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Inhalation Toxicology
International Forum for Respiratory Research
Volume 24, 2012 - Issue 2
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Letter to the Editor

Letter to the editor in response to Finkelstein et al. (2012)

, &
Pages 141-142 | Published online: 09 Feb 2012

Dear Editor,

We are delighted to have the opportunity to respond to the comments from Dr. Murray Finkelstein regarding our recent publication in Inhalation Toxicology entitled “Asbestos fiber concentrations in the lungs of brake repair workers: commercial amphibole levels are predictive of chrysotile levels” (Marsh et al., Citation2011). In a most peculiar turn of events, Dr. Finkelstein was permitted to amend his original submission after we had responded and both letters were accepted for publication. For purposes of clarification, we will first respond to the comments in his original letter and then address the statements in his amended letter.

Regarding the alleged data errors, we have re-reviewed all our data and calculations and have verified them to be correct as published. Dr. Finkelstein’s allegations appear to stem from his misunderstanding of the values recorded on the counting sheets versus values reported in Table 1 of our manuscript. Below we address and clarify these areas of misunderstanding.

Regarding Cases 1 and 9, Dr. Finkelstein has omitted the coated fibers (asbestos bodies) in the count sheets which, when included, yield the values published in our article. In the original manuscript by CitationButnor et al. (2003) which is the source of most of the data for our current study, it is clearly stated in the Materials and Methods section that the calculations are based on total asbestos fiber concentrations, and the footnote to Table 2 clearly indicates that the columns represent the total of coated plus uncoated fibers. Similarly, in our paper, the footnote to Table 2 clearly indicates that the last column represents the total of coated plus uncoated fibers.

Regarding Cases 2, 3, 4, 8 and 9, Dr. Finkelstein has omitted the non-commercial amphibole fibers other than tremolite (actinolite and anthophyllite) in the count sheets, which, when included, yield the published values in our article. In Cases 2 and 4, the non-commercial amphiboles (TAA) identified were anthophyllite, in Case 3 actinolite, in Case 8 actinolite and tremolite, and in Case 9 anthophyllite and tremolite. In the original manuscript by Butnor et al. (Citation2003) the Materials and Methods section clearly states that non-commercial amphiboles included actinolite, anthophyllite and tremolite and the Results section notes that non-commercial amphiboles, principally tremolite, with some actinolite and anthophyllite, predominated. Similarly, in Table 2, it is clearly indicated that the non-commercial amphiboles were combined for purposes of this analysis.

In our paper, this is again mentioned similarly in the Introduction section: “non-commercial asbestos fibers (principally tremolite, with some actinolite and anthophyllite, measured as a marker of chrysotile exposure)” (Marsh et al., Citation2011). Tremolite and actinolite are part of a single mineral series, with the distinction based on demonstrable iron content in the latter, and anthophyllite being more closely related to talc. All three non-commercial amphiboles have been mentioned as contaminants of chrysotile (Roggli & Coin, Citation2004; Churg, Citation1986).

With respect to Case 6, one asbestos body was counted but not analyzed. We were left with the option of ignoring this coated fiber or to assume that it was likely a commercial amphibole (as it is in 96% of coated fibers that we have analyzed) (Roggli & Sharma, Citation2004). We arbitrarily chose the latter option. Either way, this sample was not considered to be different from our background levels. With respect to Case 9, two samples were analyzed and the findings were nearly identical. The results reported in our paper were the weighted average of the two samples (i.e., the total number of fibers combined and the total weight of tissue combined). This was the only case that had two samples analyzed by electron microscopy.

After the submission of our original response, Dr. Finkelstein noted that he had learned from Dr. Roggli that the fiber counts reported were the sum of uncoated fibers 5 µm or greater in length plus asbestos bodies (there was no direct communication with Dr. Finkelstein regarding this information). He further states that this was nowhere reported in the paper (see the discussion above) and that this is an unusual procedure. He has thus further compounded his error. It is not at all uncommon for researchers to report their findings by electron microscopy as the total fiber count for any particular fiber type or group without distinction as to whether or not the fibers are coated or uncoated (Churg & Vedal, Citation1994; Gibbs et al., Citation1991). Indeed, we have done so on many occasions (Roggli & Sanders, Citation2000; Roggli et al., Citation2002a,Citationb; Roggli & Vollmer, Citation2008; Schneider et al., Citation2010) (including the Butnor paper, 2 which Dr. Finkelstein apparently never read).

Dr. Finkelstein raises another issue in his amended letter regarding case 9, stating that this individual was exposed to friction products that contained crocidolite asbestos. No citation is provided for this statement. The company involved in this matter filed in the late 1980s answers to interrogatories stating that when Canadian mines were on strike, the company purchased ‘Russian blue’ as a substitute (CitationDeposition of Carl Liggett, 2011). Russia is the location of the largest chrysotile mine in the world and was not a source for crocidolite asbestos (Roggli & Coin, Citation2004; CitationDeposition of Carl Liggett, 2011). Thus, this company’s products never contained crocidolite, as implied by Dr. Finkelstein.

As noted in the Discussion section of our paper, two other laboratories using transmission electron microscopy (TEM) have reported similar findings to ours with respect to mesothelioma patients exposed to brake dust whose lung samples were submitted for analysis. Since the submission of our manuscript, an additional report from Dr. Bruce Case, again using TEM, reported findings similar to those of Butnor et al. (CitationCase, 2011).

Declaration of interest

A conflict of interest form is available online.

Supplemental material

Supplementary Material

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References

  • Butnor KJ, Sporn TA, Roggli VL. 2003. Exposure to brake dust and malignant mesothelioma: A study of 10 cases with mineral fiber analyses. Ann Occup Hyg 47:325–330.
  • Case BW. Exposure to brake dust and malignant mesothelioma: Lung-retained fibre analyses using transmission electron microscopy confirm previous findings at lower magnification by scanning electron microscopy (abstr.), presented at the Johnson Conference of ASTM, University of Vermont, January 28, 2011.
  • Churg A. 1986. Analysis of asbestos fibers from lung tissue: Research and diagnostic uses. Sem Respir Med 7:281–288.
  • Churg A, Vedal S. 1994. Fiber burden and patterns of asbestos-related disease in workiers with heavy mixed amosite and chrysotile exposure. Am J Respir Crit Care Med 150:663–669.
  • Deposition of Carl Liggett, corporate designee, taken in Atlanta, GA on June 22, 2011.
  • Gibbs AR, Stephens M, Griffiths DM, Blight BJN, Pooley FD. 1991. Fibre distribution in the lungs and pleura of subjects with asbestos related diffuse pleural fibrosis. Br J Ind Med 48:762–770.
  • Marsh GM, Youk AO, Roggli VL. Asbestos fiber concentrations in the lungs of brake repair workers: commercial amphibole levels are predictive of chrysotile levels. Inhalation Toxicology, 2011: 1–8, Early Online.
  • Roggli VL, Coin P. Mineralogy of Asbestos, CH 1, In: Pathology of Asbestos-Associated Diseases, 2nd Ed.(Roggli VL, Oury TD, Sporn TA, eds), Springer: New York, 2004, pp. 1–16.
  • Roggli VL, Sanders LL. 2000. Asbestos content of lung tissue and carcinoma of the lung: A clinicopathologic correlation and mineral fiber analysis of 234 cases. Ann Occup Hyg 44:109–117.
  • Roggli VL, Sharma A. Analysis of Tissue Mineral Fiber Content, CH 11, In: Pathology of Asbestos-Associated Diseases, 2nd Ed.(Roggli VL, Oury TD, Sporn TA, eds), Springer: New York, 2004, pp. 309–354.
  • Roggli VL, Sharma A, Butnor KJ, Sporn T, Vollmer RT. 2002a. Malignant mesothelioma and occupational exposure to asbestos: A clinicopathological correlation of 1445 cases. Ultrastruct Pathol 26:1–11.
  • Roggli VL, Vollmer RT, Butnor KJ, Sporn TA. 2002b. Tremolite and mesothelioma. Ann Occup Hyg 46:447–453.
  • Roggli VL, Vollmer RT. 2008. Twenty-five years of fiber analysis: what have we learned? Hum Pathol 39:307–315.
  • Schneider F, Sporn TA, Roggli VL. 2010. Asbestos fiber content of lungs with diffuse interstitial fibrosis: An analytical scanning electron microscopic analysis of 249 cases. Arch Pathol Lab Med 134:457–461.

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