Correspondence / American Journal of Emergency Medicine 33 (2015) 1305–1322
2. Many of the referenced articles, differently from the present study, included mechanically ventilated patients in which changes in LUS were detected during the period of ventilation. Is this a selection bias that could engender any limitation in the analysis? 3. Pulmonary consolidation (interchangeable in some sentences with pneumonia) is defined by “the morphologic characteristics of pneumonia tissue-like or anechoic pattern and blurred, irregular margins, dynamic air bronchogram, and focal B lines.” The description of this imaging clues addressed as the main feature of LUS is seemingly, according to the quoted own authors' articles [1], mainly a mere interpretation of artifacts. We respectfully ask whether it is well established that the air bronchogram detected at the x-ray and CT corresponds to the echogenic structures often seen in patients with pneumonia. Whenever this is the case, could the authors show a typical example with a figure? 4. In this article, features of pneumonia consolidation are shortly listed and not detailed: where is the US imaging clues contribution? This is crucial to definitely confirm the flimsiness of the study. The so-called air bronchograms are tiny spots that appear in the context of the consolidation. In x-ray and CT imaging, air bronchogram sign refers to a branching, linear, tubular image representing a bronchus or bronchiole passing through airless lung parenchyma. However, this sign does not allow distinguishing among the abnormal parenchymal opacities such as pneumonia or nonobstructive atelectasis [2]. A characteristic CT finding of pneumonia-like adenocarcinoma, called bronchioloalveolar carcinoma before the new classification of lung adenocarcinoma (2011) is just the presence of air bronchograms and bubble-like lucencies or pseudocavitations [3,4]. The CT air bronchogram sign in solitary pulmonary lesions is actually significantly more common in malignant than in benign lesions [5]. Differently from CT, there is no specific pattern in transthoracic US that can help in distinguishing inflammatory lesions from other conditions, particularly malignancy. The latter generally presents with slightly irregular margins and varying degrees of hypoechogenicity and uniformity or rather as mixed hyperechoic/hypoechoic or with anechoic areas of necrosis. Ultrasound images of lung carcinomas may also have the feature of areas of air/fluid bronchogram, like those of inflammatory consolidations [6]. 5. The role of vascularization [1] in the US evaluation of pneumonia has not been explained. At this regard, we think that breathing movements represent a challenge, as the flash artifact makes color Doppler evaluation of vessels difficult or impossible [6]. 6. The aforementioned technical issues compel us to respectfully consider that the claimed [1] typical pneumonia echo pattern, established in a previous select committee conference cannot be suitable to dissemination in the clinical practice. Other points are very puzzling, and, overall, we claim the possibility of an observer's selection bias. As from the study methods' description, after a clinical evaluation, the potential diagnosis of pneumonia was ruled in, whereas other diagnoses that could potentially have a similar US appearance were ruled out. In addition, criteria of pulmonary embolism diagnosis are unclear. Did the authors make the diagnosis of pulmonary embolism and therefore exclude patients from the study only by US or by CT scan? In our opinion, the low rate of false-positive consolidation (3.1%) is probably due to the aforementioned selection bias and to the claimed exceptional expertise of operators. Nonetheless, the fact that even in selected patients, whose clinical presentation was compatible with pneumonia, 9 pulmonary consolidations interpreted as pneumonia at US were rather due to other causes (lung cancer and fibrosis) is of high clinical relevance.
1309
We think that the article [1] does not significantly contribute to the current knowledge on clinical usefulness of transthoracic US as a tool, alternative to x-ray, in the diagnosis of pulmonary consolidation that clinically, radiologically, and, sometimes, histologically is proven to be pneumonia.
Gaetano Rea, MD Department of Radiology, Ultrasound Diagnostic Unit, AORN dei Colli Monaldi Hospital, Naples, Italy Cristiana Cipriani, MD Department of Internal Medicine and Medical Disciplines “Sapienza” University of Rome, Rome, Italy Corresponding author. Cristiana Cipriani, MD, Viale del Policlinico 155 00161 Rome, Italy E-mail address: [email protected] http://dx.doi.org/10.1016/j.ajem.2015.04.019 References [1] Nazerian P, Volpicelli G, Vanni S, Gigli C, Betti L, Bartolucci M, et al. Accuracy of lung ultrasound for the diagnosis of consolidations when compared to chest computed tomography. Am J Emerg Med 2015;33:620–5. [2] Collins J, Stern EJ. Chest radiology: the essentials. 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2008 17. [3] Travis WD, Brambilla E, Noguchi M, Nicholson AG, Geisinger KR, Yatabe Y, et al. International association for the study of lung cancer/American Thoracic Society/ European Respiratory Society international multidisciplinary classification of lung adenocarcinoma. J Thorac Oncol 2011;6:244–85. [4] Bonomo L, Storto ML, Ciccotosto C, Polverosi R, Merlino B, Bellelli M, et al. Bronchioloalveolar carcinoma of the lung. Eur Radiol 1998;8:996–1001. [5] Kui M, Templeton PA, White CS, Cai ZL, Bai YX, Cai YQ. Evaluation of the air bronchogram sign on CT in solitary pulmonary lesions. J Comput Assist Tomogr 1996;20:983–6. [6] Catalano D, Trovato G, Sperandeo M, Sacco MC. Lung ultrasound in pediatric pneumonia. The persistent need of chest X-rays. Pediatr Pulmonol 2014;49:617–8.
Re: Endogenous and exogenous factors affecting the levels of carboxyhemoglobin☆
To the Editor, Thank you for providing us the opportunity to clarify additional issues regarding the coexistence of possible factors affecting carboxyhemoglobin (COHb) levels and consequently the results in our study “COHb and methemoglobin levels as prognostic markers in acute pulmonary embolism [1].” Both exogenous (CO inhalation by cigarette use) and endogenous CO contribute to the levels of COHb. Since COHb levels is a biomarker for cigarette use, we excluded smokers from our study. In addition, multiple physiologic processes or pathologic conditions possibly modulate the levels of endogenous COHb. Hematologic disease has been reported as a possible modulator of endogenous COHb levels [2], and concerns have been raised about a possible interaction of this pathology with the data provided by our study. Regarding these concerns, we would like to provide some additional data concerning our study population. Our final study sample consisted of 156 patients, 16% of which with cancer diagnosed either earlier or during the standard evaluation after pulmonary embolism diagnosis. All of ☆ Conflict of interest: The authors declare that they have no conflict of interest or financial ties to disclose.
1310
Correspondence / American Journal of Emergency Medicine 33 (2015) 1305–1322
these cases concerned solid (mainly lung) tumors. In the remaining cases analyzed in our study, pulmonary embolism was considered as idiopathic or the result of trauma, fracture, or other form of immobilization of the patient. Clearly, the possibility of occult hematologic disease cannot be completely ruled out, especially in cases considered as idiopathic. Nevertheless, the analysis of the data coming up from patients' medical record, clinical examination, or laboratory tests does not support such a possibility. On the other hand, second-hand smoking could represent an additional limitation of our retrospective study, although it is difficult to estimate the extent of this limitation. We should also take into account the difficulty in assessing passive smokers' exposure to environmental tobacco smoke. Although medical history taking in our hospital checks for exposure to cigarette smoking, it does not comprise a standard questionnaire for the semiquantitative evaluation of passive smoking. Two patients who spontaneously reported a very high exposure to passive smoking were classified as smokers and were excluded from the study. Ideally, the quantification of exposure to passive smoking should be based on the information reported by parents and verified by the measurement of cotinine levels in saliva or urine to support their statements [3]. Of course, this was impossible in our study due to its retrospective nature. Furthermore, although passive smoking has been repeatedly reported to acutely increase COHb levels, most of these measurements have been carried out during participants' exposure to second-hand smoking or shortly after this. Moreover, this effect appears to be dose dependent. Thus, lower levels or shorter durations of smoke exposure fail to significantly increase COHb levels [4]. Generally, exogenously delivered CO presents a half-life of 5 to 6 hours without supplemental oxygen administration [5]. Therefore, it is not surprising that COHb had poor discriminating ability for passive smoking in when evaluated later after the exposure during the preoperative process [6,7]. We consider this clinical setting to present more similarities with our study compared with other studies involving the acute effects of environmental tobacco smoke exposure under experimental conditions. Yours sincerely Sotirios Kakavas, MD, MSc, PhD⁎ Aggeliki Papanikolaou, MD Evangelos Balis, MD, PhD Nikolaos Tatsis, MD Christina Goga, MD Georgios Tatsis, MD Pulmonary Department, Evangelismos General Hospital of Athens Ypsilanti 45-47, 10676, Athens, Greece ⁎Corresponding author. Tel.: +30 213 2041 631; fax: +30 210 7232 370 E-mail addresses: [email protected] (S. Kakavas) [email protected] (A. Papanikolaou) [email protected] (E. Balis), [email protected] (N. Tatsis) [email protected] (C. Goga) [email protected] (G. Tatsis)
[4] Yarlioglues M, Kaya MG, Ardic I, Dogdu O, Yarlioglues H, Zencir C, et al. Dosedependent acute effects of passive smoking on left ventricular cardiac functions in healthy volunteers. J Investig Med 2012;60:517–22. [5] Scherer G. Carboxyhemoglobin and thiocyanate as biomarkers of exposure to carbon monoxide and hydrogen cyanide in tobacco smoke. Exp Toxicol Pathol 2006;58:101–24. [6] Cardwell K, Pan Z, Boucher R, Zuk J, Friesen RH. Screening by pulse CO-oximetry for environmental tobacco smoke exposure in preanesthetic children. Paediatr Anaesth 2012;22:859–64. [7] Yee BE, Ahmed MI, Brugge D, Farrell M, Lozada G, Idupaganthi R, et al. Second-hand smoking and carboxyhemoglobin levels in children: a prospective observational study. Paediatr Anaesth 2010;20(1):82–9.
Endogenous and exogenous factors affecting the levels of carboxyhemoglobin
To the Editor, We read with great interest the article “Carboxyhemoglobin and methemoglobin levels as prognostic markers in acute pulmonary embolism” written by Kakavas et al [1]. We think that the factors affecting the carboxyhemoglobin (COHb) level were not expressed clearly, and some patients who should be excluded from the study may have been included in this research that examined the COHb and methemoglobin level in patients with pulmonary embolism. Therefore, COHb levels were higher than expected, and the study results could be affected. Carbon monoxide (CO) poisoning is a condition that affects many systems especially the cardiovascular and central nervous systems [2-6]. Older erythrocytes are removed from the circulation, and when the Heme they contain are demolished, CO occurs. Carbon monoxide originating from the human body generates 1% of COHb. Endogenous CO rises to the level of 4% to 6% in some hematologic diseases [7]. Otherwise, COHb level of patients being smoker and also passive smoker rises. Carboxyhemoglobin level of a passive smoker has been reported to be twice as much than the normal level of COHb in studies [8,9]. Therefore, we consider that not questioning the conditions causing an increase in COHb levels such as passive smoker and hematologic diseases in addition to smokers in study exclusion criteria was one of limitations of study, and this situation should be explained in the study. Y. Emrah Eyi, MD Department of Emergency Medicine, Gulhane Military Medical Academy, Ankara, Turkey Corresponding author at: Gulhane Military Medical Academy Etlik, Ankara, Turkey. Tel.: +90 532 582 2802; fax: +90 312 304 1194. E-mail address: [email protected] Memduh Yetim, MD Van Military Hospital, Van, Turkey
http://dx.doi.org/10.1016/j.ajem.2015.05.006 Sukru Tekindur, MD Department of Anesthesiology and Reanimation Gulhane Military Medical Academy, Ankara, Turkey
References [1] Sotirios Kakavas, Aggeliki Papanikolaou, Evangelos Ballis, Nikolaos Tatsis, Christina Goga, Georgios Tatsis. Carboxyhemoglobin and methemoglobin levels as prognostic markers in acute pulmonary embolism. Am J Emerg Med 2015. http://dx.doi.org/10. 1016/j.ajem.2015.01.046. [2] Nielsen VG, Pearson EC, Smith MC. Increased carbon monoxide production by hemeoxygenase-1 caused by device-mediated hemolysis: thrombotic phantom menace? Artif Organs 2013;37(11):1008–14. [3] Jarvis M, Tunstall-Pedoe H, Feyerabend C, Vesey C, Salloojee Y. Biochemical markers of smoke absorption and self reported exposure to passive smoking biochemical markers of smoke absorption and self reported exposure to passive smoking. J Epidemiol Community Health 1984;38(4):335–9.
http://dx.doi.org/10.1016/j.ajem.2015.05.005
References [1] Sotirios Kakavas, Aggeliki Papanikolaou, Evangelos Ballis, Nikolaos Tatsis, Christina Goga, Georgios Tatsis. Carboxyhemoglobin and methemoglobin levels as prognostic markers in acute pulmonary embolism. Am J Emerg Med 2015. http://dx.doi.org/10. 1016/j.ajem.2015.01.046.
2. Many of the referenced articles, differently from the present study, included mechanically ventilated patients in which changes in LUS were detected during the period of ventilation. Is this a selection bias that could engender any limitation in the analysis? 3. Pulmonary consolidation (interchangeable in some sentences with pneumonia) is defined by “the morphologic characteristics of pneumonia tissue-like or anechoic pattern and blurred, irregular margins, dynamic air bronchogram, and focal B lines.” The description of this imaging clues addressed as the main feature of LUS is seemingly, according to the quoted own authors' articles [1], mainly a mere interpretation of artifacts. We respectfully ask whether it is well established that the air bronchogram detected at the x-ray and CT corresponds to the echogenic structures often seen in patients with pneumonia. Whenever this is the case, could the authors show a typical example with a figure? 4. In this article, features of pneumonia consolidation are shortly listed and not detailed: where is the US imaging clues contribution? This is crucial to definitely confirm the flimsiness of the study. The so-called air bronchograms are tiny spots that appear in the context of the consolidation. In x-ray and CT imaging, air bronchogram sign refers to a branching, linear, tubular image representing a bronchus or bronchiole passing through airless lung parenchyma. However, this sign does not allow distinguishing among the abnormal parenchymal opacities such as pneumonia or nonobstructive atelectasis [2]. A characteristic CT finding of pneumonia-like adenocarcinoma, called bronchioloalveolar carcinoma before the new classification of lung adenocarcinoma (2011) is just the presence of air bronchograms and bubble-like lucencies or pseudocavitations [3,4]. The CT air bronchogram sign in solitary pulmonary lesions is actually significantly more common in malignant than in benign lesions [5]. Differently from CT, there is no specific pattern in transthoracic US that can help in distinguishing inflammatory lesions from other conditions, particularly malignancy. The latter generally presents with slightly irregular margins and varying degrees of hypoechogenicity and uniformity or rather as mixed hyperechoic/hypoechoic or with anechoic areas of necrosis. Ultrasound images of lung carcinomas may also have the feature of areas of air/fluid bronchogram, like those of inflammatory consolidations [6]. 5. The role of vascularization [1] in the US evaluation of pneumonia has not been explained. At this regard, we think that breathing movements represent a challenge, as the flash artifact makes color Doppler evaluation of vessels difficult or impossible [6]. 6. The aforementioned technical issues compel us to respectfully consider that the claimed [1] typical pneumonia echo pattern, established in a previous select committee conference cannot be suitable to dissemination in the clinical practice. Other points are very puzzling, and, overall, we claim the possibility of an observer's selection bias. As from the study methods' description, after a clinical evaluation, the potential diagnosis of pneumonia was ruled in, whereas other diagnoses that could potentially have a similar US appearance were ruled out. In addition, criteria of pulmonary embolism diagnosis are unclear. Did the authors make the diagnosis of pulmonary embolism and therefore exclude patients from the study only by US or by CT scan? In our opinion, the low rate of false-positive consolidation (3.1%) is probably due to the aforementioned selection bias and to the claimed exceptional expertise of operators. Nonetheless, the fact that even in selected patients, whose clinical presentation was compatible with pneumonia, 9 pulmonary consolidations interpreted as pneumonia at US were rather due to other causes (lung cancer and fibrosis) is of high clinical relevance.
1309
We think that the article [1] does not significantly contribute to the current knowledge on clinical usefulness of transthoracic US as a tool, alternative to x-ray, in the diagnosis of pulmonary consolidation that clinically, radiologically, and, sometimes, histologically is proven to be pneumonia.
Gaetano Rea, MD Department of Radiology, Ultrasound Diagnostic Unit, AORN dei Colli Monaldi Hospital, Naples, Italy Cristiana Cipriani, MD Department of Internal Medicine and Medical Disciplines “Sapienza” University of Rome, Rome, Italy Corresponding author. Cristiana Cipriani, MD, Viale del Policlinico 155 00161 Rome, Italy E-mail address: [email protected] http://dx.doi.org/10.1016/j.ajem.2015.04.019 References [1] Nazerian P, Volpicelli G, Vanni S, Gigli C, Betti L, Bartolucci M, et al. Accuracy of lung ultrasound for the diagnosis of consolidations when compared to chest computed tomography. Am J Emerg Med 2015;33:620–5. [2] Collins J, Stern EJ. Chest radiology: the essentials. 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2008 17. [3] Travis WD, Brambilla E, Noguchi M, Nicholson AG, Geisinger KR, Yatabe Y, et al. International association for the study of lung cancer/American Thoracic Society/ European Respiratory Society international multidisciplinary classification of lung adenocarcinoma. J Thorac Oncol 2011;6:244–85. [4] Bonomo L, Storto ML, Ciccotosto C, Polverosi R, Merlino B, Bellelli M, et al. Bronchioloalveolar carcinoma of the lung. Eur Radiol 1998;8:996–1001. [5] Kui M, Templeton PA, White CS, Cai ZL, Bai YX, Cai YQ. Evaluation of the air bronchogram sign on CT in solitary pulmonary lesions. J Comput Assist Tomogr 1996;20:983–6. [6] Catalano D, Trovato G, Sperandeo M, Sacco MC. Lung ultrasound in pediatric pneumonia. The persistent need of chest X-rays. Pediatr Pulmonol 2014;49:617–8.
Re: Endogenous and exogenous factors affecting the levels of carboxyhemoglobin☆
To the Editor, Thank you for providing us the opportunity to clarify additional issues regarding the coexistence of possible factors affecting carboxyhemoglobin (COHb) levels and consequently the results in our study “COHb and methemoglobin levels as prognostic markers in acute pulmonary embolism [1].” Both exogenous (CO inhalation by cigarette use) and endogenous CO contribute to the levels of COHb. Since COHb levels is a biomarker for cigarette use, we excluded smokers from our study. In addition, multiple physiologic processes or pathologic conditions possibly modulate the levels of endogenous COHb. Hematologic disease has been reported as a possible modulator of endogenous COHb levels [2], and concerns have been raised about a possible interaction of this pathology with the data provided by our study. Regarding these concerns, we would like to provide some additional data concerning our study population. Our final study sample consisted of 156 patients, 16% of which with cancer diagnosed either earlier or during the standard evaluation after pulmonary embolism diagnosis. All of ☆ Conflict of interest: The authors declare that they have no conflict of interest or financial ties to disclose.
1310
Correspondence / American Journal of Emergency Medicine 33 (2015) 1305–1322
these cases concerned solid (mainly lung) tumors. In the remaining cases analyzed in our study, pulmonary embolism was considered as idiopathic or the result of trauma, fracture, or other form of immobilization of the patient. Clearly, the possibility of occult hematologic disease cannot be completely ruled out, especially in cases considered as idiopathic. Nevertheless, the analysis of the data coming up from patients' medical record, clinical examination, or laboratory tests does not support such a possibility. On the other hand, second-hand smoking could represent an additional limitation of our retrospective study, although it is difficult to estimate the extent of this limitation. We should also take into account the difficulty in assessing passive smokers' exposure to environmental tobacco smoke. Although medical history taking in our hospital checks for exposure to cigarette smoking, it does not comprise a standard questionnaire for the semiquantitative evaluation of passive smoking. Two patients who spontaneously reported a very high exposure to passive smoking were classified as smokers and were excluded from the study. Ideally, the quantification of exposure to passive smoking should be based on the information reported by parents and verified by the measurement of cotinine levels in saliva or urine to support their statements [3]. Of course, this was impossible in our study due to its retrospective nature. Furthermore, although passive smoking has been repeatedly reported to acutely increase COHb levels, most of these measurements have been carried out during participants' exposure to second-hand smoking or shortly after this. Moreover, this effect appears to be dose dependent. Thus, lower levels or shorter durations of smoke exposure fail to significantly increase COHb levels [4]. Generally, exogenously delivered CO presents a half-life of 5 to 6 hours without supplemental oxygen administration [5]. Therefore, it is not surprising that COHb had poor discriminating ability for passive smoking in when evaluated later after the exposure during the preoperative process [6,7]. We consider this clinical setting to present more similarities with our study compared with other studies involving the acute effects of environmental tobacco smoke exposure under experimental conditions. Yours sincerely Sotirios Kakavas, MD, MSc, PhD⁎ Aggeliki Papanikolaou, MD Evangelos Balis, MD, PhD Nikolaos Tatsis, MD Christina Goga, MD Georgios Tatsis, MD Pulmonary Department, Evangelismos General Hospital of Athens Ypsilanti 45-47, 10676, Athens, Greece ⁎Corresponding author. Tel.: +30 213 2041 631; fax: +30 210 7232 370 E-mail addresses: [email protected] (S. Kakavas) [email protected] (A. Papanikolaou) [email protected] (E. Balis), [email protected] (N. Tatsis) [email protected] (C. Goga) [email protected] (G. Tatsis)
[4] Yarlioglues M, Kaya MG, Ardic I, Dogdu O, Yarlioglues H, Zencir C, et al. Dosedependent acute effects of passive smoking on left ventricular cardiac functions in healthy volunteers. J Investig Med 2012;60:517–22. [5] Scherer G. Carboxyhemoglobin and thiocyanate as biomarkers of exposure to carbon monoxide and hydrogen cyanide in tobacco smoke. Exp Toxicol Pathol 2006;58:101–24. [6] Cardwell K, Pan Z, Boucher R, Zuk J, Friesen RH. Screening by pulse CO-oximetry for environmental tobacco smoke exposure in preanesthetic children. Paediatr Anaesth 2012;22:859–64. [7] Yee BE, Ahmed MI, Brugge D, Farrell M, Lozada G, Idupaganthi R, et al. Second-hand smoking and carboxyhemoglobin levels in children: a prospective observational study. Paediatr Anaesth 2010;20(1):82–9.
Endogenous and exogenous factors affecting the levels of carboxyhemoglobin
To the Editor, We read with great interest the article “Carboxyhemoglobin and methemoglobin levels as prognostic markers in acute pulmonary embolism” written by Kakavas et al [1]. We think that the factors affecting the carboxyhemoglobin (COHb) level were not expressed clearly, and some patients who should be excluded from the study may have been included in this research that examined the COHb and methemoglobin level in patients with pulmonary embolism. Therefore, COHb levels were higher than expected, and the study results could be affected. Carbon monoxide (CO) poisoning is a condition that affects many systems especially the cardiovascular and central nervous systems [2-6]. Older erythrocytes are removed from the circulation, and when the Heme they contain are demolished, CO occurs. Carbon monoxide originating from the human body generates 1% of COHb. Endogenous CO rises to the level of 4% to 6% in some hematologic diseases [7]. Otherwise, COHb level of patients being smoker and also passive smoker rises. Carboxyhemoglobin level of a passive smoker has been reported to be twice as much than the normal level of COHb in studies [8,9]. Therefore, we consider that not questioning the conditions causing an increase in COHb levels such as passive smoker and hematologic diseases in addition to smokers in study exclusion criteria was one of limitations of study, and this situation should be explained in the study. Y. Emrah Eyi, MD Department of Emergency Medicine, Gulhane Military Medical Academy, Ankara, Turkey Corresponding author at: Gulhane Military Medical Academy Etlik, Ankara, Turkey. Tel.: +90 532 582 2802; fax: +90 312 304 1194. E-mail address: [email protected] Memduh Yetim, MD Van Military Hospital, Van, Turkey
http://dx.doi.org/10.1016/j.ajem.2015.05.006 Sukru Tekindur, MD Department of Anesthesiology and Reanimation Gulhane Military Medical Academy, Ankara, Turkey
References [1] Sotirios Kakavas, Aggeliki Papanikolaou, Evangelos Ballis, Nikolaos Tatsis, Christina Goga, Georgios Tatsis. Carboxyhemoglobin and methemoglobin levels as prognostic markers in acute pulmonary embolism. Am J Emerg Med 2015. http://dx.doi.org/10. 1016/j.ajem.2015.01.046. [2] Nielsen VG, Pearson EC, Smith MC. Increased carbon monoxide production by hemeoxygenase-1 caused by device-mediated hemolysis: thrombotic phantom menace? Artif Organs 2013;37(11):1008–14. [3] Jarvis M, Tunstall-Pedoe H, Feyerabend C, Vesey C, Salloojee Y. Biochemical markers of smoke absorption and self reported exposure to passive smoking biochemical markers of smoke absorption and self reported exposure to passive smoking. J Epidemiol Community Health 1984;38(4):335–9.
http://dx.doi.org/10.1016/j.ajem.2015.05.005
References [1] Sotirios Kakavas, Aggeliki Papanikolaou, Evangelos Ballis, Nikolaos Tatsis, Christina Goga, Georgios Tatsis. Carboxyhemoglobin and methemoglobin levels as prognostic markers in acute pulmonary embolism. Am J Emerg Med 2015. http://dx.doi.org/10. 1016/j.ajem.2015.01.046.
