6/16/2016

Laryngeal ndings and acoustic changes in light cigar smokers

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Home> Laryngeal ndings and acoustic changes in light cigar smokers

Laryngeal ndings and acoustic changes in

light cigar smokers
|Reprints
June 5, 2015
by Abdul-latif Hamdan, MD, FACS; Randa Al-Barazi, MD; Jihad Ashkar, MD; Sami Husseini, MD; Alexander
Dowli, MD; Nabil Fuleihan, MD

Abstract
The aim of this prospective study was to look at the laryngeal ndings and acoustic changes in light cigar
smokers in comparison to nonsmokers, in the setting of a voice clinic. A total of 22 cigar smokers and 19
nonsmokers used as controls were enrolled in the study. Demographic data included age, number of years
smoking, number of cigars per week, history of allergy, and history of reux. The confounding eects of allergy
and reux were accounted for in the control group. Subjects underwent laryngeal endoscopy and acoustic
analysis. On laryngeal endoscopy, the most common laryngeal nding was thick mucus. There was no
signicant dierence in the prevalence of any of the laryngeal ndings in cigar smokers vs. controls. In
comparison with the control group, both the fundamental frequency and habitual pitch were signicantly lower
in cigar smokers (pvalue = 0.034 and 0.004, respectively). We conclude that cigar smokers have lower
fundamental frequency and habitual pitch compared to nonsmokers.

Introduction
Cigar consumption is rapidly increasing in the United States. It rose by 44.5% from 1993 through
1996.1Based on a survey conducted among Massachusetts adults, cigar usage increased dramatically in men
aged 18 to 34 years of age between 1993 and 1997-8, in conjunction with national increases in sales and
marketing of cigars.2In 2013, a randomized survey of 60,000 noninstitutionalized adults >18 years of age
regarding the usage of dierent types of tobacco showed that 12.6% smoked cigars and 2% smoked them
daily.3This increase is partially due to the perception that cigars are a safe alternative to cigarettes. Cigar
smokers are roughly three times as likely as those who do not smoke cigars to believe cigars are a safer
alternative to cigarettes.2Despite the fact that cigar smoking poses signicant risks that lead to welldocumented morbidity and mortality, the perception that it is less harmful than cigarette smoking does not
appear to change over time.
Large, prospective cohort studies have strongly supported an association between cigar smoking and
mortality from several types of diseases.4In a prospective study from 24 British towns with a mean follow-up
of 22 years, pipe/cigar smokers showed a signicantly higher risk of major coronary heart disease, stroke,
diabetes, and cancer when compared with never-smokers.5Activation of inammation and hemostasis may be
mechanisms by which cigarette and pipe/cigar smoking increase cardiovascular risk.6,7
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Laryngeal ndings and acoustic changes in light cigar smokers

In a study by Shapiro et al, looking at the association between cigar smoking and death from tobacco-related
cancers in a large, prospective cohort of U.S. men, there was an increased risk of death from cancers of the
lung, oral cavity, pharynx, larynx, and esophagus.4Others have also shown that prolonged usage of tobacco
products, including cigars, is associated with the development of rectal cancer and increased stomach cancer
mortality in men and women.8,9
Despite the reports relating cigar smoking to the prevalence of cancer and cardiovascular diseases, no study
has looked at the laryngeal endoscopic changes and acoustic characteristics of cigar smokers. Based on a
PubMed search using words voice and cigar, we found no previous reports regarding this perspective.
The purpose of our study is to look at the laryngeal ndings and acoustic changes in light cigar smokers in
comparison to controls. The authors hypothesize that cigar smoking can aect voice and vocal fold mucosa.

Patients and methods

A total of 22 male cigar smokers were recruited for this study after signing the informed consent approved by
the Institution Review Board at the American University of Beirut. Demographic data included age, sex,
frequency of cigar smoking per week, number of years smoking, history of allergy, and history of reux. A total
of 19 male controls were also included. The confounding eects of allergy and reux were accounted for by
having a similar prevalence in both smokers and nonsmokers. All subjects were males above the age of 18
years.
Laryngeal evaluation.All subjects underwent laryngeal videostroboscopic evaluation using a 70 rigid
telescope. The presence of any vocal fold masses (polyps, cysts, nodules, edema, and granulomas), lesions
(leukoplakia, erythroplakia), and/or thick mucus or dilated vessels was reported. The presence of mucus was
reported when threads of mucus were spread at the free edges of the vocal folds.
Acoustic evaluation.Subjects also underwent acoustic analysis. While the patient was seated in a quiet
oce, his vocal signal was recorded directly into the system using a condenser microphone at a distance of 15
cm from the mouth. The following acoustic variables were measured: average fundamental frequency, relative
average perturbation, shimmer, noise-to-harmonic ratio, voice turbulence index, maximum phonation time, and
habitual pitch.
The maximum phonation time was calculated by asking the subject to take a deep breath and sustain
phonation for as long as he could. The habitual pitch was measured by asking the subject to count to 10 in a
normal voice. The remaining variables were measured by asking the subject to sustain the vowel /ah/ for 2
seconds, using the voice quality assessment module of the Visi-Pitch system (KayPENTAX; Montvale, N.J.).
The acoustic analysis test was repeated twice to provide a good estimate.
Statistical method.Frequencies, means, and standard deviation (SD) were used to describe the study
sample. We assessed dierences in the laryngeal ndings and acoustic analysis parameters between the two
groups. Nonparametric tests, the Mann-WhitneyUtest and the chi-square test, were used for continuous and
categorical variables, respectively. Apvalue <0.05 was considered signicant. All analysis was conducted
using the Statistical Package for the Social Sciences software version 22 (IBM; Armonk, N.Y.).

Results
Demographic data.The cigar-smoking group included 22 males with a mean age of 44.1 6.3 years, and the
control group included 19 males with a mean age of 29.5 6.7 years. The average number of cigars smoked
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per week was 11.6 8.5, and the duration of smoking was approximately 14 years. Five of the 22 (22.7%)2/8

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Laryngeal ndings and acoustic changes in light cigar smokers

cigar smokers vs. 4 of 19 controls (21.1%) had a history of reux, and 3 of 22 (13.6%) smokers had a history of
allergy vs. 3 (15.8%) of the controls (table 1).

Table 1. Baseline characteristics of study

population and controls

Cigar smokers (n = 22) Controls (n = 19)

Age (years), mean SD

44.1 6.3

29.5 6.7

Sex

Male

Male

No. cigars smoked/wk, mean SD) 11.6 8.5

Years of smoking, mean SD)

14.2 9.1

Reux

22.7%

21.1%

Allergy

14.0%

15.8%

Laryngeal ndings.The most common laryngeal nding in the cigar-smoking group was the presence of
excessive mucus in 7 of 22 (31.8%) subjects. Only 1 (4.5%) subject had vocal fold edema and 1 had a vocal
fold cyst. When cigar smokers were compared with the control group, there was no signicant dierence in the
prevalence of any of the laryngeal ndings (table 2).

Table 2. Laryngeal ndings in cigar smokers

and controls
Findings Cigar smokers (n = 22) Controls (n = 19) pValue
Polyps

0.0%

0.0%

Nodules 0.0%

0.0%

Edema

4.5%

0.0%

Cysts

4.5%

0.0%

Mucus

31.8%

31.6%

0.617

Acoustic analysis ndings.Both the fundamental frequency and habitual pitch were signicantly lower in the
cigar smokers than in the controls (pvalues = 0.034 and 0.004, respectively). There was no signicant
dierence in the prevalence of any of the remaining acoustic variables (table 3).

Table 3. Acoustic ndings in cigar smokers

and controls
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Cigar
Controls
smokers
pValue*

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pValue*

(n = 22)

(n = 19)

Mean

SD

Mean

SD

FO (Hz)

111.9

14.9

122.6

14.9 0.034

RAP (%)

0.85

0.61

0.7

0.48 0.677

Shimmer (%)

4.0

2.0

3.4

1.5

NHR

0.13

0.043

0.1

0.03 0.592

VTI

0.03

0.008

0.03

0.01 0.875

MPT (sec)

19.9

8.3

22.0

5.9

Habitual pitch (Hz)

109.7

15.7

124.3

15.9 0.004

0.505

0.136

*Signicant forpvalue <0.05

Key: FO = fundamental frequency; RAP = relative
average perturbation; NHR = noise-to-harmonic ratio;
VTI = voice turbulence index; MPT = maximum
phonation time.

Discussion
Cigarette smoking is known to aect voice. Its carcinogenic and inammatory eects have been thoroughly
reported in the literature. In a study examining the eect of smoking and drinking on histologic changes in
laryngeal tissue, metaplasia in the supraglottic region was found to be increased with aging, alcohol
consumption, and tobacco usage.10There was also a signicant dierence in the thickness of the epithelium
of the supraglottic region and vocal folds in smokers vs. nonsmokers.
In a study by Dosemeci et al, which examined the risks of laryngeal cancer in relation to subsites among
smokers, the highest risks were observed in the supraglottic region of the larynx.11In a histologic examination
of vocal fold specimens by Muller and Krohn, which examined the frequency of normal squamous epithelium
and precancerous lesions, namely dysplasia and carcinoma in situ, the relative frequency of normal epithelium
decreased from 83.3% in nonsmokers to 30.6% in heavy smokers, and the incidence of precancerous lesions
increased from 4.2% in nonsmokers to 47.2% in heavy smokers.12
Although all forms of smoking are harmful, smoking pipes or cigars has been associated with lower exposure
to the lethal products of tobacco and lower levels of morbidity and mortality than smoking cigarettes. In fact, in
looking at the eects of the type of smoking on biologic indices of tobacco exposure and toxicity, FunckBrentano et al showed that pipe or cigar smoking was associated with lower exposure to products of tobacco
metabolism than cigarette smoking and to an absence of cytochrome P4501A induction, which is believed to
be a major pathway activating carcinogens from tobacco smoke.13However, in a case-control epidemiologic
study conducted to determine the relationship between quantities and types of tobacco and the risk of cancers
at various head and neck sites, despite substantial variations in the tobacco-associated risk for each site, cigar
smokers experienced excess risks of cancers of the tongue, pharynx, and larynx.14
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The results of our study are not in accordance with the literature, as there was no signicant change, at least

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Laryngeal ndings and acoustic changes in light cigar smokers

endoscopically, in the vocal fold mucosa and no signicant dierence in the prevalence of any of the laryngeal
ndings in comparison with controls. There are several reasons that our results do not agree with those from
previous reports: the small sample size, the relatively short duration of smoking and, most importantly, our
subjects' light smoking (small number of cigars smoked per week). Nevertheless, our results do not mitigate
the conclusions from previous studies and should not preclude us from the belief that cigar smoking has an
eect on the laryngeal mucosa.
Besides the potential carcinogenic eect of smoking on the laryngeal mucosa, smoking has an irritant and
inammatory eect on the vocal fold mucosa, vessels, and mucociliary clearance. Smoking is considered one
of the main etiologic factors in the development of vocal fold edema and polypoid degeneration. Studies have
shown that the duration of exposure correlates with histologic changes, with longer years of smoking resulting
in more severe edema and polyp formation.15
Pechacek et al have reported in their analysis of 306 male cigar and/or pipe smokers that serum levels of
thiocyanate-a biological marker of tobacco use that can be detected in the serum or saliva of smokers-were
signicantly higher in smokers than in nonsmokers but lower than in cigarette smokers.16These results were
conrmed by other authors, as well, who have demonstrated that this serum level is also related to the amount
of product smoke.17Thiocyanate levels are signicantly higher in smokers than passive and never-smokers,
and an increased serum level has been linked to inammatory reactions leading to pulmonary brosis.
Because we did not test serum or salivary thiocyanate levels in our study, we cannot draw any conclusions
regarding the presence or absence of signicant inammatory changes in cigar smokers in relation to the
extent of their smoking. The results of our study are not in accordance with the hypothesis regarding the eect
of cigar smoking on vocal fold mucosa. The inammatory eect of cigar smoking was not very evident on
laryngeal examination; there was no signicant dierence in the prevalence of vocal fold edema or laryngitis in
smokers vs. controls, and only 1 subject had vocal fold edema. Again, this can be attributed to the light
smoking in the subjects recruited, to the small sample size, and to the imaging technique used (laryngeal
videostroboscopy). High-speed imaging and/or videokymography might be more revealing of subtle mucosal
changes and closure patterns in future investigations.
In addition to its inammatory eect, smoking is also known to decrease the mucociliary clearance of the
laryngeal mucosa, resulting in excess mucus secretions and pooling. Brown et al reported a higher prevalence
of chronic cough and phlegm (mucus) in cigar and pipe smokers when compared with nonsmokers.18
Several studies have also conrmed that allergy has a higher prevalence among smokers compared to
nonsmokers, which means that the presence of mucus could be secondary to both allergy and smoking. In a
study by Taylor et al, cigarette smoking was found to be associated with small increases in some markers of
allergy and that these changes were most likely acquired after the onset of smoking.19Likewise, to study the
relation between smoking habits, allergy, and IgE values, Zetterstrm et al investigated the adjuvant eect of
smoking on IgE antibody production.20Their results indicated an increase in IgE antibodies in smokers, which
could be due to the damaging eect of smoking on the upper airway mucosa.
In our study, the high prevalence of mucus in cigar smokers cannot be attributed solely to smoking because of
the lack of a signicant dierence between the two groups. The relatively high prevalence in both cigar
smokers (31.8%) and controls (31.6%) might be secondary to the confounding eect of allergy that was
present in 14 and 15.8%, respectively, of the cases.
With respect to acoustic analysis, studies investigating the vocal changes in smokers have demonstrated a
lowering of pitch. Guimaraes reported a decrease in pitch across all speech tasks in smokers, although
dierences did not reach statistical signicance.21Damborenea Tajada et al also reported a lower fundamental
frequency for the sustained vowel /a/ in nondysphonic smokers, along with an increase in cycle-to-cycle
variation in frequency (jitter).22Wiskirska-Woznica et al, in a study including 20 nondysphonic smokers,
showed a decrease in the fundamental frequency and an increase in jitter.23

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In our study, the cigar-smoking group also had a signicantly lower fundamental frequency and habitual pitch
compared to the control group. Hypothetically, this can be attributed to two factors. One factor is an increase
in mass with resultant decrease in pitch. The increase in mass can be in the form of a lesion, edema of the
vocal fold, or excessive mucus. The laryngeal ndings in our study can only partially support this hypothesis in
view of the high prevalence of mucus in cigar smokers and the limited vocal fold changes, namely the
presence of edema in 1 patient and a cyst in another. Another factor is the possible decrease or alteration in
breathing support as evidenced by a reduction the maximum phonation time, even though it is not signicant.
In a study using99mTc-labeled sulfur colloid particles to examine the degree to which cigar smokers inhale and
the association between self-reported inhalation and observable cigar particle deposition in the lung, results
indicated that cigar smoke is inhaled regardless of self-reported noninhalation and smoking history of the
subjects.24Thus, even though cigar smokers more often than not deny a history of smoke inhalation, as most
of our subjects reported (personal communication with the rst author), cigar smoke is inhaled and thus aects
the respiratory system. Consequently, cigar smokers may have reduced breathing support, which in turn can
aect pitch.
Our study is the rst to look at the laryngeal ndings and acoustic changes in subjects who smoke cigars.
Nevertheless, it carries some limitations: one is the lack of perceptual evaluation of the voice quality in subjects
who smoke, and another is the limited number of subjects we were able to recruit for our study.
Despite the limited number of subjects enrolled in our study, our results are in accordance with the hypothesis
that cigar smoking aects voice. Cigar smokers are more likely to have a low fundamental frequency and
habitual pitch than controls. These ndings could represent early symptoms and signs of vocal fold changes
not seen on laryngeal videostroboscopy. Videokympgraphy and/or high-speed imaging might be better at
detecting subtle glottic changes. The lack of signicant vocal fold changes in our study can also be attributed
to the small sample size and the light smoking.
In conclusion, the dramatic rise in cigar consumption brings with it the need to promote early-prevention
programs and to incorporate cigar smoking into tobacco cessation programs.

References
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mortality in US adults: The Cancer Prevention Study II. Int J Cancer 2002; 101 (4): 380-9.
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9. Sharpe CR, Siemiatycki JA, Rachet BP. The eects of smoking on the risk of colorectal cancer. Dis Colon
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on biological indices of tobacco exposure and toxicity. Lung Cancer 2006; 54 (1): 11-18.
14. Stockwell HG, Lyman GH. Impact of smoking and smokeless tobacco on the risk of cancer of the head
and neck. Head Neck Surg 1986; 9 (2): 104-10.
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thiocyanate measures. JAMA 1985; 254 (23): 3330-2.
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tobacco smoke exposure? Am J Public Health 1987; 77 (11): 1412-16.
18. Brown CA, Woodward M, Tunstall-Pedoe H. Prevalence of chronic cough and phlegm among male cigar
and pipe smokers: Results of the Scottish Heart Health Study. Thorax 1993; 48 (11): 1163-7.
19. Taylor RG, Gross E, Joyce H ,et al. Smoking, allergy, and the dierential white blood cell count. Thorax
1985; 40 (1): 17-22.
20. Zetterstrm O, Osterman K, Machado L, Johansson SG. Another smoking hazard: Raised serum IgE
concentration and increased risk of occupational allergy. Br Med J (Clin Res Ed) 1981; 283 (6301): 121517.
21. Guimaraes I. An electrolaryngographic study of dysphonic Portuguese speakers [PhD Dissertation].
London, UK:University of London (University College London); 2002.
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acoustic voice analysis [in Spanish]. Acta Otorrinolaring Esp 1999; 50 (6): 448-52.
23. Wiskirska-Woznica B, Obrebowski A, Swidziski P ,et al. Eect of smoking on phonation [in Polish]. Przegl
Lek 2004; 61 (10): 1068-70.
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From the Department of Otolaryngology, American University of Beirut Medical Center, Beirut, Lebanon.
Corresponding author: Abdul-latif Hamdan, MD, American University of Beirut Medical Center, PO Box
110236, Beirut, Lebanon. Email:ah77@aub.edu.lb[1]
Ear Nose Throat J. 2015 June;94(6):231-235

Topics
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