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Prenatal mercury exposure, autism, and developmental delay, using pharmacokinetic combination of newborn blood concentrations and questionnaire data: a case control study.

McKean SJ, Bartell SM, Hansen RL, Barfod GH, Green PG, Hertz-Picciotto I - Environ Health (2015)

Bottom Line: 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.Median estimated cumulative MeHg was compared among diagnostic groups using the Kruskal-Wallis Test.This method can easily be extended to other epidemiologic studies in which there is a biomarker measurement and questionnaire data regarding exposure.

View Article: PubMed Central - PubMed

Affiliation: University of California, Davis, Davis, CA, USA. sjmckean@ucdavis.edu.

ABSTRACT

Background: 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 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.

Methods: We 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).

Results: The 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).

Conclusions: The 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.

No MeSH data available.


Related in: MedlinePlus

Distribution of cumulative prenatal MeHg exposure in each diagnostic group. All groups have similar distributions, with insignificantly different median concentrations (p = 0.92)
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Fig2: Distribution of cumulative prenatal MeHg exposure in each diagnostic group. All groups have similar distributions, with insignificantly different median concentrations (p = 0.92)

Mentions: Due to incomplete diagnoses, 36 of the 274 mother-child pairs with complete fish consumption data were excluded from analyses comparing cumulative MeHg exposure among diagnostic groups. The cumulative MeHg distributions over the entire gestational period and over the 2nd and 3rd trimesters, computed using the combined fish types MeHg concentration estimate of 42 ppb, were similar among the three diagnostic groups (Table 4, Fig. 2). The method of assigning blood volume from maternal weight gain resulted in higher cumulative MeHg concentrations versus the method based on absolute weight. Using the Kruskal-Wallis Test, we found that the median cumulative MeHg concentrations were not significantly different among the three diagnostic groups for all measurements of MeHg AUC (p-value raged form 0.91 to 0.98, depending on the comparison). The multinomial logistic regression models yielded ORs for log cumulative MeHg exposure over the gestational period for ASD vs. TD and DD/AtD vs. TD (Table 5). Models investigating cumulative exposure over the 2nd and 3rd trimesters yielded almost identical results (not shown).Table 4


Prenatal mercury exposure, autism, and developmental delay, using pharmacokinetic combination of newborn blood concentrations and questionnaire data: a case control study.

McKean SJ, Bartell SM, Hansen RL, Barfod GH, Green PG, Hertz-Picciotto I - Environ Health (2015)

Distribution of cumulative prenatal MeHg exposure in each diagnostic group. All groups have similar distributions, with insignificantly different median concentrations (p = 0.92)
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4508765&req=5

Fig2: Distribution of cumulative prenatal MeHg exposure in each diagnostic group. All groups have similar distributions, with insignificantly different median concentrations (p = 0.92)
Mentions: Due to incomplete diagnoses, 36 of the 274 mother-child pairs with complete fish consumption data were excluded from analyses comparing cumulative MeHg exposure among diagnostic groups. The cumulative MeHg distributions over the entire gestational period and over the 2nd and 3rd trimesters, computed using the combined fish types MeHg concentration estimate of 42 ppb, were similar among the three diagnostic groups (Table 4, Fig. 2). The method of assigning blood volume from maternal weight gain resulted in higher cumulative MeHg concentrations versus the method based on absolute weight. Using the Kruskal-Wallis Test, we found that the median cumulative MeHg concentrations were not significantly different among the three diagnostic groups for all measurements of MeHg AUC (p-value raged form 0.91 to 0.98, depending on the comparison). The multinomial logistic regression models yielded ORs for log cumulative MeHg exposure over the gestational period for ASD vs. TD and DD/AtD vs. TD (Table 5). Models investigating cumulative exposure over the 2nd and 3rd trimesters yielded almost identical results (not shown).Table 4

Bottom Line: 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.Median estimated cumulative MeHg was compared among diagnostic groups using the Kruskal-Wallis Test.This method can easily be extended to other epidemiologic studies in which there is a biomarker measurement and questionnaire data regarding exposure.

View Article: PubMed Central - PubMed

Affiliation: University of California, Davis, Davis, CA, USA. sjmckean@ucdavis.edu.

ABSTRACT

Background: 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 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.

Methods: We 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).

Results: The 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).

Conclusions: The 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.

No MeSH data available.


Related in: MedlinePlus