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ALS and pesticides
Aug 2. 3007
By Paule Hjertaas
-motor neuron disease
n.
(include ALS)
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.
Don't have access to the full text? Click here for options.
Antinuclear Antibodies in Mice Exposed to Pesticides
Published by the American Society of Agricultural and Biological Engineers, St. Joseph, Michigan
www.asabe.org
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.
American Society of Agricultural and Biological Engineers
2950 Niles Road, St. Joseph, MI 49085 | phone 269.429.0300 | fax 269.429.3852 | [email protected]
-2.
July 2004, 15:4 > ANTINUCLEAR ANTIBODIES: ASSOCIATION...
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ARTICLE LINKS:
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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
--
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 antiSS-A/Ro (8%; 95%CI: 0.5-15.5%), followed by dsDNA, RNP, and Scl-70 (each 2%; 0.05.9%). 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.
--
Note: Performing your original search, anti-nuclear antibodies and pesticides, in
PubMed will retrieve 0 citations.
All: 1
4.
Review: 0
1: J Toxicol Environ Health A. 1999 Jun 25;57(4):225-36. 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]
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:
, pages 638 - 657
Journal of Toxicology and Environmental Health, Part A,
Volume 70, Issue 7 January 2007
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)
-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:
pages 2063 - 2069
Journal of Toxicology and Environmental Health, Part A,
Volume 69, Issue 23 June 2006 ,
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 ( 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 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
-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."
-8. Are we living in a toxic time bomb?
18.02.2006
http://www.northernstar.com.au/localnews/storydisplay.cfm?storyid=3673113&thesectio
n=localnews&thesubsection=&thesecondsubsection=
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.
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.
--
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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