Background: Arsenic is an immunotoxicant. Clinical reports observe the reactivation of varicella zoster virus (VZV) in people who have recovered from arsenic poisoning and in patients with acute promyelocytic leukemia that have been treated with arsenic trioxide.

Objective: We evaluated the association between arsenic and the seroprevalence of VZV IgG antibody in a representative sample of the U.S. population.

Methods: We analyzed data from 3,348 participants of the National Health and Nutrition Examination Survey (NHANES) 2003–2004 and 2009–2010 pooled survey cycles. Participants were eligible if they were 6–49 years of age with information on both VZV IgG and urinary arsenic concentrations. We used two measures of total urinary arsenic (TUA): TUA1 was defined as the sum of arsenite, arsenate, monomethylarsonic acid, and dimethylarsinic acid, and TUA2 was defined as total urinary arsenic minus arsenobetaine and arsenocholine.

Results: The overall weighted seronegative prevalence of VZV was 2.2% for the pooled NHANES sample. The geometric means of TUA1 and TUA2 were 6.57 μg/L and 5.64 μg/L, respectively. After adjusting for age, sex, race, income, creatinine, and survey cycle, odds ratios for a negative VZV IgG result in association with 1-unit increases in natural log-transformed (ln)-TUA1 and ln-TUA2 were 1.87 (95% CI: 1.03, 3.44) and 1.40 (95% CI: 1.0, 1.97), respectively.

Conclusions: In this cross-sectional analysis, urinary arsenic was inversely associated with VZV IgG seroprevalence in the U.S. population. This finding is in accordance with clinical observations of zoster virus reactivation from high doses of arsenic. Additional studies are needed to confirm the association and evaluate causal mechanisms.

Citation: Cardenas A, Smit E, Houseman EA, Kerkvliet NI, Bethel JW, Kile ML. 2015. Arsenic exposure and prevalence of the varicella zoster virus in the United States: NHANES (2003–2004 and 2009–2010). Environ Health Perspect 123:590–596;  http://dx.doi.org/10.1289/ehp.1408731

Address correspondence to M.L. Kile, School of Biological and Population Health Sciences, College of Public Health and Human Sciences, Oregon State University, 15 Milam, Corvallis, OR 97330 USA. Telephone: (541) 737-1443. Email: molly.kile@oregonstate.edu

This work was supported by grants K01ES017800, P30ES000210, P42ES016465, and R01ES023441 from the National Institute of Environmental Health Sciences, National Institutes of Health.

The authors declare they have no actual or potential competing financial interests.

Received: 23 May 2014 Accepted: 28 January 2015 Advance Publication: 30 January 2015 Final Publication: 1 June 2015