onset of SLE. Some chemicals, like formaldehyde and other volatile organic compounds are thought to induce tissue-specific autoimmune reactions by acting as haptens. These low molecular weight molecules will bind to various tissues in the body, making a new antigenic combination. The immune system then makes an antibody to this new combination, which can attack the parent tissue with or without the chemicals being present. Chemically exposed individuals will often present with elevated antibodies to certain body tissues including: anti-myelin, anti-parietal, anti-brush border, and anti-smooth muscle.117 A study of 298 patients with exposure to industrial chemicals showed the following abnormalities:118

1. NK activity - chemically exposed patients when compared to controls show either very low activity, or very high activity.

2. Lymphocyte blastogenic response to T-cell mitogens (PHA, CONA) and B-Cell mitogens were between 30-45% lower than controls.

3. Elevated IgG and IgM levels against formaldehyde, trimellitic anhydride, phthalic anhydride, and benzene ring. These rates were usually higher in persons with elevated T4/T8 ratio that was found in almost 15% of the exposed patients.

4. Autoantibodies against their own tissue

For a good review of numerous studies of the immunotoxicity of pesticides, the author recommends the book: Pesticides and the Immune System; The Public Health Risks, published by the World Resources Institute in Baltimore, MD. For a broader view of toxin-related autoimmunity, please refer to the papers developed for the Workshop on Linking Environmental Agents to Autoimmune Diseases.119


Walter J. Crinnion, ND

Healing Naturally, Inc.

11811 NE 128th Street, Suite 202

Kirkland, Washington 98034 USA


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