Seafood intake and urine concentrations of total arsenic, dimethylarsinate and arsenobetaine in the US population

Abstract

Background: Seafood is the main source of organic arsenic exposure (arsenobetaine, arsenosugars and arsenolipids) in the population. Arsenosugars and arsenolipids are metabolized to several species including dimethylarsinate (DMA).

Objective: Evaluate the association of seafood intake with spot urine arsenic concentrations in the 2003-2006 National Health Nutrition and Examination Survey (NHANES).

Methods: We studied 4276 participants ≥ 6 years. Total arsenic was measured using inductively coupled plasma dynamic reaction cell mass spectrometry (ICPMS). Urine DMA and arsenobetaine were measured by high-performance liquid chromatography coupled with ICPMS.

Results: Participants reporting seafood in the past 24-h had higher urine concentrations of total arsenic (median 24.5 vs. 7.3 μg/L), DMA (6.0 vs. 3.5 μg/L), arsenobetaine (10.2 vs. 0.9 μg/L) and total arsenic minus arsenobetaine (11.0 vs. 5.5 μg/L). Participants reporting seafood ≥ 2/wk vs. never during the past year had 2.3 (95% confidence interval 1.9, 2.7), 1.4 (1.2, 1.6), 6.0 (4.6, 7.8) and 1.7 (1.4, 2.0) times higher (p-trend <0.001) concentrations of total arsenic, DMA, arsenobetaine and total arsenic minus arsenobetaine, respectively. In participants without detectable arsenobetaine and in analyses adjusted for arsenobetaine, seafood consumption in the past year was not associated with total arsenic or DMA concentrations in urine.

Conclusion: Seafood intake was a major determinant of increased urine concentrations of total arsenic, DMA, arsenobetaine and total arsenic minus arsenobetaine in the US population. Epidemiologic studies that use total arsenic, DMA, the sum of inorganic arsenic, methylarsonate and DMA, and total arsenic minus arsenobetaine as markers of inorganic arsenic exposure and/or metabolism need to address seafood intake.

Figure 1

Contribution of major forms of arsenic in seafood (arsenobetaine, arsenosugars and arsenolipids) to total urine arsenic following recent seafood intake. Given inter-individual differences in arsenobetaine, arsenosugars and arsenolipids excretion patterns, the time frame to define “recent seafood intake” can be different across people. Arrows represent direct contributions. For instance, the frequency of seafood intake in the past year is related to the likelihood of recent seafood intake. Bolded elements correspond to variables that are available in NHANES 2002–2006.

Figure 2

Relationship of urine arsenobetaine and blood mercury with total arsenic, dimethylarsinate (DMA) and total arsenic minus arsenobetaine in NHANES 2003–2006. Lines represent dose-response relationships based on restricted quadratic spline models that adjusted for urine creatinine concentrations. Correlation coefficients represent spearman correlation coefficients (all are highly statistically significant, p<0.001).

Figure 3

Urine arsenic concentrations by self-reported seafood intake in the past 24-h. Horizontal lines within boxes represent medians; boxes, interquartile range; error bars, values within 1.5 times the interquartile range; circles, outlying data points.