Whilst facing a worldwide fast increase of food and environmental allergies, the medical community is also confronted with another inhomogeneous group of environment-associated disabling conditions, including multiple chemical sensitivity (MCS), fibromyalgia, chronic fatigue syndrome, electric hypersensitivity, amalgam disease and others. These share the features of poly-symptomatic multi-organ cutaneous and systemic manifestations, with postulated inherited/acquired impaired metabolism of chemical/physical/nutritional xenobiotics, triggering adverse reactions at exposure levels far below toxicologically-relevant values, often in the absence of clear-cut allergologic and/or immunologic involvement.

Due to the lack of proven pathogenic mechanisms generating measurable disease biomarkers, these environmental hypersensitivities are generally ignored by sanitary and social systems, as psychogenic or “medically unexplained symptoms”. The uncontrolled application of diagnostic and treatment protocols not corresponding to acceptable levels of validation, safety, and clinical efficacy, to a steadily increasing number of patients demanding assistance, occurs in many countries in the absence of evidence-based guidelines.

De Luca et. al. revised available information supporting the organic nature of these clinical conditions. Following intense research on gene polymorphisms of phase I/II detoxification enzyme genes, so far statistically inconclusive, epigenetic and metabolic factors are under investigation, in particular free radical/antioxidant homeostasis disturbances. The finding of relevant alterations of catalase, glutathione-transferase and peroxidase detoxifying activities significantly correlating with clinical manifestations of MCS, has recently registered some progress towards the identification of reliable biomarkers of disease onset, progression, and treatment outcomes.

Literature:

De Luca C, Raskovic D, Pacifico V, Thai JC, Korkina L., The search for reliable biomarkers of disease in multiple chemical sensitivity and other environmental intolerances, Tissue Engineering & Skin Pathophysiology Laboratory and 2nd Dermatology Division, Dermatological Research Institute (IDI IRCCS), Via Monti di Creta 104, Rome 00167, Italy; Int J Environ Res Public Health. 2011 Jul;8(7):2770-97. Epub 2011 Jul 1.

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Daily chemical exposures at low doses can affect our health

ROME – On September 24, 2010, from 8:30 a.m. to 5:30 p.m., the congress “New Environmental Diseases” was held at the Chamber of Deputees Congress Hall in Rome. The event was organized by A.M.I.C.A. (Association for Environmental and Chronic Toxic Injury), the Italian organization that works for the rights of people with MCS and EHS, and it was supported by Mep Domenico Scilipoti, an oncologist, holistic doctor, and rapporteur of a draft to become law on environmental diseases and disabilities and also for the phasing out of dental amalgam.

“More and more scientific evidence shows how daily chemical exposures at low doses can affect our health. With this event we would like to create a bridge between science and politics in order to have a new legislation, particularly for the protection of those affected by Multiple Chemical Sensitivity, Electromagnetic Hyper Sensitivity, Chronic Fatigue Syndrome and Fibromyalgia. These diseases seem to be correlated one to another,” Francesca Romana Orlando, Vice President of A.M.I.C.A., commented. She has just published the book Il Cerchio Perfetto (The Perfect Circle) about the link between industry, politics, academics, and media and its role in the hiding of toxic dangers to the public.

“Just a few weeks ago, at the Senate Commission for Health, the debate about the draft to become law for the recognition of MCS as an epidemic disease started. The prevalence of this illness is about 10% of the population and in Italy the patients still don’t have any hospital to receive any medical treatment in a proper environment,” Silvia Bigeschi, Vice President of A.M.I.C.A., adds.

There are ten projects to become law for the recognition of MCS as an epidemic disease at the Italian Parliament and, just the day before of the congress, A.M.I.C.A. presented a petition with more than 10,000 signature asking for the approval of a law for MCS and also a petition to the Ministry of Health for the total phase out of dental mercury (amalgam), since many cases of MCS, CFS and EHS seem to be triggered by amalgam fillings.

The congress was divided in four sessions. The first one was about “Diagnostic approaches” for MCS, CFS and FM. Prof. Giuseppe Genovesi of the University of Rome La Sapienza and Dr. Chiara De Luca, Head of the Laboratory BILARA at the Dermatological Institute Immacolata of Rome, presented the results of a study on oxidative stress and genetics in MCS patients, that was recently published on Toxicology Applied Pharmacology (Apr. 26, 2010).

While Dr. De Luca focused on the clear evidence of oxidative stress in these patients, such as the lack of enzyme catalysis and GST, Prof. Genovesi stressed the fact that the results don’t show the prevalence of one specific genetic polymorphism, but most of the patients had one or more genetic factors inducing a lower detoxification. He also announced that they are going to test the genetic predisposition of the enzyme catalysis, since this is so typically low in MCS patients.

Dr. Alberto Migliore, the chief of Rheumatology Department at the S. Pietro Fatebenefratelli Hospital in Rome, published a study about the comorbidity of MCS and Sjogren Syndrome. Dr. Lorenzo Bettoni presented a lecture about the environmental causes of CFS and FM, with an hypothesis about the role of chemicals, EMF pollution, and physical/mental stress on the triggering of these illnesses.

Dr. Giacomo Rao, who works for the Italian National Insurance of Workers (INAIL, the public institute that gives compensation and pension to the workers injured at workplace), talked about the legal aspects of the recognition of these illnesses as a disability. He showed that there are several impact life factors to consider and that in Italy there are now many MCS disability certificates, even if it is always very difficult to convince the commissions about the severity of this illness. He added that the final judgment depends only on the good will of the commissioners to study a new issue.

In the second session entitled “New Paradigms of Toxicology and Environmental Medicine,” Martin L. Pall, Professor Emeritus of Biochemistry and Basic Medical Sciences, Washington State University, presented his theory about the biochemical vicious cycle ON/ONOO – induced by the combination of high NOS activity and Tetrahydrobiopterin (BH4) depletion – and how it is able to explain not only MCS, CFS or FM, but also other emerging neuro-degenerative illnesses such AD, Parkinson or ALS. He commented that the De Luca – Genovesi study about oxidative stress represents a full confirmation of his theory.

Dr. Peter Ohnsorge, President of the European Academy for Environmental Medicine (EUROPAEM), has already applied Pall’s theory to his clinical approach in order to reduce NMDA in the cerebral metabolism. He proceeds in treating inflammation first, by supplementing enzymes, antioxidants, minerals and Vitamins. Then, he offers a chelation therapy, when possible, and also hemapheresis (Membrane Differential Filtration), gut therapy and detoxification. He also uses sauna therapy since the heat helps to increase BH4 and to oppose the vicious NO/ONOO cycle.

Recently, Dr. Ohnsorge was commissioned by the German Ministry of Health and Social Affairs, to do a controlled randomized study about the efficacy of therapies for MCS patients with the double aim of detoxification of lipophilic toxins and improving the complaints. He found out that using a complex therapeutic regime usually allows the patients to recover slowly, but surely.

The MCS people in the audience asked him several questions, for example about the bad secondary effects of supplementation of glutathione (GSH) and about the tests of compatibility of drugs and dental materials. He explained that supplementation has to be given always with very low doses at the beginning in order to avoid violent breaks in the detoxification mechanisms. Moreover, he suggested using the Lymphocyte Transformation Test (LTT) to find out reactions to drugs, metals, plastics and environmental toxins, while the basophil degranulation test is suggested when inflammation is suspected induced by metals, like in the case of titanium implants.

In the same second session, Dr. Ernesto Burgio, Coordinator of the Scientific Committee of ISDE Italia (Doctors for the Environment), gave a lecture about the epigenetic damages caused by environmental toxins and EMFs. The epigenome represents the interface between the information from the environment and the genome, and even in the absence of chromosomal or gene mutations, there still can be a change in the expression of the gene (DNA Methylation) because of an epigenetic injury. “With a few exceptions, cellular differentiation almost never involves a change in the DNA sequence itself,” commented Dr. Burgio.

Since the environment changed too quickly in the latest decades, the capacity of adaptation of the (epi) genome is not enough to compensate it. Thus, a toxic exposure from the parents, in the womb, or during the early childhood can induce a chronic disabling illness later in life.

New studies are being explored on how a lead exposure in infants can be associated to Alzheimer’s disease (AD)-like symptoms years later or how the mother’s exposure to high levels of folic acid, vitamin B12 or to cigarette smoke can induce epigenetic changes that can repress gene transcription and, then, induce phenotypes of asthma (i.e. allergic airway inflammation) in the offspring. These findings could lead to the conclusion that our society is on the edge of a “disevolution.”

In the third section on “Heavy Metals Toxicity,” Dr. Raimondo Pische, President of the International Academy of Bio-Dentistry (AIOB) talked about the risks associated with the exposure to the metals of dental amalgam. In particular, he presented a video of an amalgam fillings showing how mercury vapors are easily released by the amalgam. He underlined the fact that the dentists are the first ones at risk when they pose and remove amalgam fillings and that dental mercury represents the main source of exposure to mercury vapors in not occupational environments. This is no longer acceptable since mercury is the most toxic element in nature after the radioactive elements.

Dr. Antonello Maria Pasciuto, Italian member of the European Academy for Environmental Medicine (EUROPAEM), talked about the LTT-MELISA, the Lymphocyte Transformation Test for the proof of late allergy to metals (type IV). This kind of allergy was observed in patients with MCS, CFS, MS, FM, ALS and autoimmune diseases and it usually improves, as well as the symptoms, after the safe removal of dental metals.

Dr. Gianpaolo Guzzi of the Italian Organization for the Research on Metals and Biocompatibility (A.I.R.M.E.B.) talked about the side effects of chelation therapies. His group studied hundreds of patients with amalgam toxic load and they reviewed the effects of EDTA, DMPS, DMSA and Glutathione. EDTA seems to redistribute metals without really getting rid of them, while DMPS seems more effective on treating elemental mercury, but with severe side effects in some cases. DMSA works to detoxify from methyl mercury and it can also get rid of elemental mercury stocked in the kidneys. Recently Dr. Guzzi’s research group is testing the efficacy of Glutathione in metal detoxification since there aren’t studies about it.

In the last session about “EMF and Health”, Dr. Fiorenzo Marinelli, researcher of the Institute of Molecular Genetics (IGM) in Bologna talked about wireless technologies such as mobile phones, Wi-Fi and Wi-Max. He pointed out the fact that thermal effects are only a part of the biological effects of EMFs, but still these are the only ones considered by international safety standard limits. There are also other effects induced by the signal information in itself. This explains why, even though UMTS has usually a lower intensity of the signal compared to GSM, it uses a wider band of frequencies, then involving a greater risk of damage in the DNA, as the recent European Reflex study showed. His research group has recently studied the effects of radars and Wi-Fi and the preliminary findings show that both these kind of EMFs promote cell proliferation (2010).

Since scientific literature clearly demonstrates that EMF in our everyday life can induce DNA breakage, genetic deregulation as well as chromosomal breakage, increase of free radicals, alteration of neurotransmitters, memory loss, hypersensitivity-allergy, aging and possibly cancer, Dr. Marinelli supports the reduction of the safety limit of exposure to 0,6 V/m, as requested by the International Commission for the Electromagnetic Safety (ICEMS) since 2002.

Finally, Prof. Olle Johansson, associate professor at The Experimental Dermatology Unit – Department of Neuroscience of the Karolinska Institute, and Professor at The Royal Institute of Technology, Sweden, also member of the famous Bioinitiative Working group, presented a lecture about Electro-Hyper-Sensitivity, which is fully recognized as a functional impairment in Sweden. He explained not only the bioeffects of EMF on EHS people, but also the social problem of disability in our modern societies. “Disability is everywhere and it can happen to anyone: I myself have a disability when I am in Italy because I can not speak Italian,” Prof. Johansson commented. He reminded that all modern democracies signed international equal rights UN treaties, but still they leave these principles un-realized when it comes to environmental disability.

Reference:

A.M.I.C.A. congress shows how environmental and chemical pollution cause health injuries and disabilities, Rome, September 25th, 2010

Photo: AMICA

Contact:

Francesca Romana Orlando
Vice President of AMICA
Associazione Malattie da Intossicazione Cronica e/o Ambientale
(Association for Environmental and Chronic Toxic Injury)
P.O. Box 3131, 00121 Rome – Italy
www.infoamica.it amica(at)infoamica.it

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Newborns of non-smoking moms exposed to secondhand smoke during pregnancy have genetic mutations that may affect long-term health, according to a University of Pittsburgh Graduate School of Public Health study published online in the Open Pediatric Medicine Journal. The abnormalities, which were indistinguishable from those found in newborns of mothers who were active smokers, may affect survival, birth weight and lifelong susceptibility to diseases like cancer.

The study confirms previous research in which study author Stephen G. Grant, Ph.D., associate professor of environmental and occupational health at Pitt’s Graduate School of Public Health, discovered evidence of abnormalities in the HPRT gene located on the X chromosome in cord blood from newborns of non-smokers exposed to environmental tobacco smoke.

In the current study, Dr. Grant confirmed smoke-induced mutation in another gene called glycophorin A, or GPA, that is representative of oncogenes – genes that transform normal cells into cancer cells and cause solid tumors. The GPA mutation was the same level and type in newborns of mothers who were active smokers and of non-smoking mothers exposed to tobacco smoke. Likewise, the mutations were discernable in newborns of women who had stopped smoking during their pregnancies, but who did not actively avoid secondhand smoke.

“These findings back up our previous conclusion that passive, or secondary, smoke causes permanent genetic damage in newborns that is very similar to the damage caused by active smoking,” said Dr. Grant. “By using a different assay, we were able to pick up a completely distinct yet equally important type of genetic mutation that is likely to persist throughout a child’s lifetime. Pregnant women should not only stop smoking, but be aware of their exposure to tobacco smoke from other family members, work and social situations.”

Literature: University of Pittsburgh Schools of the Health Sciences, Exposure to secondhand smoke in the womb has lifelong impact, June 30, 2010

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STANFORD, Calif. — Got diabetes? If so, you probably know that the adult-onset form of the disease can be triggered by, among other things, obesity and a fatty diet. You’re also more likely to develop diabetes if other family members have it. But a new study by researchers at the Stanford University School of Medicine suggests that you should also begin looking suspiciously at other aspects of your life — like your past exposure to certain pesticides or chemicals and even one form of vitamin E.

In fact, the association of some of these so-called “environmental” cues with diabetes surpasses that of the best genetic markers scientists have identified for the disease.

Identifying relationships between a person’s environment (such as tobacco exposure) and specific health repercussions (such as cancer) is nothing new. Epidemiological studies of large groups of people have been doing just that for decades. But they are limited in their ability to assess the hundreds or even thousands of variables that comprise the intricate fabric of our everyday lives. (What’s your risk of heart disease if you smoke sparingly and eat fatty foods, but are also a marathoner?) They’re also not open-ended: The researcher has to begin with presuppositions about possible relationships. (Does folic acid prevent birth defects?)

In this new study, the scientists relied instead on an unconventional approach that treats environmental variables as “genes.” That conceptual shift allowed them to use some of the same techniques initially developed to identify the many sections of DNA throughout the genome that might contribute to disease development. Bioinformatics expert Atul Butte, MD, PhD, assistant professor of pediatric cancer biology, compared the data generated by the new approach to the amount and types of information gleaned from a DNA microarray.

“This approach catapults us from being forced to ask very simple, directed questions about environment and disease into a new realm in which we can look at many, many variables simultaneously and without bias,” said Butte, who is also director of the Center for Pediatric Bioinformatics at Lucile Packard Children’s Hospital. “In the future, we’ll be able to analyze the effect of genes and environment together, to find, perhaps, that a specific gene increases the risk of a disease only if the person is also drinking polluted well water.”

Specifically, in this study, Butte and his coworkers used the technique to identify a previously known association between people with type-2 diabetes and a class of organic compounds called polychlorinated biphenyls, or PCBs, commonly used for many applications until the late 1970s. They also uncovered a strong, but unexpected, relationship between diabetes and high levels of a form of vitamin E called gamma-tocopherol, which is prevalent in fruits, vegetables, nuts and milk.

The scientists are careful to caution, however, that an association doesn’t necessarily mean that vitamin E or pollutants cause type-2 diabetes, and that more research is needed to fully understand these complex relationships.

Butte is a senior author of the research, which will be published May 20 in the online journal PLoS ONE. The genetic studies on which the research is based are called “genome wide association studies” or GWAS. In a nod to its origin, the scientists coined the term “environment wide association studies,” or EWAS, for the new technique. They expect that EWAS will be useful in the analysis of many complex diseases.

“We’ve known for decades that environmental factors play a major role in diseases like diabetes, cancer and heart disease,” said Jeremy Berg, PhD, director of the National Institute of General Medical Sciences, which partially supported the work. “By enabling us to measure the impact of these factors, this new approach will shed light on how genes and the environment influence our health and could provide insights into new ways to control some of our nation’s most serious health problems.”

Graduate student Chirag Patel conceived of, designed and executed the computer software for the EWAS. He, Butte and associate professor of medicine Jayanta Bhattacharya, MD, PhD, used existing population studies conducted from 1999 to 2006 by the U.S. Centers for Disease Control and Prevention as part of the National Health and Nutrition Examination Survey. The researchers realized that the databases contained a goldmine of information, including the levels of pollutants and vitamins in subjects’ blood and urine as well as clinical measurements such as fasting blood sugar levels.

In all, the scientists analyzed the relationship of 266 unique environmental variables to the likelihood that a person’s fasting blood sugar level was 126 milligrams or higher per deciliter (between 70 and 110 mg/dL is considered normal). Higher-than-normal blood sugar levels after an overnight fast are a telltale sign of diabetes. They adjusted for the subjects’ age, gender, body mass index, socioeconomic status and ethnicity. Finally, they grouped related variables into 21 classes — such as dioxins, polychlorinated biphenyls, phthalates, etc. — similar to how individual genes are assigned to chromosomal units in GWAS.

Butte and his colleagues found that people with relatively higher levels of the pesticide-derivative heptachlor epoxide (a chemical whose use stopped in the ’80s but is still prevalent in food, soil and water) in their blood were more likely than those with lower levels to also have high fasting blood sugar levels (odds ratio = 1.7). The same was true for those with high levels of PCBs (OR = 2.2) and the gamma-tocopherol form of vitamin E (OR = 1.5). In contrast, high beta-carotene levels were slightly protective (OR = 0.6).

Scientists have recently made large strides in measuring genetic associations to complex disease, but are still far from using genes to predict risk for complex chronic diseases or even plan preventive measures. On the other hand, our environmental profile is potentially more modifiable and also may provide a more complete model of disease risk when combined with genetic information.

“Studying relationships between a person’s environment and their disease burden in this manner is going to be far more impactful,” said Butte. “We can now imagine what it might be to look at everything in the environment, in the same way that we’ve been doing with the genome for the past decade. Imagine one day wearing a chip on your clothing that assesses your exposure to hundreds or thousands of environmental toxins. You could bring that in to your annual physical and you and your doctor could incorporate the information into discussions about disease risk and prevention.”

The researchers are planning to conduct similar EWAS studies focused on other diseases, including cancers. They’ll also try to reproduce the data from the National Health and Nutrition Examination Survey studies on specific populations in California.

Literatur: Stanford University, New associations between diabetes, environmental factors found by novel Stanford analytic technique, May 20, 2010

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Approach could shed light on many complex diseases

Like many complex diseases, diabetes results from the interplay of genetic and environmental factors. To examine genetic risk factors, scientists pore over the human genome sequence. Environmental factors have been trickier to pin down because there is no way to evaluate them comprehensively.

Now, researchers at Stanford University present what they call an environment-wide association study (EWAS) or to systematically examine the contributions of hundreds of factors in the development of Type 2 diabetes. This “enviromics” approach, which mirrors genome-wide association studies, harnesses high-speed computers and publicly accessible databases.

The first-of-its-kind study, which was funded by the National Institutes of Health (NIH), appears in the May 20, 2010, issue of PLoS One. The article is titled An Environment-Wide Association Study (EWAS) on Type 2 Diabetes Mellitus.

The authors examined 226 separate environmental factors like nutrition and exposure to bacteria, viruses, allergens and toxins. They found that certain factors, notably a pesticide derivative and the environmental contaminant PCB, were strongly associated with the development of diabetes. Other factors, including the nutrient beta-carotene, served a protective role.

The scientists describe their work as a demonstration that computational approaches can reveal as much about environmental contributions to disease as about genetic factors. They posit that the technique could be applied to other complex diseases like obesity, hypertension and cardiovascular disorders.

The authors acknowledge that many challenges remain, including the fact that, unlike the genome, “the environment is boundless.”

Literature:

NIH/National Institute of General Medical Sciences, Computers analyze environmental factors in diabetes, 20-May-2010.