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Editorials: Point and Counterpoint |

Rebuttal From Drs Kopp and Stavas FREE TO VIEW

Vincent J. Kopp, MD; Joseph M. Stavas, MD
Author and Funding Information

FINANCIAL/NONFINANCIAL DISCLOSURES: The authors have reported to CHEST the following: J. M. S. consults for Cook, Inc. (West Lafayette, IN) and Excelerate Health Ventures, Inc. (Durham, NC). None declared (V. J. K.).

CORRESPONDENCE TO: Vincent J. Kopp, MD, Department of Anesthesiology, Campus Box 7010, N2198 UNC Hospitals, Chapel Hill, NC 27599-7010


Copyright 2016, American College of Chest Physicians. All Rights Reserved.


Chest. 2016;149(2):308-309. doi:10.1016/j.chest.2015.10.072
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Published online

We thank Drs Christopher and Repine. We rebut with three points and a reiterative call for a lowest oxygen level acceptable (LOLA) standard based on the “as low as reasonably achievable” standard used in radiology.

Although we do not contest oxygen’s capacity to save lives when used properly, we eschew any “what you see is what you get” approach to oxygen use and risk/benefit analysis.

Simply put, clinical benefit does not preclude subclinical or collateral toxicity. Absence of apparent harm at a given observational level does not mean absence of any harm at all levels. Clinical trial data and population data cannot describe a specific patient’s subclinical or collateral toxicity status in the absence of biomarker or genetic probe assessment. Basic science data must be brought to bear on development of clinical care rationales. Radiation epidemiology recognizes this; the oxygen-use community lags behind.

Radiation and oxygen share homologous injury mechanisms. These involve unmeasured/immeasurable energy transfers and stoichiometric reactions. Oxidative damage results at every submolecular and molecular level. Evidence continues to accumulate that disease and aging inevitably follow oxidative stress.

Unfortunately, the bio-energetic mechanisms governing damage reactions respect no individual. What differs among individuals—and is relevant to this pro/con debate—is an individual’s capacity to withstand/repair/recover from damage. For instance, patients with ataxia telangiectasia evince very deficient DNA repair capacities that render them susceptible to irreversible radiation-induced damage. Regarding patients with COPD vs patients without COPD on low-dose oxygen therapy (LDOT), individuals with different antioxidant/repair/recovery/prevention capacities related to pathophysiological differences will be more susceptible to oxygen’s radiation-like effects because COPD patients endorse high oxidative stress at baseline.

Progression from subclinical to clinical reactive oxygen and nitrogen species–mediated toxicity follows stochastic patterns. Cell culture experiments bear this out, as do some COPD management models.,

Patients with COPD have high comorbidity burdens. Most have radiation-oxygen injury homology foundations. Untimely emergence/exacerbation/exaggeration of comorbidities expose patients with COPD to health risks independent of COPD risks. Such risk is heightened when surgical intervention is required to address conditions such as heart attack or stroke, glaucoma, cataracts, or gastrointestinal conditions. Although we cannot prove that LDOT worsens comorbidities, excessive oxygen causes or contributes to cerebral and systemic arterial vasoconstriction, microvascular proliferation, diminished cardiac output, cataracts, and even central corneal thickening.

As with “as low as reasonably achievable” for radiation, LOLA for oxygen limits dosage to preserve benefits. Excess radiation and oxygen is harmful; oxygen deficiency (unlike radiation deficiency?) is also harmful. Should the oxygen tap then be left running and education and regulation turned off? Assuredly not.

Zhu et al showed continuous oxygen saturation monitoring in 16 patients with COPD reduced median oxygen prescriptions from 2.5 to 1.2 L/min (P < .001) with no significant effect on oxygen saturation time below 88%. A small study, it embodies LOLA’s promise. By reducing oxygen use without compromising meaningful bio-measures or function, we reduce radiation-oxygen injury homology exposure. For patients with COPD, LOLA means building new health pathways. Once built, these just might extend life better than LDOT.

Christopher K.L. .Repine J.E. . Counterpoint: does low-dose oxygen expose patients with COPD to more radiation-like risks than patients without COPD: No. Chest. 2016;149:306-308 [PubMed]journal
 
Kitahara C.M. .Linet M.S. .Rajaraman P. .Ntowe E. .de González A.B. . A new era of low-dose radiation epidemiology. Curr Envir Health Rpt. 2015;2:236-249 [PubMed]journal. [CrossRef]
 
Indo H.P. .Yen H.-C. .Nakanishi I. .et al A mitochondrial superoxide theory for oxidative stress diseases and aging. J Clin Biochem Nutr. 2015;56:1-7 [PubMed]journal. [CrossRef] [PubMed]
 
Lawless C. .Jurk D. .Gillespie C.S. .et al A stochastic step model of replicative senescence explains ROS production rate in ageing cell populations. PLoS ONE. 2012;7:e32117- [PubMed]journal. [CrossRef] [PubMed]
 
Hoogendoorn M. .Rutten-van Mölken M.P. .Hoogenveen R.T. .Al M.J. .Feenstra T.L. . Developing and applying a stochastic dynamic population model for chronic obstructive pulmonary disease. Value Health. 2011;14:1039-1047 [PubMed]journal. [CrossRef] [PubMed]
 
Soriano J.B. .Visick G.T. .Muellerova H. .Payvandi N. .Hansell A.L. . Patterns of comorbidities in newly diagnosed COPD and asthma in primary care. Chest. 2005;128:2099-2107 [PubMed]journal. [CrossRef] [PubMed]
 
Siegfried C.J. .Shui Y.-B. .Beebe D.C. . Central corneal thickness correlates with oxygen levels in the human anterior chamber angle. Am J Ophthalmol. 2015;159:457-462 [PubMed]journal. [CrossRef] [PubMed]
 
Zhu Z. .Barnette R.K. .Fussell K.M. .Rodriguez R.M. .Canonico A. .Light R.W. . Continuous oxygen monitoring—a better way to prescribe long-term oxygen therapy. Respir Med. 2005;99:136-192 [PubMed]journal
 

Figures

Tables

References

Christopher K.L. .Repine J.E. . Counterpoint: does low-dose oxygen expose patients with COPD to more radiation-like risks than patients without COPD: No. Chest. 2016;149:306-308 [PubMed]journal
 
Kitahara C.M. .Linet M.S. .Rajaraman P. .Ntowe E. .de González A.B. . A new era of low-dose radiation epidemiology. Curr Envir Health Rpt. 2015;2:236-249 [PubMed]journal. [CrossRef]
 
Indo H.P. .Yen H.-C. .Nakanishi I. .et al A mitochondrial superoxide theory for oxidative stress diseases and aging. J Clin Biochem Nutr. 2015;56:1-7 [PubMed]journal. [CrossRef] [PubMed]
 
Lawless C. .Jurk D. .Gillespie C.S. .et al A stochastic step model of replicative senescence explains ROS production rate in ageing cell populations. PLoS ONE. 2012;7:e32117- [PubMed]journal. [CrossRef] [PubMed]
 
Hoogendoorn M. .Rutten-van Mölken M.P. .Hoogenveen R.T. .Al M.J. .Feenstra T.L. . Developing and applying a stochastic dynamic population model for chronic obstructive pulmonary disease. Value Health. 2011;14:1039-1047 [PubMed]journal. [CrossRef] [PubMed]
 
Soriano J.B. .Visick G.T. .Muellerova H. .Payvandi N. .Hansell A.L. . Patterns of comorbidities in newly diagnosed COPD and asthma in primary care. Chest. 2005;128:2099-2107 [PubMed]journal. [CrossRef] [PubMed]
 
Siegfried C.J. .Shui Y.-B. .Beebe D.C. . Central corneal thickness correlates with oxygen levels in the human anterior chamber angle. Am J Ophthalmol. 2015;159:457-462 [PubMed]journal. [CrossRef] [PubMed]
 
Zhu Z. .Barnette R.K. .Fussell K.M. .Rodriguez R.M. .Canonico A. .Light R.W. . Continuous oxygen monitoring—a better way to prescribe long-term oxygen therapy. Respir Med. 2005;99:136-192 [PubMed]journal
 
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