ALS and pesticides
ALS and pesticides
Aug 2. 3007
By Paule Hjertaas
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motor neuron disease (include ALS)
n.
Any of various diseases of motor neurons, such as progressive muscular atrophy, amyotrophic lateral sclerosis, progressive bulbar paralysis, and primary lateral sclerosis.
|Source: The American Heritage® Stedman's Medical Dictionary |
|Copyright © 2002, 2001, 1995 by Houghton Mifflin Company. Published by Houghton Mifflin Company. |
ALS is one of degenerative illnesses coved under the term motor neuron disease. In Australia, a new dr coming to one particular area especially high in pesticide applications found very high levels of ALS.
Methyl bromide is used in fumigation. It is a fumigant. No sales were recorded in the partial SK sales data base from 2001-03. SK certainly uses a lot of organophosphates and carbamates which are nerve toxins.
ALS is an auto-immune disease, and many pesticides are known experimentally as well as epidemiologically to increase markers of auto-immune disease (Anti-nuclear antibodies or ANAs). A quick google search for ANA-pesticides came up with the following, certainly only the tip of the iceberg. .
I'd like to add that any neurotoxin in personal care, home care, fragrances and other products can also contribute. Well-know medical herbalists treat Multiple Sclerosis and other neurological disease as we do Multiple chemical Sensitivities, with a clean lifestyle and products.
Saskatchewan studies are # 4 and 5 below.
1.
|If you are an ASABE member or if your employer has arranged for access to the full-text, click the underlined title below to |
|view. |
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|Antinuclear Antibodies in Mice Exposed to Pesticides |
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|Published by the American Society of Agricultural and Biological Engineers, St. Joseph, Michigan |
|Citation: Journal of Agricultural Safety and Health. 5(2): 173-178 . @1999 |
|Authors: A. M. Rosenberg |
|Keywords: Antinuclear antibodies, Immunotoxicology, Pesticides, SJL mice |
|The objective of this study was to determine if pesticides induce antinuclear antibodies in mice. For the purposes of this study|
|groups of nine SJL mice received one of four commercially formulated pesticides (Dieldrin, Malathion, 2,4D or Aldicarb) orally |
|at concentrations of 10%, 25%, and 50% of the respective 50% lethal doses (LD50). Sera obtained prior to and after exposure were|
|assayed for the presence of antibodies to nuclear constituents of HEp-2 cells, a human epithelioid carcinoma cell line, by |
|indirect immunofluorescence. The results of this study showed that antinuclear antibodies occurred significantly more frequently|
|in mice exposed to Malathion as compared to those exposed to other pesticides and to unexposed control animals. The results of |
|this study show that Malathion induces antinuclear antibodies in SJL mice significantly more frequently than do other pesticides|
|and significantly more frequently than occurs spontaneously in unexposed control animals. The SJL mouse strain can serve as an |
|animal model to explore further the immunopathogenic potential of pesticides in general and the induction of antinuclear |
|antibodies and autoimmune disease in particular. |
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|American Society of Agricultural and Biological Engineers |
|2950 Niles Road, St. Joseph, MI 49085 | phone 269.429.0300 | fax 269.429.3852 | hq@ |
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|July 2004, 15:4 > ANTINUCLEAR ANTIBODIES: ASSOCIATION... |< Previous | Next > |
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ANTINUCLEAR ANTIBODIES: ASSOCIATION WITH ENVIRONMENTAL AND OCCUPATIONAL EXPOSURES TO PESTICIDES IN URBAN AND RURAL ENVIRONMENTS.
The Sixteenth Conference of the International Society for Environmental Epidemiology (ISEE)
Epidemiology. 15(4):S161-S162, July 2004.
Fahmy, Kamal; ElGaafar, Yehia Abd; Guendi, Wessam El
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3. Antinuclear antibodies among eastern-Polish rural inhabitants
Radoslaw Spiewak, Nimfa M. Stojek
Department of Occupational Biohazards, Institute of Agricultural Medicine, Lublin, Poland
Source: Spiewak R, Stojek NM. Antinuclear antibodies among eastern-Polish rural inhabitants. Ann Agric Environ Med 2003; 10 (2): 207-209.
|Background: Rural inhabitants are exposed to considerable amounts of pesticides from water, soil and air. There are indications that|
|exposure to pesticides may trigger production of antinuclear antibodies (ANA). Therefore, the question arises about the prevalence |
|of ANA in this group. |
|Methods: In 90 eastern-Polish rural inhabitants (RI) and 50 urban blood donors (BD), the presence of ANA in serum was tested using |
|EIA technique (Varelisa ReCombi ANA Profile). |
|Results: The frequency of ANA in the RI group was 2.5-fold higher than in the BD group (p=0.0175). Among RI, at least one |
|autoantibody was detected in 30% (95%CI: 20.5-39.5%). Most frequently, this was anti-dsDNA (12.2%; 95%CI: 5.5-19.0%), followed by |
|SS-A/Ro (7.8%; 2.2-13.3%), RNP and Scl-70 (each 5.6%; 0.8-10.3%), Jo-1 (3.3%; 0.0-7.0%), Sm, SS-B/La, and CENP (each 2.2%; |
|0.0-5.3%). These figures are relatively high compared to studies of other random populations. In the BD group, at least one |
|autoantibody was found in 12% (95%CI: 3.0-21.0%). Most frequently, this was anti-SS-A/Ro (8%; 95%CI: 0.5-15.5%), followed by dsDNA, |
|RNP, and Scl-70 (each 2%; 0.0-5.9%). Neither Jo-1, Sm, SS-B/La, nor CENP-autoantibodies were found in this group. These figures |
|place eastern-Polish blood donors in the middle of the range of prevalence observed among blood donors in other countries. |
|Conclusion: The occurrence of antinuclear antibodies in eastern-Polish rural population is relatively high as compared to both |
|eastern-Polish blood donors and other random populations. Possible explanation for this is the long-term exposure to pesticides. |
|Key words: immunotoxicology, rural population, farmers, agricultural chemicals, environmental exposure, pesticides, health effects, |
|autoimmunity, autoantibodies, antinuclear antibodies, agricultural workers' diseases, epidemiology, Poland. |
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|[pic]1: J Toxicol Environ Health A. 1999 Jun 25;57(4):225-36. [pic]Links |
|Prevalence of antinuclear antibodies in a rural population. |
|Rosenberg AM, Semchuk KM, McDuffie HH, Ledingham DL, Cordeiro DM, Cessna AJ, Irvine DG, Senthilselvan A, Dosman JA. |
|Department of Pediatrics, Centre for Agricultural Medicine, College of Nursing, University of Saskatchewan and National Water |
|Research Institute, Saskatoon, Canada. |
|Exposure to environmentally and occupationally encountered toxicants can be associated with the development of certain |
|autoimmune diseases and with the induction of antinuclear antibodies (ANA). Some chemicals used in the agricultural industry are|
|known to affect immune function but their roles in the induction of autoimmunity in general, and ANA in particular, have not |
|been reported previously. This study was undertaken to establish the prevalence of ANA in a rural population and to determine |
|environmental and occupational exposures with which they are associated. This cross-sectional study represented one component of|
|an interdisciplinary project (Prairie Ecosystem Study [PECOS], Eco-Research Program, Tri-Council Secretariat of Canada) designed|
|to explore, in a rural population, the roles of environmental exposures as determinants of human health status. Information |
|regarding lifetime, current, and main occupational exposures in the rural-dwelling study population was derived from a |
|self-administered questionnaire. Sera from consenting subjects, collected during the months of February and March 1996, were |
|assayed for ANA by indirect immunofluorescence on HEp-2 cells. The study population comprised 322 adult subjects (mean age |
|49.3+/-14.7 yr; range 16-87 yr). Statistical analyses adjusted for age and sex revealed that the presence of ANA among the |
|participants was associated with a current agricultural occupation that included oilseed production, hog production, or poultry |
|production. There was a significant association between ANA positivity and a current main farming operation of crop production. |
|There was also an association among individual participants between lifetime exposure to the insecticide class of pesticides and|
|the presence of ANA. In this rural study population, ANA positivity was significantly associated with lifetime exposure |
|specifically to carbamate, organochlorine (including aldrin, chlordane, dieldrin, endrin, heptachlor, and lindane, but excluding|
|DDT and methoxychlor), and pyrethroid insecticides and to phenoxyacetic acid herbicides, including 2,4-D. After adjustment for |
|age, sex, and other insecticide exposures, multivariate analyses indicated that ANA positivity was associated with current |
|oilseed production and with lifetime exposure to pyrethroid insecticides. In a rural population, ANA were associated with |
|production of certain crops and certain animals and exposure to specific pesticides. The data indicate that some occupational |
|exposures related to the agricultural industry are associated with the presence of ANA, a serologic expression of autoimmunity. |
|PMID: 10406347 [PubMed - indexed for MEDLINE] |
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5. Antinuclear Antibodies and Bromoxynil Exposure in a Rural Sample
Authors: Karen M. Semchuk a; Alan M. Rosenberg b; Helen H. McDuffie c; Allan J. Cessna d; Punam Pahwa e; Donald G. Irvine f
|Affiliations: |a College of Nursing, University of Saskatchewan, Saskatoon, Saskatchewan, Canada |
| |b Department of Pediatrics, College of Medicine, University of Saskatchewan, Saskatoon, Saskatchewan, |
| |Canada |
| |c Institute of Agricultural, Rural, and Environmental Health, Department of Medicine, University of |
| |Saskatchewan, Saskatoon, Saskatchewan, Canada |
| |d Agriculture and Agri-Food Canada, Lethbridge, Alberta, Canada |
| |e Department of Community Health and Epidemiology and Institute of Agricultural, Rural, and Environmental |
| |Health, University of Saskatchewan, Saskatoon, Saskatchewan, Canada |
| |f Toxicology Group, University of Saskatchewan, Saskatoon, Saskatchewan, Canada |
DOI: 10.1080/15287390600974593
Publication Frequency: 24 issues per year
Published in: [pic]Journal of Toxicology and Environmental Health, Part A, Volume 70, Issue 7 January 2007 , pages 638 - 657
Subjects: Environmental & Ecological Toxicology; Environmental Health;
Formats available: HTML (English) : PDF (English)
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|Abstract |
|Previous research suggests that farmers may have an increased risk of developing autoimmunity and that exposure to certain |
|pesticides may alter immune function. Little is known, however, about the immunologic effects of farming and pesticide |
|exposures. As part of the Prairie Ecosystem Study, associations between detection of antinuclear antibodies (ANA), an |
|autoimmunity indicator, and exposure to the herbicide bromoxynil (3,5-dibromo-4-hydroxybenzonitrile) were investigated in a |
|cross-sectional study of 208 residents (94 women, 114 men) of a cereal-producing region in Saskatchewan, Canada, during spring |
|herbicide application, 1996. The ANA were assayed in serum by indirect immunofluorescence on HEp-2 cells. Bromoxynil was |
|measured in plasma by gas chromatography/mass spectrometry analysis. Associations were explored between ANA detection and |
|detection of bromoxynil in plasma, self-reported use of bromoxynil and other pesticides, farming exposures, gender, age, body |
|mass index (BMI), and residency. The mean age (SD) of the participants was 50.8 (13.6) yr [women: 49.7 (13.5) yr, men: 51.6 |
|(13.6) yr]. ANA prevalence was 37.5% (women: 39.4%, men: 36%,) at 1:40 serum dilution, 17.3% (women: 20.2%, men: 14.9%) at 1:80,|
|and 10.1% (women: 13.8%, men: 7%) at 1:160. In the multiple-variable Generalized Estimating Equation (GEE) logistic regression |
|analyses, female gender was a positive predictor of ANA detection and gender differences were observed in the relative |
|importance of other study factors. None of the variables examined in the multiple-variable GEE analysis were statistically |
|significant predictors of ANA detection for women. For many of these variables, however, the point estimates for women are |
|similar to those seen in men. For men, with adjustment for age, ANA presence was inversely associated with detection of |
|concentrations of bromoxynil in winter or spring samples and recent occupational use of 2,4-dichlorophenoxyacetic acid, and the |
|positive ANA predictors included having a BMI in the obese (BMI > 30.04 kg/m2) category, recent occupational use of trifluralin |
|or fungicides, and current exposure to oilseed, poultry, or dairy production. The inverse association between ANA detection and |
|bromoxynil exposure observed in farmers in this study is consistent with earlier empirical observations that certain pesticides |
|may suppress immune function. Further research is needed to examine whether these findings are confirmed in other populations |
|and to elucidate the biological mechanisms involved. |
|view references (110) |
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6. Occupational and Environmental Associations with Antinuclear Antibodies in a General Population Sample 1
Authors: Glinda S. Cooper a; Christine G. Parks b; Peter S. Schur c; Patricia A. Fraser d
|Affiliations: |a Department of Health and Human Services, National Institute of Environmental Health Sciences, National |
| |Institutes of Health, Durham, North Carolina, USA |
| |b National Institute for Occupational Safety and Health, Morgantown, West Virginia, USA |
| |c Brigham and Women's Hospital, Boston, Massachusetts, USA |
| |d Center for Blood Research, Harvard Medical School and Brigham and Women's Hospital, Boston, |
| |Massachusetts, USA |
DOI: 10.1080/15287390600746165
Publication Frequency: 24 issues per year
Published in: [pic]Journal of Toxicology and Environmental Health, Part A, Volume 69, Issue 23 June 2006 , pages 2063 - 2069
Subjects: Environmental & Ecological Toxicology; Environmental Health;
Formats available: HTML (English) : PDF (English)
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|Abstract |
|Antinuclear antibodies are a hallmark feature of the autoimmune disease systemic lupus erythematosus, and can occur many years |
|before onset of symptoms. The objective of this study was to examine the association between exposures and high-titer |
|antinuclear antibodies in the general population (i.e., people who do not have lupus or other systemic autoimmune diseases). |
|Serum was collected from 266 population-based controls who had been frequency-matched to the age and gender distribution of |
|lupus cases in a 60-county study area in the southeastern United States. A detailed occupational history was collected using a |
|structured interview; information was also collected on hair dye use. Antinuclear antibodies were assayed using HEp-2 cells as |
|substrate. Logistic regression was used to estimate the odds ratio (OR) as a measure of association between exposures and |
|high-titer antinuclear antibody levels, adjusting for age, gender, and race. High-titer antinuclear antibodies ( [pic]1:160) |
|were observed in 21 subjects (8%). A twofold increased prevalence of high-titer antinuclear antibodies was seen with some |
|occupational exposures (silica dust, pesticides, and sunlight), although none of these individual estimates were statistically |
|significant. The association seen with use of hair dyes was weaker (OR 1.4). There was a suggestion of a dose response with a |
|combined measure based on the summation of exposures (ORs of 1.7, 2.1, and 5.9 for 1, 2, and [pic]3 exposures). These data |
|suggest that occupational exposures may influence the expression of antinuclear antibodies. Larger studies addressing these |
|exposures may provide insights into the mechanisms by which various environmental factors affect the development of |
|autoantibodies and the progression to clinical disease. |
|1 *This study was supported by the Division of Intramural Research, National Institute of Environmental Health Sciences (Dr. |
|Cooper), and by ES10295 and ES10457 from the National Institute of Environmental Health Sciences to Dr. Fraser. |
|view references (17) : view citations |
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7. PANUPS: April 12, 2007 ( NOTE: motor neurone disease =ALS)
Methyl bromide
Fumigant findings stir anger in New Zealand. Port workers in the town of Nelson have been dying from motor neurone disease and their widows believe the deaths are linked to methyl bromide used to fumigate timber for export. The Campaign Against Toxic Sprays demanded an investigation. Finally, after a long delay, New Zealand's Environment Court confirmed that the workers and nearby residents were likely exposed to dangerous levels of methyl bromide escaping from storage sheds. According to TV New Zealand, under a "worst-case scenario, residents would face gas levels twice the workplace safety standard". A spokesperson for Genera, the company using the fumigant, dismissed the court's findings as "unscientific". But Genera is now considering installing a system "that will capture all the gas."
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8. Are we living in a toxic time bomb?
18.02.2006
|By MEGAN KINNIMENT |
|Research points to link between deadly disease and pesticides exposure |
|IT CAN start with a slight twitch in your face, or a loose grip on your coffee mug. |
|However, within two years, sometimes three, the fatal Motor Neurone Disease (MND) ravages the body to the point where the |
|sufferer can no longer breathe or swallow. |
|It eventually leads to paralysis. And there is no known cure. |
|However, new research by Sydney University scientists may shed some light on the cause of the horrific disease, which has killed|
|thousands of Australians including former Lismore mayor Bob Gates. |
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|[pic][pic][pic][pic] |
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|But the findings will also sound warning bells for agricultural communities such as the Northern Rivers, which has a |
|significantly higher rate per population of neurological disease than the rest of NSW. |
|The studies by Sydney University neurologist Dr Roger Pamphlett have uncovered a deadly link between exposure to pesticides and |
|the degenerative disease MND. |
|With pesticide exposure a daily occurrence for many on the North Coast, could the ‘green and clean‘ region we call home be |
|harbouring a toxic time bomb? |
|After being diagnosed with MND in 2002, former Lismore mayor Bob Gates naturally wondered what had caused it. Tragically, seven |
|months after his diagnosis, with his movement limited and barely able to breathe, Cr Gates died without discovering the answer. |
|Three years later his widow, Helen Gates, is still asking why. |
|"He was very health conscious, there was no history of illness in the family, he was never underweight, never overweight...it |
|was just out of the blue," said Mrs Gates, president of the NSW MND Association Northern Rivers Support Group. |
|Before he died, Cr Gates had been an active man; a surf lifesaver with the Ballina SLSC who had watched what he ate, barely |
|drank and knew of no previous incidence of MND in his family history. |
|As he faced death he reflected on a lifetime growing up on the Northern Rivers and the environmental factors that may have led |
|to his MND. |
|"After he got MND we were trying to work out ‘how?’," Mrs Gates said. "Bob said maybe it was from his work as a quarry manager."|
| |
|Or, perhaps, she said, it was from his exposure as a child to pesticide residue in the Richmond River. |
|"As a child he used to swim in the river and in those days everything went in — pesticides, slops from the piggery, everything. |
|You wouldn’t let your kids swim in it these days," she said. |
|Helen Gates joins the growing number of local families who have lost loved ones to the mysterious disease. |
|North Coast Area Health Service statistics from 2000/01 show the Northern Rivers has a significantly higher number of |
|hospitalisations for nervous system disorders, compared with other areas of NSW. |
|On the Northern Rivers, 1533.22 men per 100,000 of population were hospitalised with nervous system disorders, compared with |
|1491.85 statewide; while 1465.68 Northern Rivers women were hospitalised, compared with 1385.7 statewide. |
|After three decades of practice, Lismore neurologist Dr Geoffrey Boyce has seen so many cases of MND in the past two years it |
|has left him shaking his head. |
|"I’ve seen more cases of Motor Neurone Disease in the Northern Rivers in the past two years than in the 10 years I worked in |
|Cairns," he said. |
|Dr Boyce said the incidence of degenerative Parkinson’s Disease and Multiple Sclerosis was also higher than average on the |
|Northern Rivers. But he cannot pinpoint why. |
|The Sydney University research may provide a clue. Dr Pamphlett’s study of 900 people, including 300 with MND, has suggested |
|regular exposure to pesticides may increase a person’s risk of developing the condition. |
|In particular, the Sydney University studies found that some patients with the progressive paralysing disease have differences |
|in a gene known as paraoxynase, involved in the breakdown of organophosphates, the active ingredient of many commonly-used |
|pesticides. |
|"We have found that people who had regular contact with pesticides, such as once a week for six months, are at greater risk of |
|getting Motor Neurone Disease," Dr Pamphlett said. |
That there is a high incidence of Motor Neurone Disease in this region, and that scientists are now making links between MND and pesticides, comes as no real surprise to environmental scientist and National Toxics Network president Jo Immig.
Ms Immig, of Possum Creek, has devoted her scientific career to raising awareness of the hidden dangers of pesticides residue in our food, water and air.
She has instigated changes to NSW environmental legislation regulating agricultural pesticides, making NSW the first State where it is mandatory for farmers to undertake training in using pesticides and farmers are now required to keep records of what pesticides they use.
From 2007, it will be also mandatory for the public to be notified if pesticides are to be sprayed in a public place.
Ms Immig said organophosphates, the group of pesticides targeted in the Sydney University studies on MND, were known nerve poisons.
"They derived from World War II nerve gases,’ she said.
"They kill insects by disrupting the nervous system.
"What hasn’t been explored is the low-level impact these toxins have over time.
"We’re only beginning to see the wave of illnesses coming through.
"It takes about 30 years for these degenerative diseases to manifest. I think what we are seeing here is the tip of the iceberg."
It is the tip of an iceberg scientists have been bumping into for decades, ever since organophosphates were introduced, first as weapons of war, then as weapons against agricultural pests.
Dr Pamphlett stresses that a larger scientific study is needed to prove his initial findings, but he said it was not the first time pesticides had been linked with neurological disease.
He said the connection had been made between pesticides and Parkinson’s Disease, and studies in the Northern Hemisphere had shown that farmers regularly exposed to pesticides were two times more at risk of contracting MND.
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9. Motor Neuron Disease Linked to Gene-Environment Interactions
(Beyond Pesticides, April 8, 2008) A team of University of Michigan scientists discover interactions between genes and organophosphate exposure cause some forms of motor neuron disease (MND). The study, which appears in the March issue of the American Journal of Human Genetics, shows the mutations in one key gene (neuropathy target esterase, or NTE) that causes a previously unknown type of inherited MND. The scientists also find the mutations caused changes in a protein already known to be involved when people develop neurologic disorders as a result of exposure to toxic organophosphate chemicals commonly used in solvents and insecticides and also as “nerve gas” agents.
Motor neuron disease is a rare, devastating illness in which nerve cells that carry brain signals to muscles gradually deteriorate. One form of it is Lou Gehrig’s disease or ALS (amyotrophic lateral sclerosis). For most MND patients, the cause is unknown. Figuring out why these people develop the disease, which causes muscles to weaken, atrophy and cease to function, is an important step in developing therapies to treat or prevent motor neuron disease. Motor neuron disease affects five per 100,000 people.
“Our findings support the possibility that toxic organophosphates contribute to motor neuron disease in genetically vulnerable people,” says John K. Fink, M.D., professor of neurology at the U-M Medical School and senior author of the study. He believes the results suggest that altered activity of the gene found in patients in the study may also contribute to other motor neuron disorders, possibly including ALS. The findings are an exciting first step in uncovering a possible link between the environment and motor neuron disease, says Shirley Rainier, a research assistant professor at the U-M Department of Neurology and the first author of the study. “Why does one person in a family get it, and another doesn’t?”
Dr. Fink examined members of two families who had progressive weakness and tightness in their legs, as well as muscle atrophy in their hands, shins and feet. James Albers, M.D., Ph.D., a U-M professor of neurology and an expert in neuromuscular disorders, studied nerve and motor function. Dr. Rainier performed genetic studies and determined that the gene for the condition was on a region of chromosome 19. Mark Leppert, Ph.D., co-chair of human genetics at the University of Utah, and his team performed genetic analysis that confirmed this location and excluded other areas in the genome. Among the many genes in this region of chromosome 19, one gene stood out as particularly likely: the gene that encodes for NTE. Because of its known role in organophosphate-induced neurological disease, the NTE gene was considered an important candidate gene and was studied immediately.
Analysis showed that the affected people in each family had NTE gene mutations. These mutations altered a critical part of the NTE protein called the esterase domain. Dr. Fink has named the inherited condition “NTE motor neuron disease.” It begins in childhood and progresses slowly, with symptoms of weakness and spasticity in the legs and muscle atrophy in the hands and lower legs.
Next, Dr. Fink and his team want to learn if mutations in the NTE gene happen in other types of motor neuron disease such as ALS, and if the mutations make a person more vulnerable to neurological damage from organophosphate exposure. Dr. Fink’s lab is currently using fruit flies as a model to study the NTE mutations, with the goal of finding treatments for people with motor neuron disease.
Posted in Motor neuron disease by: Beyond Pesticides
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