A new study in China has found that people with higher levels of pesticide exposure are more likely to have suicidal thoughts. The study was carried out by Dr Robert Stewart from the Institute of Psychiatry at King’s College London together with scientists from Tongde Hospital Zhejiang Province. 

The agricultural pesticides commonly used in China are organophosphates which are in wide use in many lower income countries but have been banned in many Western nations. It is well known that they are very dangerous if ingested as an overdose but there is also biological evidence that chronic low-grade exposure to these chemicals, which are very easily absorbed into the body through the skin and lungs, may have adverse effects on mental health. This study is the first epidemiological evidence to suggest possible effects on suicidal thoughts. 

The study was carried out in central/coastal China, a relatively wealthy area with a rapidly developing economy. In a very large survey of mental health in rural community residents, participants were also asked about how they stored pesticides. The study found that people who stored pesticides at home, i.e. those with more exposure, were more likely to report recent suicidal thoughts. Supporting this, the survey also found suicidal thoughts to be associated with how easily accessible these pesticides were in the home and that the geographic areas with highest home storage of pesticides also had highest levels of suicidal thoughts in their populations. 

Given the high level of pesticide exposure and the high suicide risk in rural China, clarification of the causal mechanisms underlying this association and the development of appropriate interventions should be priorities for public health and health policy. 

Dr Robert Stewart comments: ‘Organophosphate pesticides are widely used around the world although are banned in many countries because of their risk to health. They are particularly lethal chemicals when taken in overdose and are a cause of many suicides worldwide. Our research findings that suggest that higher exposure to these chemicals might actually increase the risk of suicidal thoughts provides further support for calls for tighter international restrictions on agricultural pesticide availability and use.’

Dr Jianmin Zhang, Associate Chief Psychiatrist, Tongde Hospital of Zhejiang Province, and Vice Director, Zhejiang Office of Mental Health, China added: “The findings of this study suggested potential causal links and might partially account for the much higher incidence of suicide in rural than urban areas of China. However, further studies particularly with more precisely defined and assessed exposure are critically needed, as awareness of safer access to pesticides is important both to policy-makers and pesticide users.”

Reference: King’s College London, Pesticides exposure linked to suicidal thoughts, October 22, 2009  

Notes:

Pesticide exposure and suicidal ideation in rural communities in Zhejiang province, China by Jianmin Zhang, Robert Stewart, Michael Phillips, Qichang Shi & Martin Prince was published in the October issue of the WHO Bulletin. The full article can be accessed on http://www.who.int/bulletin/volumes/87/10/08-054122.pdf 

The analysis involved data from a survey of a representative sample of 9,811 rural residents in Zhejiang province who had been asked about the storage of pesticides at home and about whether or not they had considered suicide within the two years before the interview. The Chinese version of the 12-item General Health Questionnaire (GHQ) was administered to screen for mental disorder.

Breakthrough study on Multiple Chemical Sensitivity shows MCS is an epidemic caused by toxic chemicals; peer-reviewed paper is published in prestigious toxicology reference work.

A major paper on multiple chemical sensitivity by Professor Martin L. Pall is to be published October 23, 2009 as chapter XX in a prestigious reference work for professional toxicologists, “General and Applied Toxicology, 3rd Edition” (John Wiley & Sons).  Multiple chemical sensitivity (MCS) is also known as chemical sensitivity, chemical intolerance and toxicant-induced loss of tolerance, with this last name emphasizing the role of chemicals in initiating cases of this disease.  Pall’s  paper, entitled Multiple Chemical Sensitivity: Toxicological Questions and Mechanisms, establishes five important facts about  MCS:

1. MCS is a stunningly common disease, even more common than diabetes.  This has been shown in a series of nine epidemiological studies from the U.S. and one study each from Canada, Germany, Sweden and Denmark.  In the U.S., approximately 3.5% of the population is affected by severe MCS, with much larger numbers, at least 12% of the population, being moderately affected.  MCS is, therefore, a very large international disease epidemic with major implications in terms of public health.

2. MCS is caused by toxic chemical exposure.  Cases of MCS are initiated by exposure to seven classes of chemicals.  These include three classes of pesticides and the very large class of organic solvents and related compounds.  In addition, published studies implicate mercury, hydrogen sulfide and carbon monoxide as initiators.  All seven of these classes of chemicals have been shown in animal studies to produce a common response in the body, excessive activity of a receptor in the body known as the NMDA receptor.  Furthermore animal studies have demonstrated that chemicals belonging to each of these seven classes can have their toxic responses greatly lowered by using drugs that lower this NMDA response.  Because excessive NMDA activity is implicated in MCS from other studies, we now have a compelling common response that explains how such diverse chemicals can produce the disease that we call MCS.

3. The role of chemicals acting as toxicants in MCS has been confirmed by genetic studies.  Four such studies have shown that genes that determine the rate of metabolism of chemicals otherwise implicated in MCS, influence susceptibility to becoming ill with MCS.  These four studies have been published by three research groups in three countries, the U.S., Canada and Germany, have collectively implicated six genes in determining susceptibility to MCS.  Each of these six genes has a role in determining the rate of metabolism of MCS-related chemicals.  The German studies by Schnakenberg and colleagues are particularly convincing on this because of the extremely high level of statistical significance of their studies implicating four of these six genes. There is only one interpretation for the role of these six genes in determining susceptibility to MCS.  It is that chemicals act as toxicants in initiating cases of MCS and that metabolizing these chemicals into forms that are either less or more active in such initiation, influences therefore, the probability that a person will become ill with MCS.  It is clear, therefore, that MCS is a toxicological phenomenon, with cases being caused by the toxic response to chemical exposure.

4. We have, a detailed and generally well supported mechanism for MCS.   This mechanism explains both the high level chemical sensitivity that is the most characteristic symptom of MCS, as well as many other symptoms and signs of this disease, can be generated.   This mechanism is centered on a biochemical vicious cycle, known as the NO/ONOO- cycle, which interacts with other mechanisms previously implicated in MCS, notably neural sensitization and neurogenic inflammation.  These act locally, in various tissues of the body, to generate local sensitivity in regions of the brain and in peripheral tissues including lungs, upper respiratory tract and regions of the skin and the GI tract.  Because of this local nature, different MCS patients differ from one another in their sensitivity symptoms, because the tissues impacted differ from one patient to another.  In addition to the evidence discussed above, this general mechanism is supported by various physiological changes found in MCS and in related illnesses, by studies of MCS animal models, by objectively measurable responses of MCS patients to low level chemical exposure and by therapeutic responses reported for MCS and related illnesses.

5. For over 20 years, some have falsely argued that MCS is a psychogenic disease, being generated in their view by some ill defined psychological mechanism.  However this view is completely incompatible with all of the evidence discussed earlier in this release. While such incompatibility is more than sufficient reason to reject these psychogenic claims, the MCS toxicology paper lists eight additional serious flaws in the psychogenic arguments.  There is a long history of false psychogenic claims in medicine, where such diseases as asthma, autism, Parkinson’s disease, ulcers, multiple sclerosis, lupus, interstitial cystitis, migraine and ulcerative colitis have been claimed to be generated by a psychological mechanism.  The 2005 Nobel Prize in physiology and medicine was give to Drs. Robin Warren and Barry Marshall for showing that ulcers are caused by a bacterial infection, and are not of psychogenic origin.  It is clear, now, that MCS is physiological disease initiated by toxic chemical exposure that has been falsely claimed to be psychogenic.

—

Martin L. Pall is Professor Emeritus of Biochemistry and Basic Medical Science, at Washington State University.

He is located on Pacific time in the U.S. and can be contacted at:  503-232-3883 and at martin_pall@wsu.edu.

His Website is: www.thetenthparadigm.org

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To examine the effects of solvent exposure on hearing function, through an audiological test battery, in a population not occupationally exposed to high levels of noise. 

One hundred ten workers from a coating factory were studied. Jobs at the factory were divided into three different levels of solvent exposure. Hearing status was assessed with a test battery including pure-tone hearing thresholds (0.5-8 kHz), high-frequency hearing thresholds (12 and 16 kHz), and dichotic listening measured through dichotic digits test. Multiple linear regression models were created to explore possible association between solvent exposure and each of the hearing outcomes. 

Significant associations between solvent exposure and the three hearing outcomes were found. Covariates such as age, gender, race, and ethnicity were also significantly associated with the studied hearing outcomes. 

Occupational exposure to solvents may induce both peripheral and central auditory dysfunction. The dichotic digits test seems as a sensible tool to detect central auditory dysfunction associated with solvent exposure. Hearing loss prevention programs may use this tool to monitor hearing in solvent-exposed workers. 

Reference:   Fuente A, Slade MD, Taylor T, Morata TC, Keith RW, Sparer J, Rabinowitz PM., Peripheral and Central Auditory Dysfunction Induced by Occupational Exposure to Organic Solvents, J Occup Environ Med. 2009 Sep 25 

From the Escuela de Fonoaudiologia [School of Speech and Hearing Sciences] (Dr Fuente), Medical Faculty, Universidad de Chile, Santiago, Chile; Occupational and Environmental Medicine Program (Mr Slade, Dr Taylor, Ms Sparer, and Dr Rabinowitz), Yale University School of Medicine, New Haven, Conn; Division of Applied Research and Technology (Dr Morata), National Institute for Occupational Safety and Health; and Division of Audiology (Dr Keith), University of Cincinnati, Cincinnati, Ohio.

Studies show chemicals act as toxicants in causing cases of Multiple Chemical Sensitivity; genes that metabolize these chemicals into other forms influence, therefore, susceptibility to getting MCS.

Guest post at Canary Report by Martin L. Pall, Professor Emeritus of Biochemistry and Basic Medical Sciences, Washington State University and Research Director, the Tenth Paradigm Research Group.

Martin Pall: I have emailed the following as an open letter to the Denver Post in response to the article on multiple chemical sensitivity (MCS) that was published this weekend. I think the published article was generally a step forward in terms of public understanding of MCS. But the article left out a number of important things and this letter is an attempt to deal with some of those. I have asked them to consider publishing this as an Op-Ed piece, but wanted to make it available regardless of whether or not they opt to do so.

Thank you for writing this article on multiple chemical sensitivity (MCS), the term that is used in most of the scientific literature on this disease. There are vast numbers of people who have been afflicted in this epidemic of chemical sensitivity and I am sure that they are all thanking you. I also thank you for mentioning a bit of my work on this disease.

Some of your readers have already made quite a number of important points about MCS so I can focus here on just a few remaining issues. How do chemicals act in MCS? We know now that the seven classes of chemicals implicated in MCS all produce a common toxic response in the body, excessive activity of a receptor in the body called the NMDA receptor. So even though we have a vast array of such chemicals, we know how they can produce similar responses in people.

There is compelling genetic evidence that these chemicals act as toxic agents (toxicants) in the body. Four such studies have been published by three research groups in three countries. Collectively they implicate six genes as influencing susceptibility to MCS, such that people carrying some forms of each of these genes are more susceptible to becoming chemically sensitive than are people carrying other forms of the same genes. All of these genes control the activity of enzymes that metabolize these chemicals into other forms. Most of these studies show a high level of what is called statistical significance. In the Schnakenberg and colleagues studies, the chances of getting their results by chance are less than one in a million billion. So obviously, these are not chance results. What these studies show is that chemicals are acting as toxicants in causing cases of MCS and that genes that metabolize these chemicals into other forms influence, therefore, susceptibility to getting MCS. These studies, then, provide compelling evidence that cases of MCS are caused by toxic chemical exposure. Clearly they also show that MCS is a real disease, otherwise one would not be able to do such studies clearly linking the chance of becoming ill with MCS to the action of chemicals acting as toxicants.

Dr. Herman Staudenmayer has, for some 20 years claimed just the opposite. He claims that MCS is psychogenic, caused by psychological responses and according to him, is not a toxicological phenomenon. He has maintained this claim by ignoring contrary data wherever it occurs. He has ignored all of the evidence that chemicals implicated in MCS produce a common response in the body; he has ignored the roughly two dozen studies showing that MCS patients show objectively measurable responses to low level chemical exposures, responses that differ from those of normals. He has ignored all of the evidence implicating excessive NMDA activity in MCS; he has ignored the dozens of animal model studies on MCS; he has ignored over 50 studies that show that cases of MCS typically occur following chemical exposures; he has ignored the various other measurable physiological changes reported to occur in MCS. This has all been documented in my book “Explaining – Unexplained Illnesses” and in my article on the toxicology of MCS that is coming out next month in a prestigious reference work for professional toxicologists “General and Applied Toxicology, 3rd Edition”. It is also documented on the MCS web page of my web site: The Tenth Paradigm

Clearly you cannot do science by simply ignoring the existence of vast arrays of contrary data. However, Staudenmayer provides us with a couple of other tests of his views in his book, predictions that allow us to test his theory. He predicts that psychological factors are necessary and sufficient to account for the properties of MCS. This, of course, is contradicted by all of the evidence I referred to earlier. Therefore we should reject his hypothesis based on his own prediction. He provides a second prediction as well (the exact quotes from his book on these predictions are provided on my MCS web page). He predicts that the variation of susceptibility to MCS is not caused by variable responses to toxic chemicals. Clearly the genetic studies discussed above have shown that this is false and therefore, his hypothesis should be rejected for that reason, as well.

It is clear, from the above, that Staudenmayer’s construct was basically a house of cards. Now that it has collapsed, where does that leave us?

Firstly it leaves us with reversing the errors of the past. We need to start treating MCS sufferers as victims of unsafe chemical exposure. Many of them have previously been used, abused and discarded. If we live in a society where people are not disposable items we need to “do unto others as you would have others do unto you.”

We obviously need to start regulating chemical usage much more carefully, to avoid initiating new cases of MCS. It is imperative to develop tests for chemical activity in MCS, just as we have developed tests for chemical activity as carcinogens. Then we need to use these tests to effectively regulate the use of toxic chemicals.

We need to develop specific biomarker tests for MCS, tests that can be used to objectively confirm diagnoses initially based on subjective symptoms. I think we already have several very promising approaches to doing this in the scientific literature and a minimal amount of further study may be all that is needed to develop such tests.

We need to confirm that chemical avoidance is key to therapy and to develop other therapeutic approaches to work along with avoidance. The environmental medicine physicians and others have already made very important progress in this direction and I am optimistic that further progress can be made quickly. Such progress is relevant not only to the treatment of MCS patients but also to the treatment of clearly related diseases including chronic fatigue syndrome/mylagic encephalomyelitis and fibromyalgia. All of these diseases are caused by what I have called the NO/ONOO- cycle and the way to treat them, in my judgment, is to lower the activity of that vicious cycle mechanism.

Martin L. Pall

Professor Emeritus of Biochemistry and Basic Medical Sciences, Washington State University and Research Director, the Tenth Paradigm Research Group

Reprinted with permission from the author. Dr. Pall cautions the reader that he is a PhD, not an MD, and none of this should be viewed as medical advice.

• Original Article posted by Canary Report Thank you for the permission to reprint Susie!
• Link to Martin Pall’s website: The Tenth Paradigm
• Link to an extended excerpt from Palls book Explaining “Unexplained Illnesses.”

Growing evidence shows that exposure to lead in the environment is associated with cardiovascular disease, including increased risk of hypertension. However, those studies have looked at lead concentrations in blood, not bone lead, a better indicator of cumulative lead exposure over time. In a new study, researchers at the Harvard School of Public Health (HSPH) and the University of Michigan School of Public Health found that bone lead was associated with a higher risk of death from all causes, particularly from cardiovascular disease. It is the first study to analyze the association between bone lead and mortality.

The study appears online on September 8, 2009, on the website of the journal Circulation and will appear in a later print edition. 

“The findings with bone lead are dramatic. It is the first time we have had a biomarker of cumulative exposure to lead and the strong findings suggest that, even in an era when current exposures are low, past exposures to lead represent an important predictor of cardiovascular death, with important public health implications worldwide,” said Marc Weisskopf, assistant professor of environmental and occupational epidemiology at HSPH and lead author of the study.

Air pollution was the main source of lead in the environment in recent years, though it has been decreasing since leaded gasoline was banned in the U.S. in the mid-1990s. Most of the lead circulating in the body is deposited in bone and remains there for years, unlike blood lead, which has a half life of about 30 days. Since adverse effects from lead on the cardiovascular system would be expected to show up over time, the researchers expected that bone lead would be a better marker of chronic toxicity.

The researchers, led by Weisskopf and senior author Howard Hu, professor of environmental health, epidemiology and internal medicine at the University of Michigan School of Public Health, analyzed data from 868 participants in the Department of Veterans Affairs Normative Aging Study, a study of aging in men that began in 1963. Blood lead and bone lead—analyzed using X-ray fluorescence—were measured for each of the participants. The results showed that the risk of death from cardiovascular disease was almost six times higher in men with the highest levels of bone lead compared to men with the lowest levels. The risk of death from all causes was 2.5 times higher in men with the highest levels of lead compared to those with the lowest levels. The results appeared independent of age, smoking, education, race, alcohol, physical activity, BMI, high density lipoprotein or total cholesterol levels, hypertension or diabetes.

There are a number of mechanisms, such as increased oxidative stress, by which lead exposure may result in cardiovascular mortality, say the authors. They also note that, in addition to high blood pressure, exposure to lead has been associated with widened pulse-pressure (an indicator of arterial stiffening) and heart disease.

Given that bone lead may be a better biomarker of cumulative lead exposure than blood lead, it may be the best predictor of chronic disease from exposure to lead in the environment. “In addition to spurring further public health measures to reduce exposure to lead and to begin monitoring for cumulative exposure, mechanistic and clinical research is needed to determine if opportunities exist to conduct targeted screening and treatment that can further reduce the burden of cardiovascular disease for the millions of adults who have had years of elevated lead exposure in the past,” said Hu.

Reference:    Harvard School of Public Health, Lead in bone associated with increased risk of death from cardiovascular disease in men, Boston, MA, September 9, 2009