Female mice disabled by parents' pesticide intake - golf too

[Guest guest]

Female mice disabled by parents' pesticide intake. <http://bit.ly/icUM6G>

By Lynn Markham Milwaukee Bay View Compass 28 February 2011

A white mouse is placed in the center of a maze. She is hungry because

she hasn't eaten all night. She quickly realizes that turning left at

every point gets her food. When a second mouse is set down in the center

of the maze she doesn't seem to remember that taking left turns leads to

food.

Why is it hard for the second mouse to learn? Three months earlier when

she was growing in her mother's womb, her mother was exposed to a

pesticide called chlorpyrifos at levels comparable to what humans

encounter in the environment.

more... <http://bit.ly/icUM6G>

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Paraoxonase gene variants are associated with autism in North America,

but not in Italy: possible regional specificity in gene-environment

interactions. <http://www.ncbi.nlm.nih.gov/pubmed/16027737>

D'Amelio M, Ricci I, Sacco R, Liu X, D'Agruma L, Muscarella LA,

Guarnieri V, Militerni R, Bravaccio C, Elia M, Schneider C, Melmed R,

Trillo S, Pascucci T, Puglisi-Allegra S, Reichelt KL, Macciardi F,

Holden JJ, Persico AM.

Mol Psychiatry. 2005 Nov;10(11):1006-16.

Maternal residence near agricultural pesticide applications and autism

spectrum disorders among children in the California Central Valley.

<http://www.ncbi.nlm.nih.gov/pubmed/17938740>

EM, English PB, Grether JK, Windham GC, Somberg L, Wolff C.

Environ Health Perspect. 2007 Oct;115(10):1482-9.

Organophosphates (OPs) are routinely used as pesticides in agriculture

and as insecticides within the household. Our prior work on Reelin and

APOE delineated a gene-environment interactive model of autism

pathogenesis, whereby genetically vulnerable individuals prenatally

exposed to OPs during critical periods in neurodevelopment could undergo

altered neuronal migration, resulting in an autistic syndrome. Since

household use of OPs is far greater in the USA than in Italy, this model

was predicted to hold validity in North America, but not in Europe.

Here, we indirectly test this hypothesis by assessing

linkage/association between autism and variants of the paraoxonase gene

(PON1) encoding paraoxonase, the enzyme responsible for OP

detoxification. Three functional single nucleotide polymorphisms, PON1

C-108T, L55M, and Q192R, were assessed in 177 Italian and 107

Caucasian-American complete trios with primary autistic probands. As

predicted, Caucasian-American and not Italian families display a

significant association between autism and PON1 variants less active in

vitro on the OP diazinon (R192), according to case-control contrasts

(Q192R: chi2=6.33, 1 df, P<0.025), transmission/disequilibrium tests

(Q192R: TDT chi2=5.26, 1 df, P<0.025), family-based association tests

(Q192R and L55M: FBAT Z=2.291 and 2.435 respectively, P<0.025), and

haplotype-based association tests (L55/R192: HBAT Z=2.430, P<0.025).

These results are consistent with our model and provide further support

for the hypothesis that concurrent genetic vulnerability and

environmental OP exposure may possibly contribute to autism pathogenesis

in a sizable subgroup of North American individuals.

Pubmed for

chlorpyrifos AND autis*

-> 3 cites

for

chlorpyrifos AND golf

-> 10 cites