Monthly Archive for July 2009

UCLA study reveals how tiny levels of carbon monoxide damage fetal brains

CO Exposure could make them more vulnerable to disease

A UCLA study has discovered that chronic exposure during pregnancy to miniscule levels of carbon monoxide damages the cells of the fetal brain, resulting in permanent impairment. The journal BMC (BioMed Central ) Neuroscience published the findings June 22 in its online edition.

“We expected the placenta to protect fetuses from the mother’s exposure to tiny amounts of carbon monoxide,” said John Edmond, professor emeritus of biological chemistry at the David Geffen School of Medicine at UCLA. “But we found that not to be the case.”

The researchers exposed pregnant rats to 25 parts per million carbon monoxide in the air, an exposure level established as safe by Cal/OSHA, California’s division of occupational health and safety.

Dr. Ivan Lopez, UCLA associate professor of head and neck surgery, tested the rats litters 20 days after birth. Rats born to animals who had inhaled the gas suffered chronic oxidative stress, a harmful condition caused by an excess of harmful free radicals or insufficient antioxidants.

“Oxidative stress damaged the baby rats brain cells, leading to a drop in proteins essential for proper function,” said Lopez. “Oxidative stress is a risk factor linked to many disorders, including autism, cancer, Alzheimer’s, Parkinson’s, Lou Gehrig’s disease, multiple sclerosis and cardiovascular disease. We know that it exacerbates disease.”

“We believe that the minute levels of carbon monoxide in the mother rats environment made their offspring more vulnerable to illness,” added Edmond. “Our findings highlight the need for policy makers to tighten their regulation of carbon monoxide.”

Tobacco smoke, gas heaters, stoves and ovens all emit carbon monoxide, which can rise to high concentrations in well-insulated homes. Infants and children are particularly vulnerable to carbon monoxide exposure because they spend a great deal of time in the home.

No policies exist to regulate the gas in the home. Most commercial home monitors sound an alarm only hours after concentrations reaches 70 parts per million – nearly three times the 25 parts per million limit set by Cal/OSHA.

A grant from the University of California’s Tobacco-related Disease Research Program supported the research.

Reference: Elaine Schmidt, UCLA study reveals how tiny levels of carbon monoxide damage fetal brains, UCLA, 6/25/2009

The naked Truth about MCS – Multiple Chemical Sensitivity – Including Foreword about German Situation

In June, the online magazine Delirio published an article about Multiple Chemical Sensitivity (MCS), in which Eva Caballé, the brilliant Spanish MCS blogger at NO FUN, presented herself naked in front of the camera and wrote about “The Naked Truth of MCS.”

For other countries, it often looks like chemically sensitive patients in Germany get more medical help than anywhere else since MCS is recognized as a physical disease in our country. It’s true that MCS is registered as a physical disease and has the ICD-10 code T78.4, which lists MCS in the chapter on injuries and intoxicants. MCS is recognized as a physical disability as well (26.14). But the reality for people with Chemical Sensitivity is hard and bitter. Many are fighting at court to get their disability recognized, but even when having numerous medical reports confirming their condition, they usually loose. Because, like in other countries, sickness from chemicals and modern living is not truly recognized but rather swept under the carpet even though we exist and suffer every day.

Further, in Germany, people with MCS are neglected by society. There are people who are homeless because of MCS. Many have lost their jobs or houses. Many are neglected by their relatives because family members do not understand the disease and are not willing to change habits for their sick loved one. Further still, the chemically sensitive people here in Germany are systematically declared mentally ill or having only psychosomatic symptoms.

Medical Assistance focused on Chemical Sensitivity doesn’t exist in Germany. We still have no adequate clinic with special environmentally controlled rooms where the very sick can be treated. Most environmental doctors don’t diagnose MCS because they fear harassment.

MCS is recognized as a physical disability in Germany but the “unseen” barriers are still everywhere. In public buildings you can still find air fresheners in nearly all bathrooms, harsh chemical cleaners all over the building, and perfumed employees everywhere, so none of us can go there without developing severe physical symptoms. Children who are severely chemically sensitive have no chance to visit a public school or university. We have no such thing as scent-free policies in workplaces, schools, public buildings or departments.

We people with Chemical Sensitivity here in Germany can, like people from many other countries all over the world, shake hands with the Spanish MCS sufferers, because we, too, are left naked and without any help. Our chemically sensitive people cry for help without any response each day, too.


The naked Truth about MCS

from Eva Caballé

We are born naked, they give us cologne, perfumed nappies, clothes washed with softeners, creams with all kinds of possible aromas, and they drive us in plastic stroller while we breathe nice polluted air.

We grow up and they make us believe that we can achieve anything we want, that we can write our future, that the happiness is based in buy everything and the state is here to protect and watch over us, although I had my doubts.

One day, you wake up and nothing has sense. You switch on the table lamp and your eyes get burnt; you open the window and perceive new smells that don’t let you breathe. You turn on the radio and the music booms in your head, so much that you fear it will explode. And you don’t have a hangover. It’s worse. It’s been called Multiple Chemical Sensitivity (MCS) and has come to stay. Your body has said “enough”, has been broken and starts rejecting everything that they told you was essential for your happiness. Your life has taken an unexpected turn, your mind changes, your future vanishes, you don’t have physical nor mental energy. The disease forces you to live your life behind a mask and have been in isolation from the outside world.

Multiple Chemical Sensitivity is not strange, nor a minority. It affects to the 5% of the population. It’s a chronic disease, not psychological, which causes symptoms as a response to a minimal exposure to usual and unnecessary chemical products like bleach, air fresheners, perfumes, etc. We live locked in our houses but it’s not necessary to go out to have a crisis. Your neighbour’s cloths airing outside suffocate you, make you feel sick until you loose consciousness, thanks to the wonderful toxic softeners.

The World Health Organization (WHO) don’t recognize MCS as a disease yet, in spite of having in their possession innumerable studies that prove its existence and the European Parliament includes it inside the growing number of diseases related to environmental factors. The reason is the pressure that the chemical and pharmaceutical industry exerts for not recognize it, because MCS is caused by the chemical products that we use to consume. The economical interests in front of our health. In countries which this problem is recognized, like Germany, medical assistance and financial aids towards it are provided, and in some other countries it is being considered at the moment.

And what’s the situation in Spain? We don’t exist to our paternal government. On top of the drama of suffering MCS, they abandon us, without medical assistance and without any right to a disability benefit when we can’t work. They leave us naked and unprotected, like second class citizens, because we’re the evidence that the current model of society has failed, although nobody wants to see it or to take measures to sort it out.

They too steal any hopes we might have of feeling better. Pharmacists finance research only when they can obtain any profit. As a result of this, minority diseases don’t get research, not even MCS, which affect to the 5% of the population. The chemical and pharmaceutical industry knows that we get sick because we’re intoxicated and the key is not any medicine that will make them rich. The key is to change the model of this society, decreasing the big quantity of chemical products to which we’re exposed each day. Obviously, this can’t be known and they try to deny that MCS exists, because their economical interests would be at stake.

The chemical industry, supported by the government, doesn’t have the right to subjugate the population to the involuntary exposure to chemical substances, whose effects are often unknown. When we develop MCS, we must throw away perfumes, softeners, plastics, etc., to be naked again. We born again, but it’s a new life that we don’t choose. We know by the researches that have been done that MCS has genetic components, so not anybody could develop it, although this doesn’t save you to accumulate toxics until you have a cancer or any other disease related to environmental factors.

Those who suffer MCS want the disease to be recognized; we want to have the same rights as the other chronically ill people; we want society to know the risk they are under; we want the government to protect its citizens and prevent them from getting sick at no cost for them.


We don’t want anybody feeling naked again as a result of suffering MCS.


Photos and text published with author’s permission. Thank you very much Eva!

Foreword: Silvia K. Müller, CSN – Chemical Sensitivity Network, June 2009

Original Article “The naked Truth about MCS”

Canary Report: “The naked Truth about MCS”

Document and English translation – claissification of MCS as physical disease in Germany

Exposure to bitumen fumes and genotoxic effects on asphalt workers

Toxic fumes make asphalt worker sick

Bitumen fumes consist essentially of polycyclic aromatic hydrocarbons (PAHs) and their derivatives, some of which are known to be carcinogenic or cocarcinogenic in humans. The aim of this study was to investigate exposure to asphalt fumes among Turkish asphalt workers and determine whether any effects could be detected with genotoxic tests.  

The study included 26 asphalt workers and 24 control subjects. Sister chromatid exchange (SCE) and micronucleus (MN) were determined in peripheral lymphocytes. Urinary 1-hydroxypyrene (1-OHP) excretion was used as a biomarker of occupational exposure to PAHs.  

The asphalt workers had a significant increase in SCEs and MN (for each, p < 0.001). A positive correlation existed between the duration of exposure and rates of SCE or MN frequencies (r = 0.49, p < 0.05; r = 0.53, p < 0.05, respectively). The concentration of 1-OHP in urine was higher for the asphalt workers than for the controls (p < 0.001). However, we found that there was no statistically significant correlation between the urinary 1-OHP concentration and SCEs or MN frequencies (r = 0.25, p > 0.5; r = 0.17, p > 0.5, respectively).  

This study shows that Turkish asphalt workers have an increased exposure to PAHs from bitumen fumes, and genotoxic effects could be detected by SCEs and MN tests. 

Reference: Karaman A, Pirim I., Exposure to bitumen fumes and genotoxic effects on Turkish asphalt workers, Department of Medical Genetics, State Hospital, Erzurum, Turkey, Clin Toxicol (Phila). 2009 Apr;47(4):321-6.

Research on Multiple Chemical Sensitivity (MCS)

Scientist researching about MCS - Multiple Chemical Sensitivity

Research on Multiple Chemical Sensitivity (MCS)

 

Compiled by

Professor Anne C. Steinemann and Amy L. Davis

University of Washington

 

This document lists scientific citations for peer-reviewed journal articles that support a physiological basis for MCS:

  1. Abdel-Rahman A., Shetty A.K., Abou-Donia M.B. 2002. Disruption of the blood-brain barrier and neuronal cell death in cingulate cortex, dentate gyrus, thalamus, and hypothalamus in a rat model of Gulf-War syndrome. Neurobiology of Disease 10(3): 306-26.
  2. Abel-Rahman A., Abou-Donia S., El-Masry E., Shetty A., Abou-Donia M. 2004. Stress and combined exposure to low doses of pyridostigmine bromide, DEET, and permethrin produce neurochemical and neuropathological alteration in cerebral cortex, hippocampus, and cerebellum. Journal of Toxicology and Environmental Health Part A 67(2): 163-92.
  3. Abdel-Rahman A., Dechkovskaia A.M., Goldstein L.B., Bullman S.H., Khan W., El-Masry E.M., Abou-Donia M.B. 2004. Neurological deficits induced by malathion, DEET, and permethrin, alone or in combination in adult rats. Journal of Toxicology and Environmental Health Part A 67(4): 331-56.
  4. Abou-Donia M.B 2003. Organophosphorus ester-induced chronic neurotoxicity. Archives of Environmental Health 58(8): 484-97.
  5. Abou-Donia M.B., Wilmarth K.R., Abdel-Rahman A.A., Jenseen K.F., Oehme F.W., Kurt T.L. 1996. Increased neurotoxicity following concurrent exposure to pyridostigmine bromide, DEET, and chlorpyrifos. Fundamentals of Applied Toxicology 34(2): 201-22.
  6. Abou-Donia M.B., Dechkovskaia A.M., Goldstein L.B., Shah D.U., Bullman S.L., Khan W.A. July 2002. Uranyl acetate-induced sensorimotor deficit and increased nitric oxide generation in the central nervous system in rats. Pharmacology, Biochemistry, and Behavior 72(4): 881-90.
  7. Abou-Donia M.B., Dechkovskaia A.M., Goldstein B., Abdel-Rahman A., Bullman S.L., Khan W.A. 2004. Co-exposure to pyridostigmine bromide, DEET, and/or permethrin causes sensorimotor deficit and alterations in brain acetylcholinesterase activity. Pharmacology, Biochemistry, and Behavior 77(2): 253-62.
  8. Abu-Qare A.W., Abou-Donia M.B. 2001. Combined exposure to sarin pyridostigmine bromide increased levels of rat urinary 3-nitrotyrosine and 8-hydroxy-2’deoxyguanosine, biomarkers of oxidative stress. Toxicology Letters 123(1): 51-58.
  9. Abu-Qare A.W., Abou-Donia M.B. 2001. Biomarkers of apoptosis: release of cytochrome c, activation of caspase-3, induction of 8-hydroxy-2′-deoxyguanosine, increased 3-nitrotyrosine, and alteration of p53 gene. Journal of Toxicology and Environmental Health Part B, Critical Reviews 4(3): 313-32.
  10. Abu-Qare A.W., Abou-Donia M.B. 2008. In vitro metabolism and interactions of pyridostigmine bromide, N,N-diethyl-m-toluamide, and permethrin in human plasma and liver microsomal enzymes. Xenobiotica 38(3): 294-313.
  11. Anderson R.C., Anderson J.H. 1999. Sensory irritation and multiple chemical sensitivity. Toxicology and Industrial Health 15(3-4): 339-45.
  12. Ashford N.A. 1999. Low-level chemical sensitivity: implications for research and social policy. Toxicology and Industrial Health 15(3-4): 421-47.
  13. Baldwin C.M. and Bell I.R. 1998. Increased cardiopulmonary disease risk in a community-based sample with chemical odor intolerance: implications for women’s health and health-care utilization. Archives of Environmental Health 1998 53(5): 347-53.
  14. Baldwin C.M., Bell I.R., O’Rourke M.K. 1999. Odor sensitivity and respiratory complaint profiles in a community-based sample with asthma, hay fever, and chemical odor intolerance. Toxicology and Industrial Health 15(3-4): 403-9.
  15. Bascom R., Meggs W.J., Framptom M., Hudnell K., Kilburn K., Kobal G., Medinsky M., Rea W. 1997. Neurogenic inflammation: with additional discussion of central and perceptual integration of nonneurogenic inflammation. Environmental Health Perspective 105 (Suppl. 2): 531-37.
  16. Bell I.R., Miller C.S., and Schwartz G.E. 1992. An olfactory-limbic model of multiple chemical sensitivity syndrome: possible relationships to kindling and affective spectrum disorders. Biological Psychiatry 32(3): 218-42.
  17. Bell I.R., Warg-Damiani L., Baldwin C.M., Walsh M.E., Schwartz G.E. 1998. Self-reported chemical sensitivity and wartime chemical exposures in Gulf War veterans with and without decreased global health ratings. Military Medicine 163(11): 725-32.
  18. Bell I.R., Schwartz G.E., Peterson J.M. and Amend D. 1993. Self-reported illness from chemical odors in young adults without clinical syndromes or occupational exposures. Archives of Environmental Health. 48(1): 6-13.
  19. Bell I.R., Schwartz G.E., Baldwin C.M., Hardin E.E. 1996. Neural sensitization and physiological markers in multiple chemical sensitivity. Regulatory Toxicology and Pharmacology 24(1), pt. 2: S39-S47.
  20. Bell I.R., Baldwin C.M., Schwartz G.E.R. 2001. Sensitization studies in chemically intolerant individuals: implications for individual difference research. Annals of the New York Academy of Sciences 933:38-47.
  21. Brandt-Rauf P.W., Andrews L.R., Schwarz-Miller J. 1991. Sick-hospital syndrome. Journal of Occupational Medicine 33(6): 737-39.
  22. Bronstein A.C. 1995. Multiple chemical sensitivities—new paradigm needed. Journal of Toxicology: Clinical Toxicology 33(2): 93-94.
  23. Brooks S.M., Weiss M.A., Bernstein I.L. 1985. Reactive airways dysfunction syndrome. Case reports of persistent airways hyperreactivity following high-level irritant exposures. Journal of Occupational Medicine 27(7): 473-76.
  24. Brown-DeGagne A.M., McGlone J. 1999. Multiple chemical sensitivity: a test of the olfactory-limbic model. Journal of Occupational and Environmental Medicine 41(5): 366-77.
  25. Buchwald D., Garrity D. 1994. Comparison of patients with chronic fatigue syndrome, fibromyalgia, and multiple chemical sensitivities. Archives of Internal Medicine 154(18): 2049-53.
  26. Caress S.M., Steinemann A.C. 2003. A review of a two-phase population study of multiple chemical sensitivities. Environmental Health Perspectives 111(12): 1490-97.
  27. Caress S.M., Steinemann A.C. 2004. Prevalence of multiple chemical sensitivities: A population-based study in the southeastern United States. American Journal of Public Health 94(5): 746-47.
  28. Caress S.M., Steinemann A.C. 2009. Prevalence of fragrance sensitivity in the American population. Journal of Environmental Health 71(7): 46-50.
  29. Caress S.M., Steinemann A.C. 2009. Asthma and chemical hypersensitivity: prevalence, etiology, and age of onset. Toxicology and Industrial Health 25(1): 71-78.
  30. Caress S.M., Steinemann A.C. 2004. A national population study of the prevalence of multiple chemical sensitivity. Archives of Environmental Health 59(6): 300-305.
  31. Caress S.M., Steinemann A.C. 2005. National prevalence of asthma and chemical hypersensitivity: an examination of potential overlap. Journal of Occupational and Environmental Medicine 47(5): 518-22.
  32. Caress S.M., Steinemann A.C., Waddick C. 2002. Symptomatology and etiology of multiple chemical sensitivities in the southeastern United States. Archives of Environmental Health 57(5): 429-36.
  33. Davidoff A.L., Keyl P.M., Meggs W.J. 1998. Development of multiple chemical sensitivities in laborers after acute gasoline fume exposure in an underground tunneling operation. Archives of Environmental Health 53(3):183-89.
  34. DeRosa C.T., Hicks H.E., Ashizawa A.E., Pohl H.R., Mumtaz M.M. 2006. A regional approach to assess the impact of living in a chemical world. Annals of the New York Academy of Sciences 1076:829-38.
  35. Donnay A.H. 1999. On the recognition of multiple chemical sensitivity in medical literature and government policy. International Journal of Toxicology 18(6): 383-92.
  36. Elberling J., Linneberg A., Dirksen A., Johansen J.D., Frølund L., Madsen F., et al. 2005. Mucosal symptoms elicited by fragrance products in a population-based sample in relation to atopy and bronchial hyper-reactivity. Clinical and Experimental Allergy 35(1): 75-81.
  37. Farrow A., Taylor H., Northstone K., Golding J. 2003. Symptoms of mothers and infants related to total volatile organic compounds in household products. Archives of Environmental Health 58(10): 633-41.
  38. Fernandez M., Bell I.R., Schwartz G.E. 1999. EEG sensitization during chemical exposure in women with and without chemical sensitivity of unknown etiology. Toxicology and Industrial Health 15(3-4): 305-12.
  39. Gibson P.R., Elms A.N., Ruding L.A. 2003. Perceived treatment efficacy for conventional and alternative therapies reported by persons with multiple chemical sensitivity. Environmental Health Perspectives 111(12): 1498-1504.
  40. Gilbert M.E. 1995. Repeated exposure to lindane leads to behavioral sensitivities and facilitates electrical kindling. Neurotoxicolgy and Teratology 17(2): 131-41.
  41. Greene G.J., Kipen H.M. 2002. The vomeronasal organ and chemical sensitivity: a hypothesis. Environmental Health Perspectives 110 (Suppl 4): 655-61.
  42. Haley R.W., Billecke S., La Du B.N. 1999. Association of low PON1 type Q (type A) arylesterase activity with neurologic symptoms complexes in Gulf War veterans. Toxicology and Applied Pharmacology 157(3): 227-33.
  43. Heuser G., Mena I., Alamos F. 1994. NeuroSPECT findings in patients exposed to neurotoxic chemicals. Toxicology and Industrial Health 10: 561-71.
  44. Jammes Y., DelPierre S., DelVolgo M.J., Humbert-Tena C., Burnet, H. 1998. Long-term exposure of adults to outdoor air pollution is associated with increased airway obstruction and higher prevalence of bronchial hyperresponsiveness. Archives of Environmental Health 53(6): 372-77.
  45. Johansson A., Löwhagen O., Millqvist E., Bende M. 2002. Capsaicin inhalation test for identification of sensory hyperreactivity. Respiratory Medicine 96(9): 731-35.
  46. Joffres M.R., Sampalli T., Fox R.A. 2005. Physiologic and symptomatic responses to low-level substances in individuals with and without chemical sensitivities; a randomized controlled blinded pilot booth study. Environmental Health Perspectives 113(9): 1178-83.
  47. Kelly K.J., Prezant D.J. 2005. Bronchial hyperreactivity and other inhalation lung injuries in rescue/recovery workers after the world trade center collapse. Critical Care Medicine 33 (Suppl 1): S102-S106.
  48. Kilburn K.H. 2003. Effects of hydrogen sulfide in neurobehavioral function. Southern Medical Journal 90(10): 997-1106.
  49. Kilburn K.H. 1999. Measuring the effects of chemicals in the brain. Archives of Environmental Health 54(3): 150. Read more…