Abstract
BackgroundMethylmercury (MeHg), known for well over a century as a neurotoxin in adults, has more recently been studied for potential detrimental effects during early brain development. While several studies have estimated mercury exposure, they usually rely on either a single biomarker or questionnaire data, each of which has limitations. The goal of this paper was to develop a toxicokinetic model that incorporates both biomarker and questionnaire data to estimate the cumulative exposure to MeHg through seafood consumption using data collected from the Childhood Autism Risks from Genetics and the Environment (CHARGE) study.MethodsWe utilized a previously described discrete-time model that estimates blood MeHg concentration given a piecewise-constant ingestion rate and single-compartment pharmacokinetics. We measured newborn bloodspot Hg concentrations and obtained information pertaining to maternal fish consumption using a questionnaire. Using MeHg concentration estimates from the toxicokinetic model, cumulative MeHg exposure was estimated in children with autism, children with developmental delay, and typically developing children. Median estimated cumulative MeHg was compared among diagnostic groups using the Kruskal-Wallis Test. Multinomial logistic regression models were constructed to assess the association between cumulative MeHg concentration and the risk of autism and developmental delay (vs. typical development).ResultsThe estimated average MeHg concentration of for all fish species consumed by mothers was 42 ppb. Median cumulative MeHg over gestation was similar across diagnostic groups (p-values raged from 0.91 to 0.98). After adjusting for potential confounding, we found no association between cumulative MeHg exposure and the risk of autism (OR = 0.95, 95 % CI: 0.95, 1.12) or developmental delay (OR = 1.00, 95 % CI: 0.89, 1.13).ConclusionsThe toxicokinetic model described in this paper yielded fish MeHg concentration estimates that are consistent with fish species containing lower levels of MeHg. Overall, cumulative MeHg exposure does not appear to detectably elevate the risk of autism or developmental delay. Based on the regression standard error for the association between ASD and TD, we would have reported statistical significance for an adjusted odds ratio of 1.09 or larger. This method can easily be extended to other epidemiologic studies in which there is a biomarker measurement and questionnaire data regarding exposure.
Highlights
Methylmercury (MeHg), known for well over a century as a neurotoxin in adults, has more recently been studied for potential detrimental effects during early brain development
Sampling frame and recruitment Children diagnosed with autism or developmental delay were identified through the California Department of Developmental Services (DDS), which, through its system of Regional Centers (RCs), coordinates services and support to individuals with developmental disabilities
The autism spectrum disorder (ASD) group had a higher proportion of males than the Developmentally delayed (DD)/atypically developing (AtD) and typically developing (TD) groups
Summary
Methylmercury (MeHg), known for well over a century as a neurotoxin in adults, has more recently been studied for potential detrimental effects during early brain development. While several studies have measured biomarker mercury concentrations to estimate exposure, they are often limited by the number and timing of measurements (typically one sample per participant) This is especially true when measuring exposure over longer durations of time (on the order of months or years, e.g. the entire duration of a pregnancy), without relying on an unrealistic but common assumption that blood mercury concentrations are at steady-state. To estimate the ingested dose, this method often relies on published food toxicant concentration values external to the study [7] This approach becomes less reliable when concentrations vary widely within or across sources of exposure, as is the case with MeHg in populations with access to a range of seafood options. Evidence suggests that long-term MeHg exposures based solely on food frequency questionnaires are overestimated, possibly resulting from the over report of fish consumption and the utilization of literature-based (versus directly measured) MeHg concentrations for food items [8,9,10]
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