Functional paraoxonase 1 variants modify the risk of Parkinson's disease due to organophosphate exposure.
Identifieur interne : 000178 ( PubMed/Corpus ); précédent : 000177; suivant : 000179Functional paraoxonase 1 variants modify the risk of Parkinson's disease due to organophosphate exposure.
Auteurs : Pei-Chen Lee ; Shannon L. Rhodes ; Janet S. Sinsheimer ; Jeff Bronstein ; Beate RitzSource :
- Environment international [ 1873-6750 ] ; 2013.
English descriptors
- KwdEn :
- Aged, Agriculture, Aryldialkylphosphatase (genetics), Aryldialkylphosphatase (metabolism), Female, Genetic Predisposition to Disease (epidemiology), Genotype, Humans, Male, Middle Aged, Odds Ratio, Organophosphates (toxicity), Parkinson Disease (epidemiology), Parkinson Disease (genetics), Parkinson Disease (metabolism), Pesticides (toxicity), Polymorphism, Single Nucleotide.
- MESH :
- chemical , genetics : Aryldialkylphosphatase.
- chemical , metabolism : Aryldialkylphosphatase.
- epidemiology : Genetic Predisposition to Disease, Parkinson Disease.
- genetics : Parkinson Disease.
- metabolism : Parkinson Disease.
- chemical , toxicity : Organophosphates, Pesticides.
- Aged, Agriculture, Female, Genotype, Humans, Male, Middle Aged, Odds Ratio, Polymorphism, Single Nucleotide.
Abstract
We previously demonstrated that carriers of the "slower metabolizer" MM genotype of paraoxonase (PON1) who were also exposed to ambient organophosphate (OP) pesticides at their residences were at increased risk of developing Parkinson's disease (PD). Here, with a larger sample size, we extend our previous investigation to consider additional sources of ambient exposure and examined two additional functional PON1 variants.
DOI: 10.1016/j.envint.2013.03.004
PubMed: 23602893
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pubmed:23602893Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Functional paraoxonase 1 variants modify the risk of Parkinson's disease due to organophosphate exposure.</title><author><name sortKey="Lee, Pei Chen" sort="Lee, Pei Chen" uniqKey="Lee P" first="Pei-Chen" last="Lee">Pei-Chen Lee</name><affiliation><nlm:affiliation>Department of Epidemiology, Fielding School of Public Health, University of California at Los Angeles, CA, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Rhodes, Shannon L" sort="Rhodes, Shannon L" uniqKey="Rhodes S" first="Shannon L" last="Rhodes">Shannon L. Rhodes</name></author><author><name sortKey="Sinsheimer, Janet S" sort="Sinsheimer, Janet S" uniqKey="Sinsheimer J" first="Janet S" last="Sinsheimer">Janet S. Sinsheimer</name></author><author><name sortKey="Bronstein, Jeff" sort="Bronstein, Jeff" uniqKey="Bronstein J" first="Jeff" last="Bronstein">Jeff Bronstein</name></author><author><name sortKey="Ritz, Beate" sort="Ritz, Beate" uniqKey="Ritz B" first="Beate" last="Ritz">Beate Ritz</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2013">2013</date><idno type="RBID">pubmed:23602893</idno><idno type="pmid">23602893</idno><idno type="doi">10.1016/j.envint.2013.03.004</idno><idno type="wicri:Area/PubMed/Corpus">000178</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000178</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Functional paraoxonase 1 variants modify the risk of Parkinson's disease due to organophosphate exposure.</title><author><name sortKey="Lee, Pei Chen" sort="Lee, Pei Chen" uniqKey="Lee P" first="Pei-Chen" last="Lee">Pei-Chen Lee</name><affiliation><nlm:affiliation>Department of Epidemiology, Fielding School of Public Health, University of California at Los Angeles, CA, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Rhodes, Shannon L" sort="Rhodes, Shannon L" uniqKey="Rhodes S" first="Shannon L" last="Rhodes">Shannon L. Rhodes</name></author><author><name sortKey="Sinsheimer, Janet S" sort="Sinsheimer, Janet S" uniqKey="Sinsheimer J" first="Janet S" last="Sinsheimer">Janet S. Sinsheimer</name></author><author><name sortKey="Bronstein, Jeff" sort="Bronstein, Jeff" uniqKey="Bronstein J" first="Jeff" last="Bronstein">Jeff Bronstein</name></author><author><name sortKey="Ritz, Beate" sort="Ritz, Beate" uniqKey="Ritz B" first="Beate" last="Ritz">Beate Ritz</name></author></analytic><series><title level="j">Environment international</title><idno type="eISSN">1873-6750</idno><imprint><date when="2013" type="published">2013</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Agriculture</term><term>Aryldialkylphosphatase (genetics)</term><term>Aryldialkylphosphatase (metabolism)</term><term>Female</term><term>Genetic Predisposition to Disease (epidemiology)</term><term>Genotype</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Odds Ratio</term><term>Organophosphates (toxicity)</term><term>Parkinson Disease (epidemiology)</term><term>Parkinson Disease (genetics)</term><term>Parkinson Disease (metabolism)</term><term>Pesticides (toxicity)</term><term>Polymorphism, Single Nucleotide</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Aryldialkylphosphatase</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Aryldialkylphosphatase</term></keywords><keywords scheme="MESH" qualifier="epidemiology" xml:lang="en"><term>Genetic Predisposition to Disease</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" type="chemical" qualifier="toxicity" xml:lang="en"><term>Organophosphates</term><term>Pesticides</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Agriculture</term><term>Female</term><term>Genotype</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Odds Ratio</term><term>Polymorphism, Single Nucleotide</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">We previously demonstrated that carriers of the "slower metabolizer" MM genotype of paraoxonase (PON1) who were also exposed to ambient organophosphate (OP) pesticides at their residences were at increased risk of developing Parkinson's disease (PD). Here, with a larger sample size, we extend our previous investigation to consider additional sources of ambient exposure and examined two additional functional PON1 variants.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">23602893</PMID><DateCreated><Year>2013</Year><Month>04</Month><Day>29</Day></DateCreated><DateCompleted><Year>2013</Year><Month>08</Month><Day>02</Day></DateCompleted><DateRevised><Year>2016</Year><Month>10</Month><Day>25</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1873-6750</ISSN><JournalIssue CitedMedium="Internet"><Volume>56</Volume><PubDate><Year>2013</Year><Month>Jun</Month></PubDate></JournalIssue><Title>Environment international</Title><ISOAbbreviation>Environ Int</ISOAbbreviation></Journal><ArticleTitle>Functional paraoxonase 1 variants modify the risk of Parkinson's disease due to organophosphate exposure.</ArticleTitle><Pagination><MedlinePgn>42-7</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.envint.2013.03.004</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0160-4120(13)00066-4</ELocationID><Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">We previously demonstrated that carriers of the "slower metabolizer" MM genotype of paraoxonase (PON1) who were also exposed to ambient organophosphate (OP) pesticides at their residences were at increased risk of developing Parkinson's disease (PD). Here, with a larger sample size, we extend our previous investigation to consider additional sources of ambient exposure and examined two additional functional PON1 variants.</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">From 2001 to 2011, we enrolled incident cases of idiopathic PD and population controls living in central California. We genotyped three well-known functional PON1 SNPs: two exonic polymorphisms (PON1L55M and PON1Q192R) and the promoter region variant (PON1C-108T). Ambient exposures to diazinon, chlorpyrifos, and parathion at residential and workplace addresses were assessed using a validated geographic information system-based model incorporating records of agricultural pesticide applications in California.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">The odds ratio (OR) for Caucasians exposed to OPs at either residential or workplace addresses varied by PON1 genotype; for exposed carriers of the "faster" metabolizer genotypes, ML or LL, we estimated lower odds ratios (range, 1.20-1.39) than for exposed carriers of the "slower" metabolizer genotype MM (range, 1.78-2.45) relative to unexposed carriers of the faster genotypes. We observed similarly increased ORs for exposure across PON1Q192R genotypes, but no differences across PON1C-108T genotypes. The largest ORs were estimated for exposed carriers of both PON1192QQ and PON155MM (OR range, 2.84-3.57).</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">Several functional PON1 variants may act together to modify PD risk for ambient OP exposures. While either PON1L55M or PON1Q192R may be sufficient to identify increased susceptibility, carriers of both slow metabolizer variants seem most susceptible to OP exposures.</AbstractText><CopyrightInformation>Copyright © 2013 Elsevier Ltd. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Lee</LastName><ForeName>Pei-Chen</ForeName><Initials>PC</Initials><AffiliationInfo><Affiliation>Department of Epidemiology, Fielding School of Public Health, University of California at Los Angeles, CA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rhodes</LastName><ForeName>Shannon L</ForeName><Initials>SL</Initials></Author><Author ValidYN="Y"><LastName>Sinsheimer</LastName><ForeName>Janet S</ForeName><Initials>JS</Initials></Author><Author ValidYN="Y"><LastName>Bronstein</LastName><ForeName>Jeff</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Ritz</LastName><ForeName>Beate</ForeName><Initials>B</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>P01 ES016732</GrantID><Acronym>ES</Acronym><Agency>NIEHS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 ES010544</GrantID><Acronym>ES</Acronym><Agency>NIEHS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>U54 ES012078</GrantID><Acronym>ES</Acronym><Agency>NIEHS NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2013</Year><Month>04</Month><Day>16</Day></ArticleDate></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>Environ Int</MedlineTA><NlmUniqueID>7807270</NlmUniqueID><ISSNLinking>0160-4120</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D010755">Organophosphates</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D010575">Pesticides</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.1.8.1</RegistryNumber><NameOfSubstance 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