International Journal of Occupational and Environmental Health Features Discovery of Asbestos-Related Pain Origin from Scientists at the Karmanos Cancer Institute in Detroit 

Scientists at the Barbara Ann Karmanos Cancer Institute’s National Center for Vermiculite and Asbestos-Related Cancers (NCVAC) have discovered a probable reason for the unrelenting chest pain experienced in certain patients with asbestos-related diseases and cancers. The findings, featured in the July 20, 2009 edition of the International Journal of Occupational and Environmental Health, were published in an academic peer-reviewed manuscript by principal author Michael Harbut, M.D., MPH, co-director of the NCVAC and chief of the Center for Occupational and Environmental Medicine, affiliated with Wayne State University.  

Harbut reported the findings after studying a patient who was exposed to taconite dust as a child.  

Using a new radiography approach developed by Carmen Endress, M.D., FACR, associate professor of Radiology, Wayne State University School of Medicine and radiologist at the NCVAC, there was a documented increase in pleural plaques, causing erosion on the interior wall of the ribs. 

“This action of the pleural plaque against the covering of the bone and the bone itself is a biologically plausible and an anatomically logical explanation of the unrelenting pain which some patients experience,” said Dr. Harbut.

This new imaging approach involves enhancing images obtained on the 64-slice high resolution CT scan using the Vitrea(R) imaging software program by Vital Images. By using this imaging approach, Dr. Harbut was able to demonstrate that: 

Evidence based on the CT findings, the physical examination, pulmonary function studies, epidemiology and history of the patient’s intractable pleural pain meets the criteria for diagnosis of asbestosis. Combined with the known science of taconite dust, a link between the mine where the patient’s father worked and the patient’s disease was established.  

Due to the clarity and definition of this new imaging approach, it is more likely to detect asbestos-related diseases and cancer at an earlier stage.  

Earlier detection will allow the possibility for additional treatment options to manage the pain caused by pleural plaque beyond the narcotics often prescribed for patients with advanced stages of asbestos disease. This includes exploring other forms of traditional and nontraditional methods to control pain.  

The patient, studied since 2004 and currently 55 years of age, was exposed as a child to taconite dust unknowingly by her father, a taconite miner from 1962 – 1969, who carried the taconite dust on his work clothes. Taconite is used in the production of steel and road-patching material. It has been mined in Michigan and Minnesota. 

The patient has experienced increasing pain on her right side for the past 31 years, a persistent cough and wheezing. As the pain increased so did her medication. Using the new imaging approach, Dr. Harbut was able to show the progression of the patient’s pleural plaque over a three year period, from 2005 – 2008. The patient’s pleuritic pain, as well as the findings of her pulmonary function, physical exam and symptomology are consistent with those diagnosed with asbestosis and pleural plaques, as established by the American Thoracic Society.  

These findings also support earlier human and animal reports that dusts produced by taconite mining can evoke the same biological responses as do other fibers already defined as asbestos or asbestiform materials. 

Harbut added, “Patients often require a lifetime of narcotics to allow functioning, but we are hopeful that with this new imaging technology, more selective pain management approaches with fewer side effects can be instituted resulting in a better quality of life.”

Finally, the report supports the identification of taconite, which has not yet been categorized as asbestos but causes a disease consistent with asbestosis, and recommends a reevaluation of the definition of asbestos. This is especially important within the context of legislative efforts to prohibit the use of asbestos. 

Karmanos scientists are continuing their series of patient studies and will submit similar findings for peer review later this summer.  

In addition to Dr. Harbut, co-authors of the report include Carmen Endress, M.D., FACR; John J. Graff, Ph.D., MS, assistant professor, Wayne State University School of Medicine, and chief, Cancer Surveillance Research at the Barbara Ann Karmanos Cancer Institute; Christopher Weis, Ph.D., National Enforcement Investigations Center, United States Environmental Protection Agency; and Harvey Pass, M.D., director, New York University’s Division of Thoracic Surgery.  

About the National Center for Vermiculite and Asbestos-Related Cancers (NCVAC at Karmanos)  

In response to the United States Environmental Protection Agency’s (EPA) identification of major sources of public asbestos exposure in Michigan, and to address the need for early diagnosis and aggressive treatment of asbestos-related diseases, the Barbara Ann Karmanos Cancer Institute and the Center for Occupational and Environmental Medicine (COEM) affiliated with Wayne State University established Karmanos’ National Center for Vermiculite and Asbestos-Related Cancers. The NCVAC is co-directed by Michael Harbut, M.D., MPH, Karmanos Cancer Institute and Chief of the Center for Occupational and Environmental Medicine; and John J. Graff, Ph.D. MS, chief of Cancer Surveillance Research, Karmanos Cancer Institute and assistant professor, Department of Family Medicine and Public Health Sciences, Wayne State University School of Medicine. 

Reference: Barbara Ann Karmanos Cancer Institute, International Journal of Occupational and Environmental Health Features Discovery of Asbestos-Related Pain Origin from Scientists at the Karmanos Cancer Institute in Detroit , US Newswire, DETROIT, July 20, 2009.

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

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)

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…

Many parents worry about their child’s exposure to phthalates, the chemical compounds used as plasticizers in a wide variety of personal care products, children’s toys, and medical devices. Phthalate exposure can begin in the womb and has been associated with negative changes in endocrine function. A new study soon to be published in the Journal of Pediatrics examines the possibility that in utero phthalate exposure contributes to low birth weight in infants. Low birth weight is the leading cause of death in children under 5 years of age and increases the risk of cardiovascular and metabolic disease in adulthood.  

To investigate the associations between in utero phthalate exposure and low birth weight, Dr. Renshan Ge of the Population Council and colleagues from Fudan University and Second Military Medical University in Shanghai studied 201 pairs of newborns and their mothers between 2005 and 2006. Of the 201 infants studied, 88 were born with low birth weight. The researchers analyzed samples of the infants’ meconium, the first bowel movement that occurs after birth, and cord blood to determine phthalate levels.  

They found quantifiable levels of phthalate and phthalate metabolites in more than 70% of the samples. Infants with low birth weight had consistently higher levels of phthalates. According to Dr. Ge, “The results showed that phthalate exposure was ubiquitous in these newborns, and that prenatal phthalate exposure might be an environmental risk factor for low birth weight in infants.” Although these associations are not conclusive, this study supports the accelerating efforts to minimize phthalate exposure. 

Reference: The study, reported in “Phthalate Levels and Low Birth Weight: A Nested Case-Control Study of Chinese Newborns” by Zhang Y, PhD, Lin L, MD, Cao Y, PhD, Chen B, MD, Zheng L, MSC, Ge R, MD, appears in the Journal of Pediatrics, DOI 10.1016/j.jpeds.2009.04.007, published by Elsevier. EurekAlert, June 25, 2009.