• Users Online: 151
  • Home
  • Print this page
  • Email this page
Home About us Editorial board Ahead of print Current issue Search Archives Submit article Instructions Subscribe Contacts Login 

 Table of Contents  
Year : 2021  |  Volume : 7  |  Issue : 1  |  Page : 41-46

Acute electrocardiographic changes during smoking and tobacco chewing: A Cross-sectional study

1 Department of Cardiology, Post Graduate Institute of Medical Education and Research, Chandigarh, India
2 Department of Cardiology, All India Institute of Medical Sciences, New Delhi, India

Date of Submission15-Dec-2020
Date of Decision03-Mar-2021
Date of Acceptance12-Mar-2021
Date of Web Publication24-Apr-2021

Correspondence Address:
Sivasubramanian Ramakrishnan
Department of Cardiology, All India Institute of Medical Sciences, New Delhi
Login to access the Email id

Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jpcs.jpcs_112_20

Rights and Permissions

Background: Smoking increases the risk of coronary artery disease. Very few studies have evaluated the temporal relationship of electrocardiographic changes with smoking. We sought to study and compare the electrocardiogram (ECG) changes during smoking and tobacco chewing in current smokers and tobacco chewers presenting with atypical chest pain with either negative or mild positive exercise ECG test (treadmill test [TMT]). Materials and Methods: We screened male smokers and tobacco chewers with atypical chest pain with TMT. A total of 60 patients, 30 in each group in whom TMT was either negative or mildly positive, underwent a 24-h Holter monitoring. We asked patients to note down their time of smoking and tobacco chewing along with the timing of symptoms if any. Results: All patients were male with an average age of 45 years in smokers and 42 years in the tobacco chewer group. The mean number of cigarettes consumed was 6 ± 2.8 and tobacco chewed was 5 ± 4.7 g/day. Heart rate (HR) in smokers increased from 82.5 ± 14.56/min 10 min before smoking to 90.63 ± 15.34/min, during smoking with peak HR achieved at the time of smoking (P < 0.0001). HR in the tobacco chewers peaked at 10 min after chewing from 80.62 ± 13.52/min 10 min before to 87.89 ± 13.86/min 10 min after chewing (P < 0.0001). Smoking was associated with a significant increase in supraventricular ectopics (VEs) from 3.98/h before smoking to 7.43/h during and 6.92/h after smoking (P < 0.0001). Two patients in the smoker subgroup had spontaneous smokeless tobacco -T changes lasting for 10–25 min. Smoking was associated with a significant decrease in HR variability (HRV) index than the controls (P = 0.023). Tobacco chewing was not associated with any significant changes in the HRV parameter. Conclusions: Smoking and tobacco chewing both significantly increase the HR acutely. Smoking leads to an increase in both supraventricular and VEs. We observed reduced HRV in patients who smoked cigarettes.

Keywords: Cigarette smoking, ectopics, heart rate variability, smokeless tobacco

How to cite this article:
Gupta H, Bhargava B, Seth S, Pruthvi C R, Ramakrishnan S. Acute electrocardiographic changes during smoking and tobacco chewing: A Cross-sectional study. J Pract Cardiovasc Sci 2021;7:41-6

How to cite this URL:
Gupta H, Bhargava B, Seth S, Pruthvi C R, Ramakrishnan S. Acute electrocardiographic changes during smoking and tobacco chewing: A Cross-sectional study. J Pract Cardiovasc Sci [serial online] 2021 [cited 2023 May 28];7:41-6. Available from: https://www.j-pcs.org/text.asp?2021/7/1/41/314471

  Introduction Top

Cigarette smoking is the strongest risk factor for cardiovascular disease (CVD).[1] Although the increased risk with cigarette smoking is dose dependent, as few as 4–5 cigarettes/day also significantly increase the risk.[2] Smoking has acute unfavorable effects on the blood pressure and sympathetic tone. It reduces the myocardial oxygen supply. It is involved in the pathogenesis of atherothrombosis in various vascular beds by various mechanisms.[3],[4] Compared to nonsmokers, smokers have an increased incidence of coronary vasospasm and reduced threshold for ventricular arrhythmias.[4],[5],[6] It is also associated with reduced exercise capacity and chronotropic incompetence.[5],[7],[8]

Nicotine is the major addicting substance in tobacco and is thought to be responsible for most of the adverse effects associated with its use. The mean nicotine content of chewing tobacco used in India is 13.8–65 mg/g of product. In India, smokeless tobacco (ST) consumption is more common than smoking. ST consumption is found in 38.1% of men and 9.9% of women as compared to smoking, which is found in 33.3% of men and 1.6% of women.[9]

Unlike smoking, which produces rapid peaks and troughs, ST use causes more prolonged, sustained nicotine levels, often lasting for 60 min.[10] Regular users of ST products end up taking as much nicotine per day as regular smokers.[10],[11],[12] Acute cardiovascular effects, similar to those caused by cigarette smoking, are also seen after the use of ST.

The importance of the autonomic nervous system (ANS) in CVD is well known.[13] Studies have shown changes in heart rate (HR) and HR variability (HRV) associated with acute passive smoking and exposure to respirable suspended particles (RSP).

Reduced HRV in general populations is associated with an increased risk of coronary artery disease (CAD) and death.[14],[15],[16] Similarly, acute tobacco smoke exposure is associated with significant HRV changes.[13] Smoking cessation is associated with an immediate increase in HRV.[17],[18] However, there is no study exploring the acute effects of tobacco chewing on HRV or incidence of ectopic heartbeats.

  Materials and Methods Top

Study design

Our study was a single tertiary care center cross-sectional study of electrocardiogram (ECG) changes during smoking and tobacco chewing with the help of Holter monitoring among current smokers and tobacco chewers presenting with atypical chest pain with either negative or mild positive exercise ECG test (treadmill test [TMT]).

Materials and Methods

Current smokers and tobacco chewers with atypical chest pain, aged between 25 and 65 years, who were undergoing TMT for the diagnosis of CAD were screened. Patients with moderate or strongly positive TMT were excluded. Diagnosed case of obstructive CAD, unstable coronary syndromes, inability to exercise on a treadmill, baseline ECG changes including Left bundle branch block (LBBB), ST depression >1 mm that precludes the interpretation of TMT and Holter test, and significant arrhythmias were the other exclusions.

The institute's ethical committee approved the study. Patients were asked to maintain a regular daily routine during the Holter test and note the time of smoking and any other relevant symptoms.

ECGs were recorded digitally (a sampling rate of 256 Hz/channel) on removable flashcards using a lightweight, 12-channel, ambulatory ECG monitor (Delma Reynolds's Life Card). The signal was recorded continuously throughout the study period. The ECG digital recordings were processed using PC-based software (life card). Only normal-to-normal beat (NN) intervals were included in the analysis. The Holter test was analyzed for the minimum, maximum, and average HR and arrhythmias. HR and ischemic changes were specifically noted 10 min before the smoking and after that every 10 min for the next 60 min. HRV analysis was also done. Any ECG changes which appeared during chest pain, dyspnea or palpitations were also analyzed.

HRV measures were calculated using time-domain measures. The measures included are presented in [Table 1]. The normal values of these measures are presented in [Table 1]. We had analyzed HRV data of 10 age-matched normal subjects to compare it with smokers and tobacco chewers. After the completion of Holter test, the patients were strongly counseled to quit smoking and tobacco chewing.
Table 1: Definitions of heart rate variability parameters and normal values of heart rate variability - time domain

Click here to view

Ethical consideration

Institute's ethics committee approved our study protocol, and informed consent was obtained from every patient or appropriate legally authorized relative. The study conforms to the ethical guidelines of the Declaration of Helsinki.

Statistical analysis

All the study subjects' data were entered into a Microsoft Excel spreadsheet (Microsoft Excel 2016TM, Microsoft Corporation, USA). The data were analyzed using SPSS software (SPSS Inc., version 23.0TM; IBM Corporation, Chicago, USA). Data were collected in a preset pro forma. The Kolmogorov–Smirnov test was used to assess the distribution of continuous variables, and the results were expressed as median and interquartile range or mean with standard deviations (SD). The significance of differences between the means of normally distributed data was evaluated using the Student's t-test and that of nonnormally distributed data was evaluated using the Mann–Whitney U-test. Categorical variables were shown as percentages and numbers. Comparison of categorical variables between the study groups was performed by the Chi-square test with the Yates' correction for continuity or the Fisher's exact test if the minimum expected count in the cell was <5. All probability values were calculated using two-sided tests, and P < 0.05 was considered statistically significant.

  Results Top

We had enrolled a total of 60 patients. All were male with an average age of 45 years in the smoker subgroup and 42 years in the tobacco chewer subgroup. The baseline characteristics are presented in [Table 2].
Table 2: Baseline characteristics

Click here to view

Average HR for smokers was 82.5 ± 14.56/min, and maximum and minimum HR was 123/min and 55/min, respectively. The average HR for tobacco chewers was 80.62 ± 13.52, and the maximum and minimum HR was 120/min and 54/min, respectively. An overview of Holter findings is presented in [Table 3].
Table 3: Holter data

Click here to view

HR was monitored 10 min before smoking/tobacco chewing, during smoking/tobacco chewing, and during the next 10 min for up to 60 min. Pairwise comparisons of HR showed that the HR rises within 10 min of smoking and tobacco chewing. It was significantly elevated for the next 20 min and came to baseline after 30 min. HR in smokers was maximum at the time of smoking, whereas HR in tobacco chewers tend to rise to a maximum at 10 min. HR at 20 min was significantly more elevated in tobacco chewers as compared to smokers [Table 4] and [Figure 1].
Figure 1: Increase in heart rate per min.

Click here to view
Table 4: Increase in heart rate from baseline

Click here to view

Arrhythmias per hour were analyzed. They were correlated with smoking and chewing episodes. Four (13.3%) patients in the smoker group and 7 (23.3%) in the tobacco-chewing group did not have even a single ectopic. We tried to correlate all these arrhythmic episodes with smoking and tobacco chewing events. Smoking significantly increased the total number of supraventricular ectopics (SVEs) and ventricular premature complexes (VPCS) from a mean of 5.03–9.99/h during smoking to 11.02 during the next hour after smoking. When arrhythmias were analyzed individually, there was a significant increase in SVEs after smoking [Figure 2]. However, the increase in VPCs did not reach statistical significance [Figure 3]. On the other hand, there was some increase in the mean number of ectopics in the tobacco-chewing group from 3.3 before to 5.3 during and 6.1 in the hour after tobacco chewing, but it did not reach statistical significance. No runs of Non sustained ventricular tachcardia (NSVT) or Ventricular tachycardia (VT) were observed in the study.
Figure 2: Supraventricular ectopics per min.

Click here to view
Figure 3: Ventricular ectopic per min.

Click here to view

Ischemic changes were monitored during Holter recording and tried to correlate with smoking and tobacco chewing. Ischemic changes were seen in 2 of the 30 patients in the smoker subgroup. No patient in the tobacco-chewing subgroup developed any significant ischemic ST-T changes.

HRV analysis [Table 5] was within the normal range, except for the HRV index. When smokers were compared with normal subjects, the HRV index was significantly less (P = 0.023). HRV parameters in tobacco chewers were normal, and no statistically significant differences were found as compared to controls.
Table 5: Heart rate variability parameters

Click here to view

  Discussion Top

Cigarette smoking significantly increases the risk of CAD.[19] Smoking reduces myocardial oxygen supply by increasing blood pressure and sympathetic tone acutely. Smokers are more prone to ventricular arrhythmias as compared to nonsmokers.[2],[3] Very few studies have evaluated the temporal relationship of electrocardiographic changes with smoking.[20]

On the other hand, the relationship of tobacco chewing with CAD and SCD is not certain.[21],[22],[23],[24] No large study has studied the acute effects of tobacco chewing on HR, ectopic beats, and HRV. In our study, the HR increased acutely and returned to baseline only after 30 min. Invasive studies have documented similar acute increases in HR during smoking.[20],[25] Pregnant females who smoke have increased fetal HRs.[26]

In tobacco chewers, the HR increased after some time period which was similar to previous studies.[10] This is an expected finding considering the slower absorption in tobacco chewing compared to smoking.

Smoking acutely increased SVEs. By decreasing parasympathetic tone and increasing sympathetic tone in atrial conduction tissues, smoking is shown to increase conduction velocities and decrease the effective refractory period, which could be the reason behind excess SVEs.[9] Smoking also increased ventricular ectopics (VEs) in our study, but this increase did not reach statistical significance similar to earlier studies.[20]

SVEs and VEs increased in tobacco chewers but did not reach statistical significance. To the best of our knowledge, no previous studies have explored the effects of acute tobacco exposure on arrhythmias. One-fourth of patients in the tobacco-chewing subgroup did not have an ectopic. Ectopics may also be related to the unburnt particles in smoke.

During smoking, ischemic episodes frequently remain inert, as was in our study.[27],[28] We did not observe any ST-segment elevation episode during or following smoking.

Smoking adversely affects the heart by increasing heart rate, causing hypercoagulable state, coronary vasospasm, endothelial dysfunction and decreasing oxygen carrying capacity of blood.[3],[4] The prognostic significance of the ST–T changes in the absence of obstructive CAD needs to be established in smokers.

No patients in the tobacco subgroup had ischemic ST-T changes, although only a small number of patients in our study and the results of this study are not generalizable. On the other hand, prior studies generally point toward the fact that the magnitude of vasoconstriction due to smoking and tobacco chewing is comparable, and this effect is likely due to nicotine or a common component of tobacco rather than due to smoke or carbon monoxide.[29] Stimulation of coronary α adrenergic receptors by circulating or locally released catecholamines may be responsible for this effect.[30] Prior studies have shown significant vasoconstriction after acute exposure to chewable tobacco.[31]

There has been a growing recognition of the importance of the ANS in CVD. Various measures of HRV provide specific, well-defined, quantitative indicators of cardiac autonomic function.[32] Large epidemiological studies have also linked an increased risk of coronary artery disease, death, and cardiac mortality with decreased HRV in general populations.[33]

The studied HRV parameters including SD normal-to-normal (SDNN), SD of average normal-to-normal (SDANN), and root mean square value of square differences (RMSSD) were within the normal range, but the HRV index was significantly less in smokers. SDNN and HRV index are the parameters expressing the overall HRV. SDANN is a marker of the spectral component with a long period, and RMSSD is a marker of a component with a short period. These methods do not substitute each other but supplant each other mutually. HRV index is a more sensitive and specific HRV analysis method, as it uses the geometrical method.[13] As in the present study, when 24 h Holter monitoring is used, the HRV index remains an important parameter of HRV. The main advantage of the geometrical method (HRV index) resides in its independence from the quality of the analyzed NN interval. The disadvantage is it requires a long period of recording.

Previous studies have shown significant HRV changes with acute tobacco smoke exposure, as in our study.[12],[19] Studies have also shown an increase in HRV immediately after smoking cessation.[16],[17]

HRV parameters in the tobacco-chewing subgroup did not vary as compared to controls. No study previously has shown any significant change in HRV parameters with tobacco chewing, although other components of the autonomic system like HR are significantly affected by tobacco chewing. Which component of tobacco smoke is responsible for autonomic dysfunction is still not clear. Carbon monoxide was implemented in some studies.[34] The role of nicotine is still not clear in autonomic dysfunction because nicotine patches release a high nicotine level. Still, it has a minimal effect on HRV.[35] RSP may be the main culprit.[36] A study of healthy volunteers demonstrated 100-μg/m3 increase in 4-hr RSP exposure which was associated with approximately a 25-m s decline in both SDNN and r-MSSD.[12]

  Conclusions Top

Both smoking and tobacco chewing significantly increase the HR acutely. Smoking leads to an increase in both supraventricular and VEs. Smoking was associated with a reduced HRV index.

Ethics clearance

Ethical clearance of the study was taken from the institute.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

Keto J, Ventola H, Jokelainen J, Linden K, Keinänen-Kiukaanniemi S, Timonen M, et al. Cardiovascular disease risk factors in relation to smoking behaviour and history: A population-based cohort study. Open Heart 2016;3:e000358.  Back to cited text no. 1
Ezzati M, Henley SJ, Thun MJ, Lopez AD. Role of smoking in global and regional cardiovascular mortality. Circulation 2005;112:489-97.  Back to cited text no. 2
Barua RS, Ambrose JA, Srivastava S, DeVoe MC, Eales-Reynolds LJ. Reactive oxygen species are involved in smoking-induced dysfunction of nitric oxide biosynthesis and upregulation of endothelial nitric oxide synthase: An in vitro demonstration in human coronary artery endothelial cells. Circulation 2003;107:2342-7.  Back to cited text no. 3
Bazzano LA, He J, Muntner P, Vupputuri S, Whelton PK. Relationship between cigarette smoking and novel risk factors for cardiovascular disease in the United States. Ann Intern Med 2003;138:891-7.  Back to cited text no. 4
Akishima S, Matsushita S, Sato F, Hyodo K, Imazuru T, Enomoto Y, et al. Cigarette-smoke-induced vasoconstriction of peripheral arteries: Evaluation by synchrotron radiation microangiography. Circ J 2007;71:418-22.  Back to cited text no. 5
Caralis DG, Deligonul U, Kern MJ, Cohen JD. Smoking is a risk factor for coronary spasm in young women. Circulation 1992;85:905-9.  Back to cited text no. 6
Lauer MS, Pashkow FJ, Larson MG, Levy D. Association of cigarette smoking with chronotropic incompetence and prognosis in the Framingham Heart Study. Circulation 1997;96:897-903.  Back to cited text no. 7
Srivastava R, Blackstone EH, Lauer MS. Association of smoking with abnormal exercise heart rate responses and long-term prognosis in a healthy, population-based cohort. Am J Med 2000;109:20-6.  Back to cited text no. 8
D'Alessandro A, Boeckelmann I, Hammwhöner M, Goette A. Nicotine, cigarette smoking and cardiac arrhythmia: An overview. Eur J Prev Cardiol 2012;19:297-305  Back to cited text no. 9
Benowitz NL, Porchet H, Sheiner L, Jacob P 3rd. Nicotine absorption and cardiovascular effects with smokeless tobacco use: Comparison with cigarettes and nicotine gum. Clin Pharmacol Ther 1988;44:23-8.  Back to cited text no. 10
Benowitz NL, Jacob P 3rd, Yu L. Daily use of smokeless tobacco: Systemic effects. Ann Intern Med 1989;111:112-6.  Back to cited text no. 11
Wennmalm A, Benthin G, Granström EF, Persson L, Petersson AS, Winell S. Relation between tobacco use and urinary excretion of thromboxane A2 and prostacyclin metabolites in young men. Circulation 1991;83:1698-704.  Back to cited text no. 12
Pope CA 3rd, Eatough DJ, Gold DR, Pang Y, Nielsen KR, Nath P, et al. Acute exposure to environmental tobacco smoke and heart rate variability. Environ Health Perspect 2001;109:711-6.  Back to cited text no. 13
Camm J, Malik M, Bigger T Jr, Breithardt G, et al. Heart rate variability. Standards of measurement, physiological interpretation, and clinical use. Task Force of the European Society of Cardiology and the North American Society of Pacing and Electrophysiology. Eur Heart J 1996;17:354-81.  Back to cited text no. 14
Dekker JM, Crow RS, Folsom AR, Hannan PJ, Liao D, Swenne CA, et al. Low heart rate variability in a 2-minute rhythm strip predicts risk of coronary heart disease and mortality from several causes: The ARIC Study. Atherosclerosis Risk In Communities. Circulation 2000;102:1239-44.  Back to cited text no. 15
de Bruyne MC, Kors JA, Hoes AW, Klootwijk P, Dekker JM, Hofman A, et al. Both decreased and increased heart rate variability on the standard 10-second electrocardiogram predict cardiac mortality in the elderly: The Rotterdam Study. Am J Epidemiol 1999;150:1282-8.  Back to cited text no. 16
Stein PK, Rottman JN, Kleiger RE. Effect of 21 mg transdermal nicotine patches and smoking cessation on heart rate variability. Am J Cardiol 1996;77:701-5.  Back to cited text no. 17
Yotsukura M, Koide Y, Fujii K, Tomono Y, Katayama A, Ando H, et al. Heart rate variability during the first month of smoking cessation. Am Heart J 1998;135:1004-9.  Back to cited text no. 18
Prasad DS, Kabir Z, Dash AK, Das BC. Smoking and cardiovascular health: A review of the epidemiology, pathogenesis, prevention and control of tobacco. Indian J Med Sci 2009;63:520-33.  Back to cited text no. 19
[PUBMED]  [Full text]  
Ramakrishnan S, Bhatt K, Dubey AK, Roy A, Singh S, Naik N, et al. Acute electrocardiographic changes during smoking: An observational study. BMJ Open 2013;3:e002486.  Back to cited text no. 20
Bolinder G, Alfredsson L, Englund A, de Faire U. Smokeless tobacco use and increased cardiovascular mortality among Swedish construction workers. Am J Public Health 1994;84:399-404.  Back to cited text no. 21
Hergens MP, Alfredsson L, Bolinder G, Lambe M, Pershagen G, Ye W. Long‐term use of Swedish moist snuff and the risk of myocardial infarction amongst men. J Intern Med 2007;262:351-9.  Back to cited text no. 22
Teo KK, Ounpuu S, Hawken S, Pandey MR, Valentin V, Hunt D, et al. Tobacco use and risk of myocardial infarction in 52 countries in the INTERHEART study: A case-control study. Lancet 2006;368:647-58.  Back to cited text no. 23
Piano MR, Benowitz NL, Fitzgerald GA, Corbridge S, Heath J, Hahn E, et al. Impact of smokeless tobacco products on cardiovascular disease: Implications for policy, prevention, and treatment: A policy statement from the American Heart Association. Circulation 2010;122:1520-44.  Back to cited text no. 24
Zhu BQ, Parmley WW. Hemodynamic and vascular effects of active and passive smoking. Am Heart J 1995;130:1270-5.  Back to cited text no. 25
Graça LM, Cardoso CG, Clode N, Calhaz-Jorge C. Acute effects of maternal cigarette smoking on fetal heart rate and fetal body movements felt by the mother. J Perinat Med 1991;19:385-90.  Back to cited text no. 26
Conti CR, Bavry AA, Petersen JW. Silent ischemia: Clinical relevance. J Am Coll Cardiol 2012;59:435-41.  Back to cited text no. 27
Valle GA, Lemberg L. Silent ischemia: A clinical update. Chest 1990;97:186-91.  Back to cited text no. 28
Salahuddin S, Prabhakaran D, Roy A. Pathophysiological mechanisms of tobacco-related CVD. Glob Heart 2012;7:113-20.  Back to cited text no. 29
Winniford MD, Wheelan KR, Kremers MS, Ugolini V, van den Berg E Jr., Niggemann EH, et al. Smoking-induced coronary vasoconstriction in patients with atherosclerotic coronary artery disease: Evidence for adrenergically mediated alterations in coronary artery tone. Circulation 1986;73:662-7.  Back to cited text no. 30
Ramakrishnan S, Thangjam R, Roy A, Singh S, Ramakrishnan L, Seth S, et al. Acute effects of tobacco chewing on the systemic, pulmonary and coronary circulation. Am J Cardiovasc Drugs 2011;11:109-14.  Back to cited text no. 31
Camm J, Malik M, Bigger T Jr, Breithardt G. Heart rate variability: Standards of measurement, physiological interpretation and clinical use. Task Force of the European Society of Cardiology and the North American Society of Pacing and Electrophysiology. Circulation 1996;93:1043-65.  Back to cited text no. 32
Hillebrand S, Gast KB, de Mutsert R, Swenne CA, Jukema JW, Middeldorp S, et al. Heart rate variability and first cardiovascular event in populations without known cardiovascular disease: Meta-analysis and dose-response meta-regression. Europace 2013;15:742-9.  Back to cited text no. 33
Hirakawa H, Nakamura T, Hayashida Y. Effect of carbon dioxide on autonomic cardiovascular responses to systemic hypoxia in conscious rats. Am J Physiol 1997;273:R747-54.  Back to cited text no. 34
Niedermaier ON, Smith ML, Beightol LA, Zukowska-Grojec Z, Goldstein DS, Eckberg DL. Influence of cigarette smoking on human autonomic function. Circulation 1993;88:562-71.  Back to cited text no. 35
Huang W, Zhu T, Pan X, Hu M, Lu SE, Lin Y, et al. Air pollution and autonomic and vascular dysfunction in patients with cardiovascular disease: Interactions of systemic inflammation, overweight, and gender. Am J Epidemiol 2012;176:117-26.  Back to cited text no. 36


  [Figure 1], [Figure 2], [Figure 3]

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5]


Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
Access Statistics
Email Alert *
Add to My List *
* Registration required (free)

  In this article
   Materials and Me...
   Article Figures
   Article Tables

 Article Access Statistics
    PDF Downloaded130    
    Comments [Add]    

Recommend this journal