In the original article, there was a mistake in the footnotes for Table 3 and 4 as published. Previously, all units were reported as (mcg/mL). However, serum selenium values should be reported in (ng/mL), and hair/nail samples should be reported in (mcg/g). The corrected footnotes appear below.
“Table 3. Median Cu, Zn, and Se levels for cases and controls, stratified by sex. Serum zinc and copper levels are presented in units mcg/mL. Serum selenium levels are presented in units ng/mL. Bolded p-value denotes significance.”
“Table 4. Median Se levels between cases and controls, stratified by sex. Hair and nail levels are presented in units mcg/g. Bolded p-value denotes significance. 66 participants provided hair samples (26 ASD, 40 controls), and 62 provided nail samples (23 ASD, 39 controls). Only one ASD female provided hair/nail samples in this study, therefore female-specific comparisons were not conducted.”
Additionally, in the original article, there was an error in the units of measurement that we reported in our results. Previously, all units were reported as (mcg/mL). However, serum selenium values should be reported in (ng/mL), and hair/nail samples should be reported in (mcg/g).
A correction has been made to the Abstract. The corrected paragraph is shown below.
“Metal ion dyshomeostasis and disparate levels of biometals like zinc (Zn), copper (Cu), and selenium (Se) have been implicated as a potential causative factor for Autism Spectrum Disorder (ASD). In this study, we have enrolled 129 children (aged 2–4 years) in North America, of which 64 children had a diagnosis of ASD and 65 were controls. Hair, nail, and blood samples were collected and quantitatively analyzed for Zn, Cu and Se using inductively coupled plasma mass spectrometry (ICP-MS). Of the analyzed biometals, serum Se (116.83 ± 14.84 ng/mL) was found to be significantly lower in male ASD cases compared to male healthy controls (128.21 ± 9.11 ng/mL; p < 0.005). A similar trend was found for nail Se levels in ASD (1.01 ± 0.15 mcg/g) versus that of controls (1.11 ± 0.17 mcg/g) with a p-value of 0.0132 using a stratified Wilcoxon rank sum testing. The level of Se in ASD cohort was co-analyzed for psychometric correlation and found a negative correlation between total ADOS score and serum Se levels. However, we did not observe any significant difference in Zn, Cu, and Zn/Cu ratio in ASD cases versus controls in this cohort of North American children. Further studies are recommended to better understand the biology of the relationship between Se and ASD status.”
A correction has also been made to Results, Serum Analysis of Zn, Cu, and Se, Paragraphs 1 & 2. The corrected paragraphs are shown below.
“Of the 129 children enrolled, 74 provided a blood sample (52 children with ASD and 22 controls). Overall and sex-stratified comparisons were made between cases and controls (Table 3). Of these comparisons, median serum Se levels were lower in cases than controls, with significant difference among males (p = 0.004). A Receiver Operating Characteristic (ROC) curve analysis Under Curve (AUC) of 0.760 (95% CI = [0.619–0.902]; Figure 1). Among controls, there was a significant difference in serum Se levels by sex (Table 3; 109.41 ng/mL in females vs. 128.21 ng/mL in males; p < 0.001).
There were no significant differences in median serum Zn or Cu levels. The Zn/Cu ratio was similarly evaluated with no significant differences between cases and controls.”
The authors apologize for this error and state that this does not change the scientific conclusions of the article in any way. The original article has been updated.
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Summary
Keywords
autism spectrum disorder, Zn, Cu, Se, biometals
Citation
Mehta SQ, Behl S, Day PL, Delgado AM, Larson NB, Stromback LR, Huebner AR, DeGrado TR, Davis JM, Jannetto PJ, Howie F and Pandey MK (2022) Corrigendum: Evaluation of Zn, Cu, and Se Levels in the North American Autism Spectrum Disorder Population. Front. Mol. Neurosci. 15:831799. doi: 10.3389/fnmol.2022.831799
Received
08 December 2021
Accepted
10 January 2022
Published
14 February 2022
Volume
15 - 2022
Edited and reviewed by
Paul Anthony Adlard, University of Melbourne, Australia
Updates
Copyright
© 2022 Mehta, Behl, Day, Delgado, Larson, Stromback, Huebner, DeGrado, Davis, Jannetto, Howie and Pandey.
This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
*Correspondence: Sunil Q. Mehta Mehta.Sunil@mayo.eduMukesh K. Pandey Pandey.Mukesh@mayo.edu
†These authors have contributed equally to this work
This article was submitted to Brain Disease Mechanisms, a section of the journal Frontiers in Molecular Neuroscience
Disclaimer
All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.