Correspondence/Rebuttal pubs.acs.org/est
Response to Comment on “Appalachian Mountaintop Mining Particulate Matter Induces Neoplastic Transformation of Human Bronchial Epithelial Cells and Promotes Tumor Formation” †
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n a comment by Winschel, he has asked us to retract our paper entitled “Appalachian Mountain top Mining Particulate Matter Induces Neoplastic Transformation of Human Bronchial Epithelial Cells and Promotes Tumor Formation.” Given that there are no ethical issues with the paper that would merit retraction, rather a scientific disagreement with how data is reported, we decline to retract the paper. Dr. Winschel, Director of Research and Development at Consol Energy, has called into question the high molybdenum (Mo) content in particulate matter of mountain top mining (PMMTM) and the statement in the paper that Mo is a “main chemical constituent” of PMMTM. For clarification, we did not state that molybdenum is the main chemical constituent of PMMTM as determined by SEM-EDX. Methodologically, we used SEM-EDX to determine the presence of Mo and other inorganic components such as silica in the samples. SEM-EDX does not detect all elements, for example, it cannot detect organic components (and some inorganic elements). Therefore, we cannot and did not conclude that Mo is the main chemical constituent (but inorganic constituent) of PMMTM. This method was used in the study primarily to help identify potential contributors to the observed biological effects of PMMTM, and not for quantitative analysis of the sample. Because of the limited detection capacity and qualitative nature of SEM-EDX, we were careful to not state the quantitative values of PMMTM constituents. The reported values were only relative and approximate values compared to other detected elements. As indicated earlier, SEM-EDX does not detect all elements, and therefore the values cannot be compared with the absolute values for coal samples described by Winschel. Of higher importance than having a discussion about absolute or relative concentration of Mo in PMMTM, the purpose of this study was to investigate the long-term carcinogenic potential of PMMTM exposure on human bronchial epithelial cells. We have observed that PMMTM is bioactive upon chronic exposure to lung epithelial cells causing them to transform, and that noncytotoxic concentrations of Mo and other potentially unidentified constituents in PMMTM may contribute to this effect. Whether or not Mo is the causative agent or main constituent does not detract from the underlying bioactivity of PMMTM. We suggest that further risk assessment studies be conducted to verify the long-term health effect of PMMTM.
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AUTHOR INFORMATION
Corresponding Author
*Phone: 304 293 1483; fax: 304 293 2576; e-mail: suidjit@ gmail.com. Notes
The authors declare no competing financial interest.
Sudjit Luanpitpong*,†,‡,§ Michael Chen†,‡ Travis Knuckles∥ Sijin Wen⊥ Juhua Luo# Emily Ellis∇ Michael Hendryx# Yon Rojanasakul†,‡
© 2015 American Chemical Society
Department of Pharmaceutical Sciences, West Virginia University, Morgantown, West Virginia 26506, United States; ‡ Mary Babb Randolph Cancer Center, West Virginia University, Morgantown, West Virginia 26506, United States; § Siriraj Center of Excellence for Stem Cell Research, Mahidol University, Bangkok 10700, Thailand ∥ Center for Cardiovascular and Respiratory Science, West Virginia University, Morgantown, West Virginia 26506, United States; ⊥ Department of Biostatistics, West Virginia University, Morgantown, West Virginia 26506, United States; # School of Public Health, Indiana University, Bloomington, Indiana 47405, United States; ∇ Animal Models and Imaging Facility, West Virginia University, Morgantown, West Virginia 26506, United States
Published: July 24, 2015 9385
DOI: 10.1021/acs.est.5b02314 Environ. Sci. Technol. 2015, 49, 9385−9385
