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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

The effect of varying the elimination rate of MeHg from the blood and the assumed relationship between newborn blood MeHg and maternal blood MeHg concentration
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Fig1: The effect of varying the elimination rate of MeHg from the blood and the assumed relationship between newborn blood MeHg and maternal blood MeHg concentration

Mentions: The estimated MeHg concentration for tuna, other ocean fish, and fresh fish were 5 (95 % CI: −65,75), 50 (95 % CI: 8,91) and 39 (95 % CI: −29, 106) ppb, respectively. The estimated MeHg concentrations for the combined fish types were similar between the two methods of determining blood volume from maternal weight. If we assumed that maternal newborn blood mercury concentrations were 1.5 times that of the corresponding mothers, the estimated fish concentration was 42 ppb (95 % C.I. 12, 72) when blood volume was based on absolute maternal weight, and 47 ppb (95 % C.I. 15, 78) when blood volume was based on maternal weight gain. Changing the elimination rate by 2 standard deviations leads to about a 10 ppb change in the fish MeHg concentration estimate. The estimated fish MeHg concentration is directly proportional to the ratio between maternal and newborn MeHg concentrations (Fig. 1).Fig. 1


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)

The effect of varying the elimination rate of MeHg from the blood and the assumed relationship between newborn blood MeHg and maternal blood MeHg concentration
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Fig1: The effect of varying the elimination rate of MeHg from the blood and the assumed relationship between newborn blood MeHg and maternal blood MeHg concentration
Mentions: The estimated MeHg concentration for tuna, other ocean fish, and fresh fish were 5 (95 % CI: −65,75), 50 (95 % CI: 8,91) and 39 (95 % CI: −29, 106) ppb, respectively. The estimated MeHg concentrations for the combined fish types were similar between the two methods of determining blood volume from maternal weight. If we assumed that maternal newborn blood mercury concentrations were 1.5 times that of the corresponding mothers, the estimated fish concentration was 42 ppb (95 % C.I. 12, 72) when blood volume was based on absolute maternal weight, and 47 ppb (95 % C.I. 15, 78) when blood volume was based on maternal weight gain. Changing the elimination rate by 2 standard deviations leads to about a 10 ppb change in the fish MeHg concentration estimate. The estimated fish MeHg concentration is directly proportional to the ratio between maternal and newborn MeHg concentrations (Fig. 1).Fig. 1

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