Interaction between Arsenic Exposure from Drinking Water and Genetic Polymorphisms on Cardiovascular Disease in Bangladesh: A Prospective Case-Cohort Study

Epidemiologic data on genetic susceptibility to cardiovascular effects of arsenic exposure from drinking water are limited. We investigated whether the association between well-water arsenic and cardiovascular disease (CVD) differed by 170 single nucleotide polymorphisms (SNPs) in 17 genes related t...

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Published inEnvironmental health perspectives Vol. 123; no. 5; pp. 451 - 457
Main Authors Wu, Fen, Jasmine, Farzana, Kibriya, Muhammad G., Liu, Mengling, Cheng, Xin, Parvez, Faruque, Islam, Tariqul, Ahmed, Alauddin, Rakibuz-Zaman, Muhammad, Jiang, Jieying, Roy, Shantanu, Paul-Brutus, Rachelle, Slavkovich, Vesna, Levy, Diane, VanderWeele, Tyler J., Pierce, Brandon L., Graziano, Joseph H., Ahsan, Habibul, Chen, Yu
Format Journal Article
LanguageEnglish
Published United States National Institute of Environmental Health Sciences 01.05.2015
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Subjects
Adjustment
Adult
Arsenic
Arsenic - toxicity
Autopsies
Bangladesh - epidemiology
Cardiovascular disease
Cardiovascular diseases
Cardiovascular Diseases - epidemiology
Cardiovascular Diseases - genetics
Chemical vapor deposition
Cohort analysis
Contamination
Diagnostic tests
Drinking water
Drinking Water - adverse effects
Environmental aspects
Environmental Exposure
Enzymes
Exposure
Female
Genetic polymorphisms
Genetic variance
Genetics
Genotype
Health
Health aspects
Health risk assessment
Homocysteine
Humans
Inflammation
Intercellular Adhesion Molecule-1 - genetics
Lipids
Longitudinal studies
Male
Medical research
Metabolism
Metabolites
Middle Aged
Oxidative stress
Polymorphism
Polymorphism, Genetic - genetics
Polymorphism, Single Nucleotide - genetics
Population
Prospective Studies
Risk factors
Stroke
Stroke - genetics
Studies
Tumor necrosis factor-TNF
Urine
Vascular Cell Adhesion Molecule-1 - genetics
Bangladesh
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Abstract Epidemiologic data on genetic susceptibility to cardiovascular effects of arsenic exposure from drinking water are limited. We investigated whether the association between well-water arsenic and cardiovascular disease (CVD) differed by 170 single nucleotide polymorphisms (SNPs) in 17 genes related to arsenic metabolism, oxidative stress, inflammation, and endothelial dysfunction. We conducted a prospective case-cohort study nested in the Health Effects of Arsenic Longitudinal Study, with a random subcohort of 1,375 subjects and 447 incident fatal and nonfatal cases of CVD. Well-water arsenic was measured in 2000 at baseline. The CVD cases, 56 of which occurred in the subcohort, included 238 coronary heart disease cases, 165 stroke cases, and 44 deaths due to other CVD identified during follow-up from 2000 to 2012. Of the 170 SNPs tested, multiplicative interactions between well-water arsenic and two SNPs, rs281432 in ICAM1 (padj = 0.0002) and rs3176867 in VCAM1 (padj = 0.035), were significant for CVD after adjustment for multiple testing. Compared with those with GC or CC genotype in rs281432 and lower well-water arsenic, the adjusted hazard ratio (aHR) for CVD was 1.82 (95% CI: 1.31, 2.54) for a 1-SD increase in well-water arsenic combined with the GG genotype, which was greater than expected given aHRs of 1.08 and 0.96 for separate effects of arsenic and the genotype alone, respectively. Similarly, the joint aHR for arsenic and the rs3176867 CC genotype was 1.34 (95% CI: 0.95, 1.87), greater than expected given aHRs for their separate effects of 1.02 and 0.84, respectively. Associations between CVD and arsenic exposure may be modified by genetic variants related to endothelial dysfunction.
AbstractList Background: Epidemiologic data on genetic susceptibility to cardiovascular effects of arsenic exposure from drinking water are limited. Objective: We investigated whether the association between well-water arsenic and cardiovascular disease (CVD) differed by 170 single nucleotide polymorphisms (SNPs) in 17 genes related to arsenic metabolism, oxidative stress, inflammation, and endothelial dysfunction. Method: We conducted a prospective case-cohort study nested in the Health Effects of Arsenic Longitudinal Study, with a random subcohort of 1,375 subjects and 447 incident fatal and nonfatal cases of CVD. Well-water arsenic was measured in 2000 at baseline. The CVD cases, 56 of which occurred in the subcohort, included 238 coronary heart disease cases, 165 stroke cases, and 44 deaths due to other CVD identified during follow-up from 2000 to 2012. Results: Of the 170 SNPs tested, multiplicative interactions between well-water arsenic and two SNPs, rs281432 in ICAM1 ( p adj = 0.0002) and rs3176867 in VCAM1 ( p adj = 0.035), were significant for CVD after adjustment for multiple testing. Compared with those with GC or CC genotype in rs281432 and lower well-water arsenic, the adjusted hazard ratio (aHR) for CVD was 1.82 (95% CI: 1.31, 2.54) for a 1-SD increase in well-water arsenic combined with the GG genotype, which was greater than expected given aHRs of 1.08 and 0.96 for separate effects of arsenic and the genotype alone, respectively. Similarly, the joint aHR for arsenic and the rs3176867 CC genotype was 1.34 (95% CI: 0.95, 1.87), greater than expected given aHRs for their separate effects of 1.02 and 0.84, respectively. Conclusions: Associations between CVD and arsenic exposure may be modified by genetic variants related to endothelial dysfunction. Citation: Wu F, Jasmine F, Kibriya MG, Liu M, Cheng X, Parvez F, Islam T, Ahmed A, Rakibuz-Zaman M, Jiang J, Roy S, Paul-Brutus R, Slavkovich V, Islam T, Levy D, VanderWeele TJ, Pierce BL, Graziano JH, Ahsan H, Chen Y. 2015. Interaction between arsenic exposure from drinking water and genetic polymorphisms on cardiovascular disease in Bangladesh: a prospective case-cohort study. Environ Health Perspect 123:451–457;  http://dx.doi.org/10.1289/ehp.1307883
Epidemiologic data on genetic susceptibility to cardiovascular effects of arsenic exposure from drinking water are limited. We investigated whether the association between well-water arsenic and cardiovascular disease (CVD) differed by 170 single nucleotide polymorphisms (SNPs) in 17 genes related to arsenic metabolism, oxidative stress, inflammation, and endothelial dysfunction. We conducted a prospective case-cohort study nested in the Health Effects of Arsenic Longitudinal Study, with a random subcohort of 1,375 subjects and 447 incident fatal and nonfatal cases of CVD. Well-water arsenic was measured in 2000 at baseline. The CVD cases, 56 of which occurred in the subcohort, included 238 coronary heart disease cases, 165 stroke cases, and 44 deaths due to other CVD identified during follow-up from 2000 to 2012. Of the 170 SNPs tested, multiplicative interactions between well-water arsenic and two SNPs, rs281432 in ICAM1 (padj = 0.0002) and rs3176867 in VCAM1 (padj = 0.035), were significant for CVD after adjustment for multiple testing. Compared with those with GC or CC genotype in rs281432 and lower well-water arsenic, the adjusted hazard ratio (aHR) for CVD was 1.82 (95% CI: 1.31, 2.54) for a 1-SD increase in well-water arsenic combined with the GG genotype, which was greater than expected given aHRs of 1.08 and 0.96 for separate effects of arsenic and the genotype alone, respectively. Similarly, the joint aHR for arsenic and the rs3176867 CC genotype was 1.34 (95% CI: 0.95, 1.87), greater than expected given aHRs for their separate effects of 1.02 and 0.84, respectively. Associations between CVD and arsenic exposure may be modified by genetic variants related to endothelial dysfunction.
Background: Epidemiologic data on genetic susceptibility to cardiovascular effects of arsenic exposure from drinking water are limited. Objective: We investigated whether the association between well-water arsenic and cardiovascular disease (CVD) differed by 170 single nucleotide polymorphisms (SNPs) in 17 genes related to arsenic metabolism, oxidative stress, inflammation, and endothelial dysfunction. Method: We conducted a prospective case-cohort study nested in the Health Effects of Arsenic Longitudinal Study, with a random subcohort of 1,375 subjects and 447 incident fatal and nonfatal cases of CVD. Well-water arsenic was measured in 2000 at baseline. The CVD cases, 56 of which occurred in the subcohort, included 238 coronary heart disease cases, 165 stroke cases, and 44 deaths due to other CVD identified during follow-up from 2000 to 2012. Results: Of the 170 SNPs tested, multiplicative interactions between well-water arsenic and two SNPs, rs281432 in ICAM1 (padj = 0.0002) and rs3176867 in VCAM1 (padj = 0.035), were significant for CVD after adjustment for multiple testing. Compared with those with GC or CC genotype in rs281432 and lower well-water arsenic, the adjusted hazard ratio (aHR) for CVD was 1.82 (95% CI: 1.31, 2.54) for a 1-SD increase in well-water arsenic combined with the GG genotype, which was greater than expected given aHRs of 1.08 and 0.96 for separate effects of arsenic and the genotype alone, respectively. Similarly, the joint aHR for arsenic and the rs3176867 CC genotype was 1.34 (95% CI: 0.95, 1.87), greater than expected given aHRs for their separate effects of 1.02 and 0.84, respectively. Conclusions: Associations between CVD and arsenic exposure may be modified by genetic variants related to endothelial dysfunction.
BACKGROUND: Epidemiologic data on genetic susceptibility to cardiovascular effects of arsenic exposure from drinking water are limited. OBJECTIVE: We investigated whether the association between well-water arsenic and cardiovascular disease (CVD) differed by 170 single nucleotide polymorphisms (SNPs) in 17 genes related to arsenic metabolism, oxidative stress, inflammation, and endothelial dysfunction. METHOD: We conducted a prospective case-cohort study nested in the Health Effects of Arsenic Longitudinal Study, with a random subcohort of 1,375 subjects and 447 incident fatal and nonfatal cases of CVD. Well-water arsenic was measured in 2000 at baseline. The CVD cases, 56 of which occurred in the subcohort, included 238 coronary heart disease cases, 165 stroke cases, and 44 deaths due to other CVD identified during follow-up from 2000 to 2012. RESULTS: Of the 170 SNPs tested, multiplicative interactions between well-water arsenic and two SNPs, rs281432 in ICAM1 ([p.sub.adj] = 0.0002) and rs3176867 in VCAM1 ([p.sub.adj] = 0.035), were significant for CVD after adjustment for multiple testing. Compared with those with GC or CC genotype in rs281432 and lower well-water arsenic, the adjusted hazard ratio (aHR) for CVD was 1.82 (95% CI: 1.31, 2.54) for a 1-SD increase in well-water arsenic combined with the GG genotype, which was greater than expected given aHRs of 1.08 and 0.96 for separate effects of arsenic and the genotype alone, respectively. Similarly, the joint aHR for arsenic and the rs3176867 CC genotype was 1.34 (95% CI: 0.95, 1.87), greater than expected given aHRs for their separate effects of 1.02 and 0.84, respectively. CONCLUSIONS: Associations between CVD and arsenic exposure may be modified by genetic variants related to endothelial dysfunction. dx.doi.org/10.1289/ehp.1307883
Epidemiologic data on genetic susceptibility to cardiovascular effects of arsenic exposure from drinking water are limited.BACKGROUNDEpidemiologic data on genetic susceptibility to cardiovascular effects of arsenic exposure from drinking water are limited.We investigated whether the association between well-water arsenic and cardiovascular disease (CVD) differed by 170 single nucleotide polymorphisms (SNPs) in 17 genes related to arsenic metabolism, oxidative stress, inflammation, and endothelial dysfunction.OBJECTIVEWe investigated whether the association between well-water arsenic and cardiovascular disease (CVD) differed by 170 single nucleotide polymorphisms (SNPs) in 17 genes related to arsenic metabolism, oxidative stress, inflammation, and endothelial dysfunction.We conducted a prospective case-cohort study nested in the Health Effects of Arsenic Longitudinal Study, with a random subcohort of 1,375 subjects and 447 incident fatal and nonfatal cases of CVD. Well-water arsenic was measured in 2000 at baseline. The CVD cases, 56 of which occurred in the subcohort, included 238 coronary heart disease cases, 165 stroke cases, and 44 deaths due to other CVD identified during follow-up from 2000 to 2012.METHODWe conducted a prospective case-cohort study nested in the Health Effects of Arsenic Longitudinal Study, with a random subcohort of 1,375 subjects and 447 incident fatal and nonfatal cases of CVD. Well-water arsenic was measured in 2000 at baseline. The CVD cases, 56 of which occurred in the subcohort, included 238 coronary heart disease cases, 165 stroke cases, and 44 deaths due to other CVD identified during follow-up from 2000 to 2012.Of the 170 SNPs tested, multiplicative interactions between well-water arsenic and two SNPs, rs281432 in ICAM1 (padj = 0.0002) and rs3176867 in VCAM1 (padj = 0.035), were significant for CVD after adjustment for multiple testing. Compared with those with GC or CC genotype in rs281432 and lower well-water arsenic, the adjusted hazard ratio (aHR) for CVD was 1.82 (95% CI: 1.31, 2.54) for a 1-SD increase in well-water arsenic combined with the GG genotype, which was greater than expected given aHRs of 1.08 and 0.96 for separate effects of arsenic and the genotype alone, respectively. Similarly, the joint aHR for arsenic and the rs3176867 CC genotype was 1.34 (95% CI: 0.95, 1.87), greater than expected given aHRs for their separate effects of 1.02 and 0.84, respectively.RESULTSOf the 170 SNPs tested, multiplicative interactions between well-water arsenic and two SNPs, rs281432 in ICAM1 (padj = 0.0002) and rs3176867 in VCAM1 (padj = 0.035), were significant for CVD after adjustment for multiple testing. Compared with those with GC or CC genotype in rs281432 and lower well-water arsenic, the adjusted hazard ratio (aHR) for CVD was 1.82 (95% CI: 1.31, 2.54) for a 1-SD increase in well-water arsenic combined with the GG genotype, which was greater than expected given aHRs of 1.08 and 0.96 for separate effects of arsenic and the genotype alone, respectively. Similarly, the joint aHR for arsenic and the rs3176867 CC genotype was 1.34 (95% CI: 0.95, 1.87), greater than expected given aHRs for their separate effects of 1.02 and 0.84, respectively.Associations between CVD and arsenic exposure may be modified by genetic variants related to endothelial dysfunction.CONCLUSIONSAssociations between CVD and arsenic exposure may be modified by genetic variants related to endothelial dysfunction.
Audience Academic
Author Slavkovich, Vesna
Jiang, Jieying
VanderWeele, Tyler J.
Islam, Tariqul
Liu, Mengling
Chen, Yu
Pierce, Brandon L.
Rakibuz-Zaman, Muhammad
Parvez, Faruque
Kibriya, Muhammad G.
Levy, Diane
Jasmine, Farzana
Cheng, Xin
Ahsan, Habibul
Ahmed, Alauddin
Paul-Brutus, Rachelle
Wu, Fen
Graziano, Joseph H.
Roy, Shantanu
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  surname: Chen
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  organization: Department of Population Health, New York University School of Medicine, New York, New York, USA
BackLink https://www.ncbi.nlm.nih.gov/pubmed/25575156$$D View this record in MEDLINE/PubMed
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ContentType Journal Article
Copyright COPYRIGHT 2015 National Institute of Environmental Health Sciences
Copyright National Institute of Environmental Health Sciences May 2015
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DOI 10.1289/ehp.1307883
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Snippet Epidemiologic data on genetic susceptibility to cardiovascular effects of arsenic exposure from drinking water are limited. We investigated whether the...
BACKGROUND: Epidemiologic data on genetic susceptibility to cardiovascular effects of arsenic exposure from drinking water are limited. OBJECTIVE: We...
Background: Epidemiologic data on genetic susceptibility to cardiovascular effects of arsenic exposure from drinking water are limited. Objective: We...
Epidemiologic data on genetic susceptibility to cardiovascular effects of arsenic exposure from drinking water are limited.BACKGROUNDEpidemiologic data on...
Background: Epidemiologic data on genetic susceptibility to cardiovascular effects of arsenic exposure from drinking water are limited. Objective: We...
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SourceType Open Access Repository
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StartPage 451
SubjectTerms Adjustment
Adult
Arsenic
Arsenic - toxicity
Autopsies
Bangladesh - epidemiology
Cardiovascular disease
Cardiovascular diseases
Cardiovascular Diseases - epidemiology
Cardiovascular Diseases - genetics
Chemical vapor deposition
Cohort analysis
Contamination
Diagnostic tests
Drinking water
Drinking Water - adverse effects
Environmental aspects
Environmental Exposure
Enzymes
Exposure
Female
Genetic polymorphisms
Genetic variance
Genetics
Genotype
Health
Health aspects
Health risk assessment
Homocysteine
Humans
Inflammation
Intercellular Adhesion Molecule-1 - genetics
Lipids
Longitudinal studies
Male
Medical research
Metabolism
Metabolites
Middle Aged
Oxidative stress
Polymorphism
Polymorphism, Genetic - genetics
Polymorphism, Single Nucleotide - genetics
Population
Prospective Studies
Risk factors
Stroke
Stroke - genetics
Studies
Tumor necrosis factor-TNF
Urine
Vascular Cell Adhesion Molecule-1 - genetics
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Title Interaction between Arsenic Exposure from Drinking Water and Genetic Polymorphisms on Cardiovascular Disease in Bangladesh: A Prospective Case-Cohort Study
URI https://www.ncbi.nlm.nih.gov/pubmed/25575156
https://www.proquest.com/docview/1686798015
https://www.proquest.com/docview/1677885988
https://www.proquest.com/docview/1680445334
https://www.proquest.com/docview/1686434406
https://pubmed.ncbi.nlm.nih.gov/PMC4421763
Volume 123
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