Dufault RJ, Wolle MM, Kingston HMS, Gilbert SG, Murray JA. Connecting inorganic mercury and lead measurements in blood to dietary sources of exposure that may impact child development. World J Methodol 2021; 11(4): 144-159 [PMID: 34322366 DOI: 10.5662/wjm.v11.i4.144]
Corresponding Author of This Article
Renee J Dufault, PhD, Doctor, Food Ingredient and Health Research Institute, Ocean View, Naalehu, HI 96772, United States. rdufault@foodingredient.info
Research Domain of This Article
Public, Environmental & Occupational Health
Article-Type of This Article
Review
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Methodol. Jul 20, 2021; 11(4): 144-159 Published online Jul 20, 2021. doi: 10.5662/wjm.v11.i4.144
Connecting inorganic mercury and lead measurements in blood to dietary sources of exposure that may impact child development
Renee J Dufault, Mesay M Wolle, H M Skip Kingston, Steven G Gilbert, Joseph A Murray
Renee J Dufault, H M Skip Kingston, Steven G Gilbert, Food Ingredient and Health Research Institute, Naalehu, HI 96772, United States
Renee J Dufault, College of Graduate Health Studies, A.T. Still University, Kirksville, MO 63501, United States
Mesay M Wolle, H M Skip Kingston, Department of Chemistry and Biochemistry, Duquesne University, Pittsburgh, PA 15282, United States
Steven G Gilbert, Institute of Neurotoxicology and Neurological Disorders, Seattle, WA 98105, United States
Joseph A Murray, Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, MN 55905, United States
Author contributions: Dufault RJ wrote all but one section of the manuscript and created the figure, and supplementary material; Wolle MM wrote the analytical methods section and created the table; Kingston HMS, Gilbert SG, and Murray JA contributed to the format design and revision of the manuscript.
Conflict-of-interest statement: The authors declare no conflict of interests.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Renee J Dufault, PhD, Doctor, Food Ingredient and Health Research Institute, Ocean View, Naalehu, HI 96772, United States. rdufault@foodingredient.info
Received: January 28, 2021 Peer-review started: January 28, 2021 First decision: May 14, 2021 Revised: May 27, 2021 Accepted: June 16, 2021 Article in press: June 16, 2021 Published online: July 20, 2021 Processing time: 171 Days and 7.1 Hours
Abstract
Pre-natal and post-natal chemical exposures and co-exposures from a variety of sources including contaminated air, water, soil, and food are common and associated with poorer birth and child health outcomes. Poor diet is a contributing factor in the development of child behavioral disorders. Child behavior and learning can be adversely impacted when gene expression is altered by dietary transcription factors such as zinc insufficiency or deficiency or by exposure to toxic substances permitted in our food supply such as mercury, lead, or organophosphate pesticide residue. Children with autism spectrum disorder and attention deficit hyperactivity disorders exhibit decreased or impaired PON1 gene activity which is needed by the body to metabolize and excrete neurotoxic organophosphate pesticides. In this current review we present an updated macroepigenetic model that explains how dietary inorganic mercury and lead exposures from unhealthy diet may lead to elevated blood mercury and/or lead levels and the development of symptoms associated with the autism and attention deficit-hyperactivity disorders. PON1 gene activity may be suppressed by inadequate dietary calcium, selenium, and fatty acid intake or exposures to lead or mercury. The model may assist clinicians in diagnosing and treating the symptoms associated with these childhood neurodevelopmental disorders. Recommendations for future research are provided based on the updated model and review of recently published literature.
Core Tip: Connecting inorganic mercury and lead measurements in blood to dietary sources of exposure that may impact child development is a challenge. Autism spectrum disorder (ASD) and attention deficit hyperactivity disorder (ADHD) diagnoses and treatment efficacy may include the collection of the biomarker measurements of selenium, mercury, and lead levels in red blood cells and behavioral checklist data before and after healthy dietary interventions. We discuss the analytical measurement methods for determining mercury and lead levels in blood and how these biomarkers have been used in ASD and ADHD studies with and without dietary intervention.
