Olmsted on Autism: How to Completely Miss the Story
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Could Swine Flu Deaths be the Key to Understanding Autism?

Arsenic By Kent Heckenlively, Esq.

It’s long been the belief among Defeat Autism Now (DAN) practitioners and parents that some combination of toxins and infections are responsible for autism.

While many in the traditional medical community have attacked the plausibility of such a scenario, some early signs from the swine flu investigation are suggesting that this toxin/infection interaction might explain other conditions as well.

Scientists from Dartmouth Medical School and the Marine Biological Laboratory (MBL) have found that “the ability to mount an immune response to influenza A (H1N1) infection is significantly compromised by a low level of arsenic exposure that commonly occurs through drinking contaminated well water.”  (“Swine Flu: Influenza A (H1N1) Susceptibility Linked to Common Levels of Arsenic Exposure”, Science Daily, May 21, 2009 HERE.) The research was published in the journal Environmental Health Perspectives (HERE.)

According to Joshua Hamilton, Chief Academic and Science Officer from the MBL as well as study co-author, “When a normal person or mouse is infected with the flu, they immediately develop an immune response.”  The article went on to note, “However, in mice that had ingested 100 ppb (parts per billion) arsenic in their drinking water for five weeks, the immune response to H1N1 infection was initially feeble, and when a response finally did kick in days later, it was "too robust and too late" . . . There was a massive infiltration of immune cells to the lungs and a massive inflammatory response, which led to bleeding and damage to the lungs . . . Morbidity over the course of the infection was significantly higher for the arsenic-exposed animals than the normal animals.”

The swine flu has killed 83 people in Mexico and 12 in the United States.  Hamilton saw some intriguing parallels to his own research in the pattern of deaths. “One of the things that did strike us, when we heard about the recent H1N1 outbreak, is Mexico has large areas of very high arsenic in their well water, including areas where the flu cropped up.  We don’t know that the Mexicans who got the flu were drinking high levels of arsenic, but it’s an intriguing notion that it may have contributed.”

According to the U.S. Environmental Protection Agency, concentrations of arsenic at the levels of 100 ppb and higher are common in well water, especially in those areas where arsenic is geologically abundant.  A level of 10 ppb is considered "safe."

Hamilton’s laboratory discovered and first reported in 1998 the broad ways in which arsenic disrupts the working of the body.  “Most chemicals that disrupt hormone pathways target just one, such as the estrogen pathway . . . But arsenic disrupts the pathways of all five steroid hormone receptors (estrogen, testosterone, progesterone, glucocorticoids, and mineralocorticoids), as well as several other hormone pathways.  You can imagine that just this one effect could play a role in cancer, diabetes, heart disease, reproductive and developmental disorders-all the diseases that have a strong hormonal component.”

This research is interesting for many reasons.  The concept of an environmental toxin lowering the body’s immune response, and as in this case causing it to overreact to a virus or other pathogen is something which has been long theorized in autism.  It’s also in accord with the clinical observations of parents and the response and decline of their children into autism.

The multiple hormonal pathways which are disrupted by arsenic are an example of how poorly we understand the effects of so many of these toxins in a biological organism. What about the aluminum, or the mercury that’s still used in the process of making the vaccines and in many flu shots?  What about the formaldehyde, the lead, the cadmium, the monkey and dog kidney, as well as various animal and supposedly inactivated human viruses? Add to that the level of multi-system complexity and vulnerability of a young child and it’s difficult to see the current vaccination schedule as anything other than a vast, uncontrolled experiment on our children.

When the swine flu panic first surfaced many in the bio-medical community feared it would lead to a more zealous vaccination program.  Wouldn’t it be ironic if that same fear confirmed many of the doubts our community has long held about the currently existing vaccine program?

Kent Heckenlively is Legal Editor of Age of Autism


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Has anyone ever looked into the possibility of the effect of heavy metal toxicity from vaccines on the parents and their parents on the children of today that are being diagnosed autistic at an alarming rate? I keep thinking about it and have actually spoken to a man at the CDC who had sent me a link to a site a few years ago with the ingredients to all the vaccines that were supposedly mercury free, yet still contained trace amounts of mercury. I myself am allergic to nickel, latex, adhesives, bioabsorbabable materials (stitches, screws, etc..), and all kinds of medications and all kinds of other things that the allergist listed. I've passed these allergies down to my children. As far as I know, they don't share my deficiences to metals...iron and magnesium. But my two daughters with autism started showing symptoms as soon as they started receiving vaccinations. I know I have surgical implants, both metal and bioabsorbabable (they didn't screen for allergies first...I was thrilled..believe me..) and my body is rejecting them. I have been suffering memory loss since I have had them implanted. I fear for my children now, to have any more vaccinations that contain any more mercury, no matter how small. I do not want to lose any ground we have gained.


Mercury a key componant of Puerto rican Drinking Water during the times of gold mining.many elders on the island suffer lost of memory and get diagnosis error.
Murcury deadly intruduction to the puerto ricab Brain 1930,1940,1950.....

Teresa Conrick

Hans Raible,

Thanks for your enormously interesting and pertinent story about Brazil Nuts. You are a good story teller and I appreciate how you weave the past into the present. I also like how you said "The question interested me, and I collected some data"......

which is how the best information and often treatments/cures are found.

Thanks again for some good insight into the connections here.

Hans Raible

Brazil Nuts

On Sundays, I often meet a young man (19) who is autistic and who comes with his father. His treatment is Risperdal + Haldol. He also is zinc deficient which is shown by his lack of taste. His father suffers from iron overload, so the young man may also have inherited this.

For a while, I brought him Brazil nuts, and since they had a positive influence on his mental state, the father asked their psychiatrist, Dr. Roth, how many of these the young man should take. The psychiatrist of course hardly knew what Brazil nuts are and what they contain, and he said two nuts per day.

This is too little, and the young man is stimming strongly again, but he goes to work.

The question interested me, and I collected some data on the nuts.

One of these is that in our office, we have a wooden bowl with Brazil nuts, and I fill it when it is empty, and people eat what they like. Our grandchildren know where the bowl is, and they ask me: May I take one? and then eat several nuts according to taste. I also give away bags of the nuts frequently. They are very useful gift for people with cancer.

The company (Kluth) selling the shelled nuts recommends eating 50 grams of shelled nuts per day. On average, these are 14 nuts since each nut weighs about 3.5 grams.

The selenium content of the nuts varies a great deal depending on where the trees grow. One ounce (US) may contain from zero to over 500 micrograms (= 0.5 milligrams). One ounce corresponds to 8 nuts, so one nut may contain between zero and 70 micrograms of selenium. The 50 grams per day recommended by the Kluth firm might thus correspond to
14 times 70 = 980 micrograms/day which would be a good dose for a patient having cancer or AIDS, and you are likely to see a positive effect quite soon on such a dose. Higher doses such as 2000 micrograms are used for treating Ebola with *considerable* success.

50 grams of the nuts, however, is a lot of calories and may make you put on weight, so one might take along a bag of the nuts when one goes hiking, but if the job is sedentary, one would eat less, say between 2 and 10 per day.

Keshan disease in Germany
Selenium pills made from inorganic materials are no use - the selenium has to go through a plant first such as wheat or Brazil nuts. Wheat from South Dakota is immensely rich in selenium, and it saved Bavaria, one of the provinces of Germany, from an epidemic of Keshan disease back in 1945.

Bavaria formerly was glaciated, and the ice had washed out the trace elements such as iodine (hence goiter), zinc and selenium so the food grown there is very low in selenium. (Nowadays, selenium is added to fertilizer in Bavaria).

The babies born at that time had a disease where patches of mold would grow on the tiny hearts, and this looked like callus, in German Schwiele, so the (deadly) disease was called Schwielenherz (callous heart). Nobody knew then that this was Keshan disease, but an American general, Lucius D. Clay, the US High Commissioner for Germany, understood the problem and brought in shiploads of wheat from the Middle West, and the selenium in the wheat took care of the babies so they were born healthy again. (We like such generals.)

The callous heart migh also be called Acute Disseminated Cardiac Myopathy and is the equivalent of the ADEM (acute disseminated encephalitic myelinopathy) where the measles virus eats away the myelin cover on the latest formed nerve fibers (dendrites). It is just a different virus (coxsackie in Keshan, measles in ADEM), but the mechanism, and even the pattern of attack, namely patches of mold, is the same.

Bailey Banks who, thanks to the diligence of his father, could prove ADEM, owes his success in the vaccine court to the enormous financial investment of his father who had MRI pictures of his brain made, and I think the Bailey Banks case must have cost his family about 5 million dollars.

It appears wise to provide a pregnant or nursing mother with enough Brazil nuts since we do not want the moldy patches - we want healthy children, and most families cannot spend five millions on a lawsuit against the US goverment.


Teresa Conrick

Hi Kent,

I continue to be fascinated with the whole idea of metals (more specifically mercury) and its relationship to infection (bacterial/viral). Thanks for exploring this avenue of research as I believe it is a big piece historically and presently to autism.

These are some studies that show what that relationship can actually produce:

Influence of mercuric chloride on resistance to generalized infection with herpes simplex virus type 2 in mice.
Christensen MM , Ellermann-Eriksen S, Rungby J, Mogensen SC.
Department of Medical Microbiology and Immunology, University of Aarhus, Denmark.
The effect of mercuric chloride on resistance to generalized infection with herpes simplex virus type 2 (HSV-2) in mice was studied. The severity of the infection was evaluated by the amount of infectious virus in the liver. Mercury at a single dose of 20 micrograms aggravated the infection , and neither increasing the single dose to 80 micrograms nor giving repeated doses of 20 micrograms further intensified the infection. Examination of the course of infection after mercury exposure revealed an increased virus replication and dissemination during the first days of the infection, indicating that the early, nonspecific defense mechanisms were affected. Virus clearance and elimination, which is mediated by specific immunity, seemed not to be influenced. Examination of cells from the peritoneal cavity and of livers from virus-infected mice showed that mercury detectable by autometallography was exclusively found in mature peritoneal macrophages and in Kupffer cells of the liver. Inflammatory cells, recruited to the peritoneal cavity or infiltrating the infectious foci of the liver, did not show any mercury deposits. Attempts to demonstrate an effect in vivo of mercury on potential antiviral macrophage functions like interferon-alpha/ beta (IFN-alpha/beta) and tumour necrosis factor-alpha (TNF-alpha) secretion and oxidative burst capacity were not successful, possibly because recruited, inflammatory cells, which have not been exposed to the high mercury concentrations at the site of injection, take over these functions of intoxicated macrophages.

1: Vet Med (Praha). 1996 Apr;41(4):103-106
[The effect of emissions from a mercury-processing metallurgy plant on the intensity of experimental Fasciola hepatica infection in sheep]
[Article in Slovak]

Krupicer I, Velebný S, Legáth J.
Parasitological Institute, Slovak Academy of Sciences, Kosice, Slovak Republic.
A group of 14 improved Valashka lambs, aged 4 months, body weight 14-16 kg, were used in the experiment studying the effect of subchronic heavy metal intoxication on the course of experimental fasciolosis (Fasciola hepatica). The animals were divided into two groups, each of 7 lambs, 3 lambs--ewes and 4 lambs--rams. Each animal in group I was given orally for 27 days gelatinous capsules containing heavy metal emissions of the following composition: 4.5 mg Hg, 2.9 mg Pb, 147.8 mg Cu, 9.8 mg Zn, 0.9 mg Cr and 0.04 mg Cd per animal and day. Group II served as control. On Day 27, when the administration of heavy metals ceased, each animal in both groups received 250 F. hepatica metacercariae. The animals were sacrificed on Day 110 post infection, their liver necropsied and parenchymatous organs and muscles taken to examine the content of heavy metals. The heavy metal concentrations are presented in Tab. I. In the emission-intoxicate d group, the maximum permissible reference level of mercury in the kidneys, liver and muscles was exceeded on the average by 1.94, 0.87 and 0.020 mg Hg/kg, respectively. Cu exceeded the reference level only in the liver, with 261.3 mg Cu/kg. In the kidneys and muscles, Cu was below the reference levels. An analogous situation was with Zn, Cr, and Cd. The F. hepatica infection mean intensity in this animal group was 38.3 +/- 3.01 specimens (min. 34 - max. 46 specimens). In control group, the heavy metal levels were several times lower than the reference values and the infection mean intensity was 27 +/- 5.4 (min. 19 - max. 35 specimens). In subchronically intoxicated animals, the reference values for mercury were exceeded and so were partially those of copper in the parenchymatous organs and muscles. The F. hepatica infection mean intensity also increased, compared with control. The results have proved the negative effect of the metal emissions on the animal immune system, which was manifested by the increased infection intensity.

Environ Pollut. 2001;112(1):33-40.Click here to read Links
Exposure to heavy metals and infectious
disease mortality in harbour porpoises from England and Wales.
Bennett PM, Jepson PD, Law RJ, Jones BR, Kuiken T, Baker JR, Rogan E, Kirkwood JK.
Institute of Zoology, Zoological Society of London, Regent's Park, London NW1 4RY, UK. p.bennett@ucl.ac.uk
We investigate whether long-term exposure to heavy metals, including immunosuppressive metals like mercury (Hg),
is associated with infectious disease in a wild cetacean. Post-mortem investigations on 86 harbour porpoises,
Phocoena phocoena, found dead along the coasts of England and Wales revealed that 49 of the porpoises were healthy
when they died as a consequence of physical trauma (most frequently entrapment in fishing gear). In contrast,
37 porpoises died of infectious diseases caused by parasitic, bacterial, fungal and viral pathogens (most frequently
pneumonia caused by lungworm and bacterial infections). We found that mean liver concentrations of Hg, selenium (Se),
the Hg:Se molar ratio, and zinc (Zn) were significantly higher in the propoises that died of infectious disease compared
to healthy porpoises that died from physical trauma. Liver concentrations of lead (Pb), cadmium (Cd), copper (Cu) and chromium
(Cr) did not differ between the two groups. Hg, Se, and the Hg:Se molar ratio were also positively correlated with age.
The association between Zn concentration and disease status may result from Zn redistribution in response to infection.
Further work is required to evaluate whether chronic exposure to Hg may have presented a toxic challenge to the porpoises
that succumbed to infectious disease.

J Helminthol. 1997 Dec;71(4):339-44. Links
Effects of concurrently administered copper and mercury on phagocytic cell activity and antibody levels in guinea pigs with experimental ascariasis.
Soltýs J, Borosková Z, Dvoroznáková E.
Parasitological Institute, Slovak Academy of Sciences, Hlinkova 3, Kosice, Slovak Republic.
The subchronic effect of copper and mercury on selected immunological parameters in guinea pigs with experimental ascariasis was studied. Cupric sulphate and mercuric chloride administered for 28 days did not suppress the levels of specific circulating antibody in a subsequent Ascaris suum infection. Intoxication of animals significantly inhibited the phagocytic activity of peritoneal macrophages throughout the experiment. Ascaris suum infection elevated macrophage phagocytic activity but values remained significantly lower in comparison with infected non-intoxicated animals. Both the concurrently administered metal compounds changed the phagocytic ability of polymorphonuclear leucocytes in the blood. The intensity of infection assessed by the number of Ascaris larvae migrating in the lungs of animals currently intoxicated with both the metal compounds increased by 28.6%, compared with controls.

Toxicol Lett. 1996 Dec;89(1):19-28.Click here to read Links
Effects of methyl mercury on cytokines, inflammation and virus clearance in a common infection (coxsackie B3 myocarditis).
Ilbäck NG, Wesslén L, Fohlman J, Friman G.

Pharmacia and UpJohn, Helsingborg, Sweden.

A myocarditic coxsackievirus B3 (CB3) infection in Balb/c mice was used to investigate the effects of 12 weeks of methyl mercury (MeHg) exposure (3.69 mg/g diet) on inflammatory heart lesions, virus in the heart, the cytokine response, i.e. cachectin/TNF-alpha and gamma-interferon (IFN-gamma) levels in plasma, and on disease complications and mortality. This dose of MeHg did not influence mortality in this infection model. The inflammatory and necrotic lesions in the ventricular myocardium 7 days after the inoculation covered 2.2% of the tissue section area in infected control mice. This damage was increased (n.s.) by 50% (to 3.3% of the tissue section area) in MeHg-treated mice. The response pattern of lymphocyte subsets in situ in myocardial inflammatory lesions was corroborated using an immune histological technique. MeHg treatment tended to increase (2.2-fold, n.s.) the number of Mac 2+ cells (macrophages) in the heart muscle in this infection. Plasma levels of both TNF-alpha and IFN-gamma increased on day 3 of the infection in MeHg-treated as well as in non-MeHg-treated mice, but the mean IFN-gamma response was more pronounced in the MeHg-treated mice. On day 7 of the infection, when most animals still showed clinical signs of disease, cytokine levels were back to normal. MeHg-exposure in non-infected mice did not affect cytokine levels. In situ hybridization of virus RNA in myocardial tissue showed remaining virus in those mice who had the lowest plasma IFN-gamma levels. A 20% increased (P < 0.05) lymphoproliferative response to the T cell mitogen Con A was observed as a result of the MeHg treatment. Even heart tissue lesions and virus persistence tended to be influenced by MeHg in a direction compatible with the development of chronic disease.

Kathy Blanco

arsenic and lead were higher than mercury in my kids.

Heidi N

I am a big forum-searcher, and many have said their child with autism tested with very high arsenic.


I have been fighting to have millions of pounds of contaminated meat recalled that was produced using a warehouse facility that makes the PBA facility look like the Ritz. The pictures I gave to the USDA and the FDA showed RAT fecal matter and rodents nests on food ingredients and materials, I submitted documents to the USDA proving the use of this contaminated warehouse for years and was denied a recall of my own products .Why –to protect a State institution that was contracted to produce this meat for my company.
Agencies state the manufacturer must generate the recall and the FDA and USDA not having the authority to initiate this action as the reason bad food gets into the system .This is not so ,I am proof of this statement not being accurate. Even when the USDA went and found this contaminated warehouse with live rodents they never tested any product for salmonella and co-operated with the state of Florida to use possible contaminated ingredients in further meat processing.
I appeal to you to visit my blog site http://bullstone-larrym.blogspot.com/ and see the evidence of rat fecal contamination in meats produced by an instrument of the State of Florida department of Corrections. I have been battling with the USDA to issue a recall on the millions of pounds of meat the State of Florida produced under contract for my company. This meat was distributed nation wide to schools, supermarkets and institutions. When we discovered that this Florida State division was storing food supplies and edible ingredients in a rat infested warehouse we began our quest to get this information to the public and get accountability placed on those who allowed this to happen. When you read the information on my blog you will see the validity of both our stories .I support your efforts and request your support of mine. Larry Stone

Diane M.Renna

Very interesting. thanks for the posts.

Kathy Blanco

How many of us use tylenol to treat vaccine reactions (answer many of us), and why was that bad? Because it ruins the fever pathways, and lowers glutathione, and does not expel viruses like it should.

see www.rollingdigital.com/autism

María Luján

Rev Infect Dis. 1991 May-Jun;13 Suppl 6:S501-8.Links
Pathogenesis of respiratory infections due to influenza virus: implications for developing countries.Leigh MW, Carson JL, Denny FW Jr.
School of Medicine, University of North Carolina, Chapel Hill 27599.

The influenza viruses have an important and distinctive place among respiratory viruses: they change antigenic character at irregular intervals, infect individuals of all ages, cause illnesses characterized by constitutional symptoms and tracheobronchitis, produce yearly epidemics associated frequently with excess morbidity and mortality, and predispose the host to bacterial superinfections. Much is known about influenza viruses, but their role in respiratory infections among children in developing countries is poorly understood, and the risk factors that lead to the excess morbidity and mortality have not been identified clearly.
Among the many risk factors that may be important are alterations in host immunity, malnutrition, prior or coincident infections with other microorganisms, inhaled pollutants, and lack of access to medical care.

There is a great need for research that can establish more precisely the role these and other unidentified factors play in the pathogenesis of influenza infections in children in the developing world.

María Luján

Toxicol Pathol. 2009;37(2):161-9. Epub 2009 Jan 26.
Immunotoxicity and environment: immunodysregulation and systemic inflammation in children.Calderón-Garcidueñas L, Macías-Parra M, Hoffmann HJ, Valencia-Salazar G, Henríquez-Roldán C, Osnaya N, Monte OC, Barragán-Mejía G, Villarreal-Calderon R, Romero L, Granada-Macías M, Torres-Jardón R, Medina-Cortina H, Maronpot RR.
Environmental pollutants, chemicals, and drugs have an impact on children's immune system development. Mexico City (MC) children exposed to significant concentrations of air pollutants exhibit chronic respiratory inflammation, systemic inflammation, neuroinflammation, and cognitive deficits. We tested the hypothesis that exposure to severe air pollution plays a role in the immune responses of asymptomatic, apparently healthy children. Blood measurements for markers of immune function, inflammatory mediators, and molecules interacting with the lipopolysaccharide recognition complex were obtained from two cohorts of matched children (aged 9.7 +/- 1.2 years) from southwest Mexico City (SWMC) (n = 66) and from a control city (n = 93) with criteria pollutant levels below current standards. MC children exhibited significant decreases in the numbers of natural killer cells (p = .003) and increased numbers of mCD14+ monocytes (p < .001) and CD8+ cells (p = .02). Lower concentrations of interferon gamma (p = .009) and granulocyte-macrophage colony-stimulating factor (p < .001), an endotoxin tolerance-like state, systemic inflammation, and an anti-inflammatory response were also present in the highly exposed children. C-reactive protein and the prostaglandin E metabolite levels were positively correlated with twenty-four- and forty-eight-hour cumulative concentrations of PM(2.5). Exposure to urban air pollution is associated with immunodysregulation and systemic inflammation in children and is a major health threat.

Toxicol Pathol. 2008;36(2):289-310. Epub 2008 Mar 18. Links
Long-term air pollution exposure is associated with neuroinflammation, an altered innate immune response, disruption of the blood-brain barrier, ultrafine particulate deposition, and accumulation of amyloid beta-42 and alpha-synuclein in children and young adults.Calderón-Garcidueñas L, Solt AC, Henríquez-Roldán C, Torres-Jardón R, Nuse B, Herritt L, Villarreal-Calderón R, Osnaya N, Stone I, García R, Brooks DM, González-Maciel A, Reynoso-Robles R, Delgado-Chávez R, Reed W.
Air pollution is a serious environmental problem. We investigated whether residency in cities with high air pollution is associated with neuroinflammation/neurodegeneration in healthy children and young adults who died suddenly. We measured mRNA cyclooxygenase-2, interleukin-1beta, and CD14 in target brain regions from low (n = 12) or highly exposed residents (n = 35) aged 25.1 +/- 1.5 years. Upregulation of cyclooxygenase-2, interleukin-1beta, and CD14 in olfactory bulb, frontal cortex, substantia nigrae and vagus nerves; disruption of the blood-brain barrier; endothelial activation, oxidative stress, and inflammatory cell trafficking were seen in highly exposed subjects. Amyloid beta42 (Abeta42) immunoreactivity was observed in 58.8% of apolipoprotein E (APOE) 3/3 < 25 y, and 100% of the APOE 4 subjects, whereas alpha-synuclein was seen in 23.5% of < 25 y subjects. Particulate material (PM) was seen in olfactory bulb neurons, and PM < 100 nm were observed in intraluminal erythrocytes from lung, frontal, and trigeminal ganglia capillaries. Exposure to air pollution causes neuroinflammation, an altered brain innate immune response, and accumulation of Abeta42 and alpha-synuclein starting in childhood. Exposure to air pollution should be considered a risk factor for Alzheimer's and Parkinson's diseases, and carriers of the APOE 4 allele could have a higher risk of developing Alzheimer's disease if they reside in a polluted environment.
Mutat Res. 2007 Jul 10;631(1):9-15. Epub 2007 Apr 6. Links
Micronuclei induced by airborne particulate matter from Mexico City.Roubicek DA, Gutiérrez-Castillo ME, Sordo M, Cebrián-García ME, Ostrosky-Wegman P.
Particulate air pollution is an important environmental health risk. In the present study, we have investigated the ability of chemically characterized water and organic-soluble extracts of PM(10) from two different regions of Mexico City to induce micronuclei in a human epithelial cell line. We also evaluated the association between the chemical characteristics of the PM and its genotoxicity. The airborne particulate samples were collected from an industrial and a residential region; a Hi-Vol air sampler was used to collect PM(10) on glass fiber filters. PM mass was determined by gravimetric analysis of the filters. One section of each PM(10) filter was agitated either with deionized water to extract water-soluble compounds or with dichloromethane to prepare organic-soluble compounds. The chemical composition of the extracts was determined by ion and gas chromatography and atomic adsorption spectroscopy. A549-human alveolar epithelial cells were exposed to different concentrations of PM(10) extracts and the cytokinesis blocked micronucleus assay was performed to measure DNA damage. Even though the industrial region had a higher PM concentration, higher amounts of metals and PAHs were found in the residential area. Both industrial and residential extracts induced a significant concentration-related increase in the micronuclei frequency. The PM(10) water-soluble industrial extract induced significantly more micronuclei than the one of the residential region; inversely, the organic residential extract induced more micronuclei than the one from the industrial region. The association between the induction of micronuclei and the chemical components obtained by the comparative analysis of standardized regression coefficients showed that cadmium and PAHs were significantly associated with micronuclei induction. Data indicate that water-soluble metals and the organic-soluble fraction of PM(10) are both important in the production of micronuclei. Effects observed, point to the risk of PM exposure and shows the need of integrative studies.

Susan Brinchman

There is a connection between exposure to toxic mold and autism, learn more at www.schoolmoldhelp.org.

María Luján

Hi Sue
I have found these
Sci Total Environ. 1997 Nov 5;206(2-3):187-93.
Environmental pollution and child health in the Aral Sea region in Kazakhstan.Jensen S, Mazhitova Z, Zetterström R.
Department of Environmental Chemistry, Wallenberg Laboratory, Stockholm University, Sweden.

The deterioration of human health with increasing infant mortality rate, declining life expectancy at birth and increasing prevalence of serious infectious diseases in Russia and other former Soviet Republics is thought to be due to a combination of several factors such as inadequate nutrition, poor sanitation, collapse of the health care system and pollution from Soviet agriculture and industries. In the Aral Sea region in Kazakhstan, the environmental problems are of near catastrophic proportions. As a result of the implementation of a massive irrigation scheme to support the cotton fields in the former desert land, the water flow to the Aral Sea was reduced to less than half. Industrial pollutants such as PCB-compounds and heavy metals, but also the use of large quantities of pesticides to control parasites and weeds have accumulated not only in water, but also in soil and have been deposited over large areas by atmospheric transport to enter the food chain leading to humans. In a study of 15 children and of an additional 12 children referred from the region of the Aral Sea to the National Children's Rehabilitation Center in Almaty with symptoms and signs of 'ecological disease', we have found that the concentration of PCB compounds in the blood lipids is elevated in relation to healthy Swedish children. In addition, the blood lipid concentration of the beta-isomer of the hexachlorocyclohexanes was extremely high and of DDT-compounds was elevated up to 20 times. The concentrations of lead in red blood cells was moderately elevated and that of cadmium slightly elevated compared to the findings in Stockholm children. To study the role of these pollutants in the diseases found in children from the Aral Sea region accurate epidemiological studies have to be performed.

Acta Paediatr Suppl. 1999 May;88(429):49-54.Links
Child health and environmental pollution in the Aral Sea region in Kazakhstan.Zetterström R.
Department of Paediatrics, Karolinska Hospital Stockholm, Sweden.

Environmental pollutants, which may occur in breast milk and in various food products and drinking water, and which are also transferred to the foetus, constitute a severe threat to the health of infants and children. Among such compounds, various organochlorines, such as pesticides for the control of parasites (DDTs, HCHs), and products of industry and agriculture, such as dioxins and dioxin-like compounds (PCBs), are much discussed, in addition to organic mercury and heavy metals, such as lead and cadmium. The consequences of acute exposure to PCB have been documented in Japan following the ingestion of rice oil contaminated by PCBs. In Sweden birthweight has been found to be reduced and the perinatal mortality rate higher than expected in regions with high consumption of fatty fish from the Baltic Sea. In addition, from studies around Lake Michigan, it has been shown that children who have been exposed to PCBs in utero have retarded cognitive development. In the Aral Sea basin in Central Asia people have been subjected to long-term exposure to various pesticides, which have been distributed over the cotton fields in huge quantities. Organochlorines are resistant to breakdown in nature, thus they enter the food chain, eventually entering the human diet, and they may also be inhaled from dust. Such compounds accumulate in the foetus by placental transport and continue to do so postnatally if the infants are breastfed, as they may be present in high concentrations in human milk. The health of children living in the Aral Sea region is reported to be poor, with high morbidity and mortality and a high rate of chronic diseases and retarded mental and physical development. However, in addition to being subjected to environmental pollution, these children also suffer from health hazards related to poverty. Through epidemiological studies it may be possible to obtain information about to what extent exposure to environmental pollution from organochlorines contributes to the poor health of people living in the Aral Sea region.

J Cardiovasc Risk. 1996 Feb;3(1):26-41.Links
Public health implications of environmental exposure to cadmium and lead: an overview of epidemiological studies in Belgium. Working Groups.Staessen JA, Buchet JP, Ginucchio G, Lauwerys RR, Lijnen P, Roels H, Fagard R.
Department of Molecular and Cardiovascular Research, University of Leuven, Belgium.

The CadmiBel Study was a cross-sectional population study that investigated the health effects of environmental exposure to cadmium and lead. The 2327 participants constituted a random sample of the population of four Belgian districts, chosen in order to provide a wide range of environmental exposure to cadmium. After adjustment for confounding factors, such as smoking and occupational exposure, the urinary cadmium excretion, a measure of lifetime exposure, was nearly 30% higher in the polluted areas. The CadmiBel Study produced evidence inconsistent with the hypothesis that environmental exposure to cadmium and lead would lead to an increase in blood pressure and to a higher prevalence of hypertension and other cardiovascular diseases. On the other hand, the serum alkaline phosphatase activity and the urinary excretion of calcium were significantly and positively correlated with urinary cadmium in both sexes. These findings suggested that the homeostasis of calcium was gradually affected as cadmium accumulated in the body. Furthermore, several markers of renal tubular dysfunction (urinary excretion of retinol-binding-protein, N-acetyl-beta-glucosaminidase, beta 2-microglobulin and amino acids) were significantly and positively associated with urinary cadmium. Across 10 small areas of which six were polluted with cadmium, an inverse association existed between the creatinine clearance and several indexes of environmental exposure to cadmium (cadmium concentration in the soil, cadmium content of locally grown vegetables, the inhabitants' 24 h urinary cadmium excretion). In the CadmiBel Study, the creatinine clearance was also inversely correlated with the concentrations of lead and zinc protoporphyrin in the blood. Thus, environmental exposure to cadmium and lead was associated with alterations in renal function. The significance in terms of morbidity and mortality of the functional disturbances observed in the CadmiBel Study, and the possible strategies to prevent the transfer of cadmium from the environment to man are under investigation in the prospective PheeCad Study in which half of the Cadmibel participants have been enrolled (participation rate 80%).
Perhaps is this study?
Ann Univ Mariae Curie Sklodowska [Med]. 2004;59(2):397-402.Links
Heavy metal pollution and children morbidity rate in the Rejowiec Fabryczny area.Królak E, Piłat M.
Dept of Ecology and Environment Protection, Institute of Biology, University of Podlasie, Siedlce.

The concentrations of heavy metals (Pb, Cd, Cr, Cu, Mn and Zn) were analyzed in the soils of the Rejowiec Fabryczny area. The levels of these metals were also measured in the raw materials used in cement production, in cement itself, and in dust removed by electrofilters mounted over the clinker kilns. Morbidity rates were also analyzed of children up to 6 years of age examined and treated in the local ambulatory medical center in Rejowiec Fabryczny in 1982 and 2002. The soils of the Rejowiec Fabryczny area showed elevated levels of Pb, Cd, Zn and Cu, comparing to the reference values. Installation of electrofilters in the cement plant resulted in a considerable reduction of Pb and Cd discharge. It was observed that the frequency of respiratory disorders in children from the Rejowiec Fabryczny area was higher comparing to other regions. Over the last 20 years, the frequency of allergies and asthma increased.


When I heard that the mortality rate in Mexico was higher than the US, my first thought was that much of the population there is less well-nourished and, at least in Mexico City area, exposed to much higher levels of pollution than in most of the U.S. Perhaps the mortality in NY is also related to pollution levels there.

Wakefield once cited a paper in Russian that showed much higher incidence of disease/mortality rates in wild populations of some Russian rodent in areas with higher levels of heavy metals in the soil (which corresponded with higher levels in the rodents' bodies.) If anyone has the full reference to that paper translated into English, I would very much like to have and read the full reference.

Importantly, if Andy Cutler and Boyd Haley are correct, exposure to mercury messes up the body's ability to handle all kinds of minerals, and actually results in increased accumulation of heavy metals of several sorts. Plus Haley reports that the toxicity of mercury is greatly magnified in vitro by synergism with aluminum, and other heavy metals.

The problem with mainstream medicine etc. is that its proponents just don't get synergism or the real complexity of biology. They are stuck/heavily invested in thinking about disease as either a simple result of infection by a microbe, or an inevitable result of genetics, and only treatable by "war" against microbes and genetic "defects". Real-world biological understanding is light years beyond that. Anyone with any real grasp of how nature works can quickly understand that the environment, and environmental factors, have huge effects on natality, mortality, development, and the incidence and spread of disease. As our understanding of genetics changes, it is beginning to look like even gene expression is strongly affected by environment. But there is money to be made in selling drugs and vaccines. It costs money to reduce and clean up pollution. Better to make people think the their health problems are simply due to nasty microbes and unfortunate genetic accidents. Strange how humans flourished for millions of years without vaccines or antipsychotic drugs.


María Luján

There are many very recent manuscript on the topic
Yakugaku Zasshi. 2009 Mar;129(3):305-19.
Heavy metal-induced immunotoxicity and its mechanisms
Ohsawa M.
Faculty of Pharmaceutical Sciences, Teikyo University, Kanagawa, Japan.

Immunotoxic effects of heavy metals, as a typical environmental agent, and their mechanisms are reviewed based on our findings on autoimmune response induced by exposure to cadmium (Cd) as CdCl(2). Adverse immune effects of chemicals, defined as immunotoxicity, have been used as a sensitive biomarker for assessing health effects of environmental chemicals. My initial research focused on renal toxicity of heavy metals was developed to elucidate characteristics and mechanisms for immune-mediated nephritis induced by heavy metals. In our studies the most interesting finding was autoantibody production enhanced by the oral exposure to Cd at environmental levels. It was observed simultaneously with enhancement of non-specific antibody production and suppression of primed-antigen specific antibody production. Immunostimulation including induction of autoantibodies was found to be the primary immunotoxic effect of Cd, because of the dose-sensitivity, and to be associated with polyclonal B cell activation (PBA). Further mechanism studies on the PBA induced by Cd in vitro showed that it was mediated by T cells, via cytokines, dominantly Type-2 cytokines, and recognition of MHC-II antigens of cell surface. The similarity among PBAs induced by inorganic salts of Cd, mercury and lead suggests that it would be the common effect among the metals to be involved in their pathogenesis of nephritis. Finally possible health significance of chemical-induced PBA is discussed associated with an increasing trend of autoimmune diseases in industrialized countries.

Birth Defects Res B Dev Reprod Toxicol. 2008 Dec;83(6):547-60. Early-life environment, developmental immunotoxicology, and the risk of pediatric allergic disease including asthma.Dietert RR, Zelikoff JT.
Department of Microbiology and Immunology, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853, USA.
Incidence of childhood allergic disease including asthma (AD-A) has risen since the mid-20th century with much of the increase linked to changes in environment affecting the immune system. Childhood allergy is an early life disease where predisposing environmental exposures, sensitization, and onset of symptoms all occur before adulthood. Predisposition toward allergic disease (AD) is among the constellation of adverse outcomes following developmental immunotoxicity (DIT; problematic exposure of the developing immune system to xenobiotics and physical environmental factors). Because novel immune maturation events occur in early life, and the pregnancy state itself imposes certain restrictions on immune functional development, the period from mid-gestation until 2 years after birth is one of particular concern relative to DIT and AD-A. Several prenatal-perinatal risk factors have been identified as contributing to a DIT-mediated immune dysfunction and increased risk of AD. These include maternal smoking, environmental tobacco smoke, diesel exhaust and traffic-related particles, heavy metals, antibiotics, environmental estrogens and other endocrine disruptors, and alcohol. Diet and microbial exposure also significantly influence immune maturation and risk of allergy. This review considers (1) the critical developmental windows of vulnerability for the immune system that appear to be targets for risk of AD, (2) a model in which the immune system of the DIT-affected infant exhibits immune dysfunction skewed toward AD, and (3) the lack of allergy-relevant safety testing of drugs and chemicals that could identify DIT hazards and minimize problematic exposure of pregnant women and children.
Chem Res Toxicol. 2009 Jan;22(1):17-23.
Developmental immunotoxicology: focus on health risks.Dietert RR.
Department of Microbiology and Immunology, C5-135 VMC, College of Veterinary Medicine, Cornell UniVersity, North Tower Road, Ithaca, New York 14853, USA. Developmental immunotoxicity (DIT) has gained attention with the recognition that many chronic diseases of increasing incidence feature immune dysfunction as a component of the disease. The maturing immune system represents a vulnerable target for toxicants as it progresses through a series of novel prenatal and perinatal events that are critical for later-life host defense against a wide array of diseases. These critical maturational windows display a particular sensitivity to chemical disruption with the outcome usually taking the form of persistent immune dysfunction and/or misregulation. For this reason, health risks are significantly increased following early life vs adult immunotoxic exposure. Additionally, DIT-associated health risks are not readily predicted when based on adult-exposure safety data or via the evaluation of an unchallenged immune system in developmental toxicity testing. The same toxicant [e.g., heavy metals, 2,3,7,8-tetraclorodibenzo-p-dioxin (TCDD)] may disrupt different immune maturational processes depending upon the specific developmental timing of exposure and the target organ dose at a given stage of development. Therefore, a single toxicant may promote different immune-associated diseases that are dependent upon the specific window of early life exposure, the gender of the exposed offspring, and the genetic background of the offspring. This perspective considers the linkage between early life chemical exposure, DIT, and the postnatal immune dysfunctions associated with a variety of childhood and adult diseases. Because DIT is linked to a majority of the most significant childhood chronic diseases, safety testing for DIT is a pivotal issue in the protection of children's health.

Int J Immunopathol Pharmacol. 2007 Apr-Jun;20(2 Suppl 2):15-22.
Immunotoxicity and sensitizing capacity of metal compounds depend on speciation.Di Gioacchino M, Verna N, Di Giampaolo L, Di Claudio F, Turi MC, Perrone A, Petrarca C, Mariani-Costantini R, Sabbioni E, Boscolo P.
Allergy Related Diseases Unit, Ageing Research Center (CeSI) University of Chieti Foundation, Chieti, Italy.
Immunotoxicity of metal compounds is an issue of great importance due to the recent industrial application of metals with unknown toxicity on the immune system and the discovery of metal intermediary compounds not sufficiently studied yet. In this report we show results of our study on the immunotoxicity of the following metals: the Platinum group elements (Platinum, Palladium, Rhodium), Titanium and Arsenic. We applied functional and non functional assays and investigated both innate and adaptive immune systems, in particular, cell proliferation, cytokine production by PBMCs and O*2 production by neutrophils. We obtained the following results: only some Ti compounds (Titanocene, Ti ascorbate and Ti oxalate) show immunotoxicity. Trivalent As compounds (Sodium arsenite and tetraphenyl arsonium chloride) are more immunotoxic than the other investigated As compounds. Genotoxicity of Pt group compounds is in the following order: Pt > Rh > Pd. Immunotoxicity of Pt group compounds is in the following order: Pd > Pt > Rh. Lymphocytes and macrophages show a different reaction of neutrophils to metal toxicity. We can conclude that these studies show that metal immunotoxicity depends on speciation. In general speciation provides additional and often essential information in evaluating metal toxicity. However, there are many difficulties in applying speciation in investigating toxico-kinetic aspects to many metals, mainly due to the lack of information about the existence and significance of species and to the lack of analytical methods for measuring species in biological samples.

Arch Environ Contam Toxicol. 2007 Oct;53(3):450-8. Epub 2007 Jul 26.
Immunosuppressive effect of subchronic exposure to a mixture of eight heavy metals, found as groundwater contaminants in different areas of India, through drinking water in male rats.Jadhav SH, Sarkar SN, Ram GC, Tripathi HC.
Immunotoxicity is an important health hazard of heavy metal exposure. Because the risk of combined exposure in the population cannot be neglected, we examined whether subchronic exposure to a mixture of metals (arsenic, cadmium, lead, mercury, chromium, nickel, manganese, and iron) via drinking water at contemporary Indian groundwater contamination levels and at concentrations equivalent to the WHO maximum permissible limit (MPL) in drinking water can induce immunotoxicity in male rats. Data on groundwater contamination with metals in India were collected from literature and metals were selected on the basis of their frequency of occurrence and contamination level above the MPL. Male albino Wistar rats were exposed to the mixture at 0, 1, 10, and 100 times the mode concentrations (the most frequently occurring concentration) of the individual metals in drinking water for 90 days. In addition, one group was exposed to the mixture at a concentration equal to the MPL of the individual metal and another group was used as positive control for immune response studies. The end points assessed were weights of organs, hematological indices, humoral and cell-mediated immune responses, and histopathology of skin and spleen. The MPL and 1x doses did not significantly affect any of the parameters and none of the doses induced any significant changes after 30 days of exposure. The mixture at 10x and 100x doses increased the relative weight of the spleen, but that of thymus, adrenals, and popliteal lymphnodes were increased with the 100x dose. After 90 days, 10x and 100x doses decreased serum protein and globulin contents and increased the albumin:globulin ratio; the albumin level was decreased only with the 100x dose. After 60 days, the total erythrocyte count (TEC), hemoglobin (Hb) level, and packed cell volume (PCV) were decreased with the 100x dose, whereas after 90 days, 10x and 100x doses reduced the TEC, total leukocyte count, Hb level, PCV, mean corpuscular volume, and mean corpuscular hemoglobin. With the 100x dose, the lymphocyte count was decreased after 60 and 90 days, but the neutrophil number was increased after 90 days. Antibody titer was decreased after 75 days with the 100x dose, but after 90 days, it was decreased with both the 10x and 100x doses. In delayed-type hypersensitivity response, these two doses decreased ear thickness after 24 and 48 h and skin biopsies showed a dose-dependent decrease in inflammatory changes. Histologically, the spleen revealed depletion of lymphoid cells and atrophic follicles with reduced follicular activity with higher doses. The findings suggest that hematopoietic and immune systems are toxicologically sensitive to the mixture, which could lead to anemia and suppression of humoral and cell-mediated immune responses in male rats at 10 and 100 times the mode concentrations of the individual components in contaminated groundwater

Int Immunopharmacol. 2006 Mar;6(3):454-64. Epub 2005 Oct 14. Links
Synergism in immunotoxicological effects due to repeated combined administration of arsenic and lead in mice.Bishayi B, Sengupta M.
Immunology Laboratory, Department of Physiology, University College of Science and Technology, University of Calcutta 92 APC Road, Kolkata-700009, West Bengal, India.
Arsenic and lead are considered potent human hazards because of their neoplastic outcomes; increasing epidemiologic evidence indicates a link between heavy metal exposure and health risk. Since health risks of singly administered metals are well-established, in the present study we determined whether simultaneous repeated multimetal (arsenic + lead) exposure influences the development of immunotoxicity in mice exposed (in vivo) to lead acetate (10 mg/kg b.w.) and sodium arsenite (0.5 mg/kg b.w.) simultaneously. We report that in vivo multimetal exposure alters cell morphology, inhibits cell adhesion, nitric oxide release, intracellular killing ability, chemotactic migration, myeloperoxidase release, bacterial clearance from blood and spleen and increases DNA fragmentation. On measuring bacterial density in blood and spleen after 0, 24, 48 and 72 h post infection (with Staphylococcus aureus MC524) in control and multimetal treated groups, bacterial load showed delayed clearance from blood and spleen in the multimetal exposed group. We also found that in vivo exposure to the multimetal caused a decrease in cell adhesion, indicated by a fall in absorbance at 570 nm with respect to control. Exposure to multimetal led to morphological changes in macrophages, since more deformed cells were obtained in repeated combined exposure to arsenic and lead compared to control. Nitric oxide, which has a potent microbicidal activity in macrophages, was found to be released in fewer amounts in the multimetal exposed group from that of control group. It was observed that the viability of bacteria gradually decreased in control macrophage with time, whereas, in macrophages of multimetal exposed mice, the viability of S. aureus gradually increased. Chemotactic migration of splenic macrophages significantly decreased in the multimetal exposed group from that of control. Lysosomal enzyme release from splenic macrophages decreased upon simultaneous exposure to arsenic and lead, as is evident from the decrease in myeloperoxidase release in multimetal group from that in control. That the structural integrity of splenic macrophages is decreased in the multimetal exposed group is also evident from the enhanced percentage of DNA fragmentation after multimetal exposure, suggesting apoptotic death of splenic macrophage. Intracellular viable bacteria in the splenic macrophage from multimetal exposed group was 89.16 +/- 3.54% while that from control group was 49.19 +/- 1.16%, whereas single metal exposed groups showed a bacterial viability of 69.6 +/- 2.45% and 71.71 +/- 1.89% in arsenic and lead treated groups respectively. What is essentially noteworthy from the observed results is that lead and arsenic causes a greater immunotoxic effect when administered together as multimetal than when singly administered. Simultaneous exposure to lead and arsenic appears to be additive as is further established from the isobologram constructed by plotting the concentration of arsenic against the concentration of lead at which effect (in this case myeloperoxidase release) remained constant, a convex line showing synergism was demonstrated. The present study reports a definite synergistic trend of immunotoxicity during simultaneous exposure to arsenic and lead, that is, a multimetal challenge, as compared to the effects of independent exposure to them.

Toxicol Appl Pharmacol. 2005 Sep 1;207(2 Suppl):282-92.
Mercury and autoimmunity: implications for occupational and environmental health.Silbergeld EK, Silva IA, Nyland JF.
Department of Environmental Health Sciences, The Johns Hopkins University Bloomberg School of Public Health, Baltimore, MD 21205, USA.
Mercury (Hg) has long been recognized as a neurotoxicant; however, recent work in animal models has implicated Hg as an immunotoxicant. In particular, Hg has been shown to induce autoimmune disease in susceptible animals with effects including overproduction of specific autoantibodies and pathophysiologic signs of lupus-like disease. However, these effects are only observed at high doses of Hg that are above the levels to which humans would be exposed through contaminated fish consumption. While there is presently no evidence to suggest that Hg induces frank autoimmune disease in humans, a recent epidemiological study has demonstrated a link between occupational Hg exposure and lupus. In our studies, we have tested the hypothesis that Hg does not cause autoimmune disease directly, but rather that it may interact with triggering events, such as genetic predisposition, exposure to antigens, or infection, to exacerbate disease. Treatment of mice that are not susceptible to Hg-induced autoimmune disease with very low doses and short term exposures of inorganic Hg (20-200 microg/kg) exacerbates disease and accelerates mortality in the graft versus host disease model of chronic lupus in C57Bl/6 x DBA/2 mice. Furthermore, low dose Hg exposure increases the severity and prevalence of experimental autoimmune myocarditis (induced by immunization with cardiac myosin peptide in adjuvant) in A/J mice. To test our hypothesis further, we examined sera from Amazonian populations exposed to Hg through small-scale gold mining, with and without current or past malaria infection. We found significantly increased prevalence of antinuclear and antinucleolar antibodies and a positive interaction between Hg and malaria. These results suggest a new model for Hg immunotoxicity, as a co-factor in autoimmune disease, increasing the risks and severity of clinical disease in the presence of other triggering events, either genetic or acquired.

Toxicol Appl Pharmacol. 2004 Jul 15;198(2):86-94.
Developmental immunotoxicology of lead.Dietert RR, Lee JE, Hussain I, Piepenbrink M.
Department of Microbiology and Immunology, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853, USA.
The heavy metal, lead, is a known developmental immunotoxicant that has been shown to produce immune alterations in humans as well as other species. Unlike many compounds that exert adverse immune effects, lead exposure at low to moderate levels does not produce widespread loss of immune cells. In contrast, changes resulting from lead exposure are subtle at the immune cell population level but, nevertheless, can be functionally dramatic. A hallmark of lead-induced immunotoxicity is a pronounced shift in the balance in T helper cell function toward T helper 2 responses at the expense of T helper 1 functions. This bias alters the nature and range of immune responses that can be produced thereby influencing host susceptibility to various diseases. Immunotoxic responses to lead appear to differ across life stages not only quantitatively with regard to dose response, but also qualitatively in terms of the spectrum of immune alterations. Experimental studies in several lab animal species suggest the latter stages of gestation are a period of considerable sensitivity for lead-induced immunotoxicity. This review describes the basic characteristics of lead-induced immunotoxicity emphasizing experimental animal results. It also provides a framework for the consideration of toxicant exposure effects across life stages. The existence of and probable basis for developmental windows of immune hyper-susceptibility are presented. Finally, the potential for lead to serve as a perinatal risk factor for childhood asthma as well as other diseases is considered.

J Toxicol Environ Health B Crit Rev. 2009 Mar;12(3):206-23. Links
The effects of metals as endocrine disruptors.Iavicoli I, Fontana L, Bergamaschi A.
Institute of Occupational Medicine, Universita Cattolica del Sacro Cuore, Rome, Italy.

This review reports current knowledge regarding the roles that cadmium (Cd), mercury (Hg), arsenic (As), lead (PB), manganese (Mn), and zinc (Zn) play as endocrine-disrupting chemicals (EDCs). The influence of these metals on the endocrine system, possible mechanisms of action, and consequent health effects were correlated between experimental animals and humans. Analysis of the studies prompted us to identify some critical issues related to this area and showed the need for more rigorous and innovative studies. Consequently, it was recommended that future studies need to: (1) identify the mechanisms of action, because at the present time only a few have been elucidated-in this context, the possible presence of hormesis need to be determined, as currently this was reported only for exposure Cd and As; (2) study the possible additive, synergistic, or antagonistic effects on the endocrine system following exposure to a mixture of metals since there is a lack of these studies available, and in general or occupational environments, humans are simultaneously exposed to different classes of xenobiotics, including metals, but also to organic compounds that might also be EDCs; (3) assess the potential adverse effects on the endocrine system of low-level exposures to metals, as most of the information currently available on EDCs originates from studies in which exposure levels were particularly high; and (4) assess the effects on the endocrine and reproductive systems of other metals that are present in the general and occupational environment that have not yet been evaluated.

Now, Hg, Al, Pb, Cd, As mainly have not been studied in terms of combined and synergistic impact in susceptible populations ( genetically or epigenetically related)- because of immaturity of the immune system at birth or metabolic/biochemical/mitochondrial imbalances.
Al is known to generate macrophagic myofascitis and the mechanism of action is under research- the inflammasome and the impact of its activation by alum/adjuvants

J Child Neurol. 2008 Jun;23(6):614-9. Epub 2008 Feb 15.
Macrophagic myofasciitis in children is a localized reaction to vaccination.
Lach B, Cupler EJ.
Department of Pathology and Laboratory Medicine, King Faisal Specialist Hospital and Research Center, Riyadh, Saudi Arabia. boleklach2@hotmail.com
Macrophagic myofasciitis is a novel, "inflammatory myopathy" described after a variety of vaccinations, almost exclusively in adults. We examined the relevance of histological findings of this myopathy to the clinical presentation in pediatric patients. Muscle biopsies from 8 children (7 months to 6 years old) with histological features of macrophagic myofasciitis were reviewed and correlated with the clinical manifestations. Patients underwent quadriceps muscle biopsy for suspected mitochondrial disease (4 patients), spinal muscular atrophy (2 patients), myoglobinuria (1 patient), and hypotonia with motor delay (1 patient). All biopsies showed identical granulomas composed of periodic acid-Schiff-positive and CD68-positive macrophages. Characteristic aluminum hydroxide crystals were identified by electron microscopy in 2 cases. The biopsy established diagnoses other than macrophagic myofasciitis in 5 patients: spinal muscular atrophy (2), Duchenne muscular dystrophy (1), phospho-glycerate kinase deficiency (1), and cytochrome c oxidase deficiency (1). Three children with manifestations and/or a family history of mitochondrial disease had otherwise morphologically normal muscle. All children had routine vaccinations between 2 months and 1 year before the biopsy, with up to 11 intramuscular injections, including the biopsy sites. There was no correlation between histological findings of macrophagic myofasciitis in biopsies and the clinical symptoms. We believe that macrophagic myofasciitis represents a localized histological hallmark of previous immunization with the aluminum hydroxide adjuvants contained in vaccines, rather than a primary or distinct inflammatory muscle disease.

Clin Neuropathol. 2006 Jul-Aug;25(4):172-9.
Pediatric macrophagic myofasciitis associated with motor delay.
Gruis KL, Teener JW, Blaivas M.
Department of Neurology, University of Michigan Health System, Ann Arbor, MI, USA.
BACKGROUND: Macrophagic myofasciitis (MMF) is a rare inflammatory myopathy characterized by accumulation of perifascicular macrophages without muscle fiber necrosis. Few sporadic pediatric cases have been described, and MMF is recognized as a possible reaction to intramuscular injections of aluminum-containing vaccines. The association of MMF and motor delay is unclear in the pediatric population. We report the clinical evaluation and follow-up of 4 young children with MMF and review of 4 cases previously reported of sporadic, pediatric MMF to better determine the possible association of sporadic MMF in children presenting with motor delay. PATIENTS AND METHODS: Described our 4 case reports in which we observed children presenting for evaluation of motor delay with unrevealing clinical and laboratory evaluations for common causes of motor delay and histopathological evaluations consistent with macrophagic myofasciitis. Muscle data was obtained by quadriceps muscle biopsy. RESULTS: Clinical presentations were similar in all children and were characterized by motor delay, hypotonia, and failure to thrive with an unrevealing evaluation for central nervous system disease, congenital, and mitochondrial myopathies. CONCLUSIONS: Our cases and those previously reported in the literature demonstrate MMF should be considered in the evaluation of children with failure to thrive, hypotonia, and muscle weakness, as clinical outcome appears to be favorable.

Clin Rheumatol. 2008 May;27(5):667-9. 2008 Jan 8. Polyglandular autoimmunity with macrophagic myofasciitis.Theeler BJ, Simper NB, Ney JP.
Department of Neurology, Madigan Army Medical Center, 9040A Fitzsimmons Dr., Tacoma, WA 98431, USA.

We report a man with chronic fatigue, multiple autoimmune disorders, and a muscle biopsy consistent with macrophagic myofasciitis. This rare and recently described muscle disorder is seen in patients exposed to vaccinations with aluminum hydroxide adjuvant. This case highlights the relationship between macrophagic myofasciitis and autoimmunity.

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