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Michael L. Dourson
Director of Science, TERA

Michael Dourson has a PhD in toxicology from the University of Cincinnati, College of Medicine, and is a board-certified toxicologist (i.e., DABT) serving as the Director of Science at the 501c3 nonprofit organization Toxicology Excellence for Risk Assessment (TERA). Prior to this, he was Senior Advisor in the Office of the Administrator at the US EPA. Before this, he was a Professor in the Risk Science Center at the University of Cincinnati, College of Medicine and also worked at TERA and US EPA. 

He has been awarded the Arnold J. Lehman award from the Society of Toxicology, the International Achievement Award by the International Society of Regulatory Toxicology and Pharmacology, and 4 bronze medals from the U.S. Environmental Protection Agency. He has been elected as a Fellow of the Academy of Toxicological Sciences (i.e., FATS) and as a Fellow for the Society for Risk Analysis (i.e., FSRA). 

He has co-published more than 150 papers on risk assessment methods or chemical-specific analyses (4 of them winning awards), and co-authored well over 100 government risk assessment documents (many of them risk assessment guidance texts). He has made over 150 invited presentations to a variety of organizations, and has chaired over 150 sessions at scientific meetings and independent peer reviews. He has been elected to multiple officer positions in the American Board of Toxicology (including its President), the Society of Toxicology (including the presidency of 3 specialty sections), the Society for Risk Analysis (including its Secretary), and is currently the President of the Toxicology Education Foundation, a nonprofit organization with a vision to help our public understand the essentials of toxicology. In addition to numerous appointments on government panels, such as EPA’s Science Advisory Board, he is a current member on the editorial board of Regulatory Toxicology and Pharmacology and Human and Experimental Toxicology. 

A Commentary on Some Epidemiology Data for Chlorpyrifos 

Extensive animal and human studies on chlorpyrifos (CPF) point to changes in a blood enzyme as its first biological effect, and governments and health groups around the world have used this effect in the determination of its safe dose.  Preventing this first biological effect, referred to in risk assessment parlance as the critical effect, is part and parcel of chemical regulation in general and of CFP specifically.  Rauh et al. (2011), one of the published studies from the Columbia Center for Children’s Environmental Health (CCCEH), reported evidence of deficits in Working Memory Index and Full-Scale IQ in children at 7 years old as a function of prenatal CPF exposures that are much lower than levels causing cholinesterase inhibition.  Since the raw data on which Rauh et. al. (2011) publicly-funded (in part) findings were based have not been made available despite repeated requests, we show extracted data in Figures 1A and 1E of Rauh et al. (2011), and plotted these extracted data as response versus log dose, a common risk assessment approach.  Surprisingly, a significant portion of the data stated to be available in Rauh et al. (2011) were not found in these published figures, perhaps due to data point overlay.  However, the reported associations of chlorpyrifos levels with Working Memory and Full Scale IQ were also not replicated in our analysis due perhaps to this missing data.  Multiple requests were made to Rauh et al. (2011) for access to data from this, in part, publicly funded study, so that confirmation could be attempted. This general lack of data and inconsistency with cholinergic responses in other researches raises concerns about the lack of data transparency.

Data Derived Extrapolation Factors for Developmental Toxicity:  A Preliminary Research Case Study with Perfluorooctanoate (PFOA

Guidelines of the United States Environmental Protection Agency (EPA, 1991) and the International Programme on Chemical Safety (IPCS, 2005) suggest two different default positions for dosimetric extrapolation from experimental animals to humans when the dosimetry of the critical effect is not known.  The default position of EPA (1991) for developmental toxicity is to use peak concentration (or Cmax) for this dosimetric extrapolation.  In contrast, IPCS (2005, page 39) states its default position for dosimetric choice in the absence of data is to use the area under the curve (or AUC).  The choice of the appropriate dose metric is important in the development of either a Chemical Specific Adjustment Factor (CSAF) of IPCS (2005) or a Data Derived Extrapolation Factor (DDEF) of EPA (2014).  This research shows the derivation of a DDEF for developmental toxicity for perfluorooctanoate (PFOA), a chemical of current interest.  Here, identification of the appropriate dosimetric adjustment from a review of developmental effects identified by EPA (2016) is attempted.  Although some of these effects appear to be related to Cmax, most appear to be related to the average concentration or its AUC, but only during the critical period of development for a particular effect.  A comparison was made of kinetic data from PFOA exposure in mice with newly available and carefully monitored kinetic data in humans after up to 36 weeks of PFOA exposure in a phase 1 clinical trial by Elcombe et al. (2013).  Using the average concentration during the various exposure windows of concern, the DDEF for PFOA was determined to be 1.3 or 14.  These values are significantly different than comparable extrapolations by several other authorities based on differences in PFOA half-life among species.  Although current population exposures to PFOA are generally much lower than both the experimental animal data and the clinical human study, the development of these DDEFs is consistent with current guidelines of both EPA (2014) and IPCS (2005).