Manganese is a trace element essential for human health and development. The Agency for Toxic Substances and Disease Registry recommends blood manganese concentrations (BMnCs) between 4-15 μg/L. Elevated and low levels of manganese in blood can adversely affect the nervous system, potentially leading to neurobehavioral impairment. Autism Spectrum Disorders (ASDs) are complicated neurodevelopmental and behavioral disorders that manifest in early childhood and continue into later life. Limited but conflicting data have been reported regarding the potential role of manganese in the development of ASD which suggests the need for additional studies.
To investigate the association between BMnCs and ASD in Jamaican children, and to assess the role of vegetables and seafood consumption in BMnCs among these children.
The Jamaican Autism study is a NIH-supported age- and sex-matched case-control study that started recruitment in December 2009 to investigate whether environmental exposures to mercury, lead, arsenic, manganese, and cadmium have a role in the onset of autism. We administered the Autism Diagnostic Observation Schedule and the Autism Diagnostic Interview-Revised to children, 2-8 years of age, from the Jamaican Autism Database at the University of the West Indies. For each case, we identified an age- and sex- matched typically developing child as a control; using the Social Communication Questionnaire to insure that controls did not have significant ASD symptomatology. We also administered a pre-tested questionnaire to assess demographic and socioeconomic information, parental education levels, medical history of children, and potential exposure to manganese through food, with a particular focus on the types and amount of vegetables and seafood consumed by children. Finally, we collected 2 mL of whole blood from each child, which was analyzed for manganese levels. Using a General Linear Model, we assessed the association of BMnCs with ASD status and sources of exposure to manganese based on data from the available 65 matched pairs.
In our samples, 86.2% of children were male with a mean age of about 65 months. The cases and controls were 96.9% and 98.5% Afro-Caribbean, respectively. The mean BMnC for children who ate fried plantains was significantly higher than those who did not, (11.3 vs. 8.6μg/L; P=0.05). In contrast, the mean BMnC for children who ate shellfish was significantly lower than that of children who did not report consuming shellfish, (6.2 vs. 11.0μg/L; P=0.04). In univariable analysis, we did not find a significant association between BMnCs and ASD, (10.8μg/L for both cases and controls; P = 0.95). After controlling for consumption of tuna, shellfish, fried plantains, ackee, and whole wheat bread, there was no significant association between BMnCs and ASD status, (11.0 for cases vs. 10.6μg/L for controls; P=0.61). Overall, 4.6% of children in our sample had elevated BMnCs (i.e., >15μg/L) of whom 83% ate fried plantains. However, none of the children in our samples exhibited manganese deficiency (<4μg/L).
Our findings do not support an association between BMnCs and ASD in Jamaican children. However, children who ate fried plantains appear to be at a higher risk of having an elevated BMnC.
See more of: Epidemiology
See more of: Prevalence, Risk factors & Intervention