Interaction between arsenic exposure from drinking water and genetic polymorphisms on cardiovascular disease in Bangladesh

A prospective case-cohort study

Fen Wu, Farzana Jasmine, Muhammad G. Kibriya, Mengling Liu, Xin Cheng, Faruque Parvez, Tariqul Islam, Alauddin Ahmed, Muhammad Rakibuz-Zaman, Jieying Jiang, Shantanu Roy, Rachelle Paul ‑ Brutus, Vesna Slavkovich, Tariqul Islam, Diane Levy, Tyler J. Vanderweele, Brandon L. Pierce, Joseph H. Graziano, Habibul Ahsan, Yu Chen

Research output: Contribution to journalArticle

Abstract

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.

Original languageEnglish (US)
Pages (from-to)451-457
Number of pages7
JournalEnvironmental Health Perspectives
Volume123
Issue number5
DOIs
StatePublished - 2015

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Bangladesh
Arsenic
Genetic Polymorphisms
Drinking Water
Cohort Studies
Cardiovascular Diseases
Genotype
Water
Single Nucleotide Polymorphism
Genetic Predisposition to Disease
Coronary Disease
Longitudinal Studies
Oxidative Stress
Joints
Stroke
Inflammation

ASJC Scopus subject areas

  • Public Health, Environmental and Occupational Health
  • Health, Toxicology and Mutagenesis

Cite this

Interaction between arsenic exposure from drinking water and genetic polymorphisms on cardiovascular disease in Bangladesh : A prospective case-cohort study. / 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; Islam, Tariqul; Levy, Diane; Vanderweele, Tyler J.; Pierce, Brandon L.; Graziano, Joseph H.; Ahsan, Habibul; Chen, Yu.

In: Environmental Health Perspectives, Vol. 123, No. 5, 2015, p. 451-457.

Research output: Contribution to journalArticle

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', Environmental Health Perspectives, vol. 123, no. 5, pp. 451-457. https://doi.org/10.1289/ehp.1307883
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 ; Islam, Tariqul ; Levy, Diane ; Vanderweele, Tyler J. ; Pierce, Brandon L. ; Graziano, Joseph H. ; Ahsan, Habibul ; Chen, Yu. / Interaction between arsenic exposure from drinking water and genetic polymorphisms on cardiovascular disease in Bangladesh : A prospective case-cohort study. In: Environmental Health Perspectives. 2015 ; Vol. 123, No. 5. pp. 451-457.
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abstract = "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.",
author = "Fen Wu and Farzana Jasmine and Kibriya, {Muhammad G.} and Mengling Liu and Xin Cheng and Faruque Parvez and Tariqul Islam and Alauddin Ahmed and Muhammad Rakibuz-Zaman and Jieying Jiang and Shantanu Roy and {Paul ‑ Brutus}, Rachelle and Vesna Slavkovich and Tariqul Islam and Diane Levy and Vanderweele, {Tyler J.} and Pierce, {Brandon L.} and Graziano, {Joseph H.} and Habibul Ahsan and Yu Chen",
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T1 - Interaction between arsenic exposure from drinking water and genetic polymorphisms on cardiovascular disease in Bangladesh

T2 - A prospective case-cohort study

AU - Wu, Fen

AU - Jasmine, Farzana

AU - Kibriya, Muhammad G.

AU - Liu, Mengling

AU - Cheng, Xin

AU - Parvez, Faruque

AU - Islam, Tariqul

AU - Ahmed, Alauddin

AU - Rakibuz-Zaman, Muhammad

AU - Jiang, Jieying

AU - Roy, Shantanu

AU - Paul ‑ Brutus, Rachelle

AU - Slavkovich, Vesna

AU - Islam, Tariqul

AU - Levy, Diane

AU - Vanderweele, Tyler J.

AU - Pierce, Brandon L.

AU - Graziano, Joseph H.

AU - Ahsan, Habibul

AU - Chen, Yu

PY - 2015

Y1 - 2015

N2 - 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.

AB - 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.

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DO - 10.1289/ehp.1307883

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