90 Indian Dermatology Online Journal-
Dr. Ayman A. Zayed,
P.O. Box ‑ 13046,
Department of Internal
Diabetes and Metabolism,
Faculty of Medicine,
1Department of General
Surgery, Faculty of
of Anesthesia, Faculty of
and Clinical Pharmacy,
Faculty of Pharmacy,
Jordan University Hospital,
The University of Jordan,
Aims: To determine if there is a signicant association between premature hair graying and cigarette smoking.
Materials and Methods: A cross‑sectional observational study was conducted in a nonclinical setting on
207 participants on August 24 until 25, 2010. Participants were classied into two groups [premature hair
graying (PHG) and normal hair graying]. PHG was dened as the rst appearance of gray hair before the age of 30.
Data were collected using an interview questionnaire and measurements of body mass index, waist circumference,
fasting blood glucose and blood pressure. Collected data were statistically analyzed using SPSS 16, Chicago, IL.
Results: Of the 207 subjects, 104 (50.2%) had rst appearance of gray hair before the age of 30 (PHG group)
while the other 103 (49.8%) were considered normal hair graying group. The prevalence of smokers in the “PHG”
group was higher (40.2% vs. 24.7%, P=0.031). Smokers had earlier onset of hair graying (smokers: 31 (7.4)
vs. nonsmokers: 34 (8.6), P=0.034). Using multiple logistic regression with conditional likelihood, smokers
were two and half times (95% CI: 1.5‑4.6) more prone to develop PHG. Conclusion: This study suggests that
there is a signicant relation (with adjusted odds ratio of two and half) between onset of gray hair before the
age of 30 and cigarette smoking.
Key words: Jordan, premature hair graying, smoking
It is well accepted that gray hair is a natural
phenomenon of age in humans. There is
also some evidence that age is associated
with increased graying in mice as well.
Premature hair graying (PHG) has been linked
to certain autoimmune disorders such as
autoimmune thyroid disease and pernicious
anaemia and to several rare premature aging
syndromes (e.g., Werner’s syndrome). In
addition, a link between smoking and gray hair in
both men and women and between smoking and
hair loss in men has been reported.[4‑6] Because
of this, PHG has attracted the attention of the
medical community. Could PHG be a marker
of early aging of organs and thus premature
morbidity and mortality?
Research exploring the relationship of PHG to
smoking has been very little worldwide and does
not exist in the Middle East.
Because of this rarity of studies in this eld, this
particular study was undertaken to determine the
association between PHG and cigarette smoking
in the Jordanian population.
MATERIALS AND METHODS
A cross‑sectional observational study that
aimed at evaluating the association of smoking
with PHG. It was conducted in a nonclinical
setting involving 207 participants (94 men and
113 women) over a period of 2 days from August
24 until August 25, 2010. The participants
represent a random sample of Jordanian people
who participated willingly in this public health
Collected data were entered into Statistical
Package for Social Sciences (SPSS16, Chicago,
IL). Data were expressed as mean (SD). Data
were subdivided between two groups (PHG and
normal hair graying). PHG was dened as the
rst appearance of gray hair before the age of
30. Whereas in the literature, other denitions
were used. (See discussion section).
Smokers’ hair: Does smoking cause premature
Ayman A. Zayed, Awni D. Shahait1, Musa N. Ayoub2, Al‑Motassem Yousef3
Access this article online
Quick Response Code:
Zayed, et al.: Premature hair graying and smoking
Indian Dermatology Online Journal -
Data of continuous nature [age of rst appearance of gray hair,
height, weight, body mass index (BMI), waist circumference,
fasting blood glucose, systolic blood pressure and diastolic
blood pressure] were compared between the two groups by
independent Student t‑test. Data of categorical nature (gender,
smoking behavior and medical history of hypertension,
diabetes, and dyslipidemia) were compared between the two
groups by Chi square. Despite its importance, family history
was not included in this survey, because it was subjected to
recall bias since the onset of hair graying in the family members
was not exceptionally remembered by the participants. Multiple
logistic regression was utilized to discern the relationship
between signicant variables and the susceptibility to PHG.
A nonsmoker was dened as someone who never smoked.
However, the range of smoking among the smokers in this
study was between one to 70 cigarettes per year. Those who
had smoked in the past were not included in the study.
BMI was calculated by dividing the body weight in kilograms
by the height in square meters.
The total number of people who agreed to participate was
207 subjects, half of them had PHG (n=104) [Table 1]. Men
and women were equally represented in the whole sample
(men: 94 (45.4%)) and in the two subgroups (men in PHG
group: 51 (49%), P=0.29). The participants covered a wide
range of age categories with an average age of 44 (11.6)
years (range: 18‑65 years). One quarter of recruits was below
the age of 35.3 years, one quarter above the age of 53.7 and
with a median age of 44.5 years.
The average age for the rst appearance of gray hair was
31.7 years with one quarter was below the age of 25, one quarter
above the age of 40 and a median age of 30 years. There was
15 years difference in age at which hair graying was rst noted
between the two groups [25.0 (4.7) vs. 40 (5.3), P<0.001].
There was no statistically significant difference in the
demographics between the two groups. There were no
differences in their body weight [78.8 (15) vs. 78.0 (15.3) kg,
P=0.73]; height [1.67 (0.09) vs. 1.65 (0.09) m, P=0.11];
BMI [28.9 (5.3) vs. 28.1 (5.3) kg/m2, P=0.3]; waist
circumference [95.6 (14.4) vs. 96.5 (12.6) cm, P=0.67]; fasting
blood glucose [104.3 (26.8) vs. 108.5 (25.9) g/dL, P=0.29];
systolic blood pressure [121.6 (11.3) vs. 123.7 (16.7) mmHg,
P=0.32] and diastolic blood pressure [80.1 (7.5) vs.
82.0 (8.2) mmHg, P=0.11] [Table 1].
The prevalence of physician‑diagnosed diabetes was
similar between the two groups (5.8% vs. 11.7%, P=0.13).
The prevalence of hypertension was lower in subjects with
PHG (7.7% vs. 28.2%, P<0.001). The prevalence of smokers
in the “PHG” was higher (40.2% vs. 24.7%, P=0.031).
Smokers had earlier onset of hair graying [smokers: 31 (7.4)
vs. nonsmokers: 34 (8.6), P=0.034] in the whole sample.
Backward stepwise multiple logistic regression with conditional
likelihood was used to nd out the best subset of variables
to predict PHG. The logistic regression was specied for
signicance level of 0.05 for entry and at level of 0.1 for removal.
The different models were compared by conditional logistic
regression, and minus two log likelihood ratio statistic was used
in comparing the tness of combined models. Two variables
were evaluated for susceptibility; smoking behavior and medical
history of hypertension. Smoking behavior remained statistically
signicant with adjusted odds ratio of 2.5 (95% CI: 1.5‑4.6).
Besides being a well‑known risk factor for cardiovascular
disease, smoking was reported to be associated with an
increase in apparent biological age over chronological age.
Model D. indicates that people who smoke have characteristic
facial changes similar to those seen in premature aging.
Smoking was also linked to PHG. Mosley and Gibbs reported
a signicant relation between gray hair and smoking. Of their
606 patients aged over 30 years, 152 of each sex, smoked.
They indicated a signicant association between gray hair
and smoking for all age groups in both sexes with overall
odds ratio of 4.40 (3.24‑5.96). However, they did not mention
their denition of gray hair. Our cross‑sectional observational
study showed similar results. Smokers had earlier onset of
hair graying [smokers: 31 (7.4) vs. nonsmokers: 34 (8.6),
P=0.034] in the whole sample with adjusted odds ratio of 2.5
Table 1: Clinical characteristics of participants by the
onset of first appearance of gray hair
Variable Premature hair
Age (years) 40.5±12.8 52.9±11.9 <0.000
Height (m) 1.67 ±0.09 1.65±0.09 0.11
Weight (kg) 78.8±15 78±15.3 0.73
BMI (kg/m2) 28.9±5.3 28.1±5.3 0.3
95.6±14.4 96.5±12.6 0.67
104.3±26.8 108.5±25.9 0.29
Diabetes 6 (5.8) 12 (11.7) 0.13
121. 6±11 .3 123.7±16.7 0.32
80.1±7.5 82±8.2 0 .11
Hypertension 8 (7.7) 29 (28.2) <0.001
BMI: Body mass index
Zayed, et al.: Premature hair graying and smoking
92 Indian Dermatology Online Journal-
(95% CI: 1.5‑4.6). On the other hand, there was no signicant
association between PHG and BMI, waist circumference,
fasting blood glucose or blood pressure. It should be noted
that the prevalence of hypertension was lower in subjects
with PHG (7.7% vs. 28.2%, P < 0.001), despite being
smokers. This could be related to the fact that PHG group
was signicantly younger than the normal hair graying group
[40.5 (12.8) vs. 52.9 (11.9) years, P<0.000].
To our knowledge, there is no universal denition of PHG. Gould,
et al. and Glasser dened PHG if 50% of hair is gray before the
age of 50.[9,10] On the other hand, others considered participants
to have PHG if all or most of their hair is gray before the age of
40.[11,12] Whereas Trueb adopted the threshold of PHG to be at
the age of 20 in Caucasian and at the age of 30 in Africans, but
he did not specify the percentage of gray hair. In our study, we
considered participants to have PHG if the onset of visible gray
hair is before the age of 30. The reason that this age was chosen
because it has been proposed that for every decade after the
age of 30, there is a decrease of 10‑20% in pigment‑producing
epidermal melanocytes.[14,15] This melanocyte decrease is one
of the proposed mechanisms of hair graying.
The mechanisms by which smoking causes hair graying are
incompletely understood. The color of hair mainly relies on
the presence or absence of melanin pigment produced by the
melanocytes. It has been indicated that smoking could be
associated with generating huge amounts of reactive oxygen
species leading to increased oxidative stress. This pro‑oxidant
effect of smoking could lead to damage the melanin‑producing
cells, the melanocytes. This theory is supported by the observation
that melanocytes in gray hair bulbs are frequently highly
vacuolated, a common response to increased oxidative stress.
A limiting factor throughout this study was that there is no
temporal relationship and it is impossible to distinguish between
cause and effect. For this reason surveys such as this can be
regarded as hypothesis‑generation and not hypothesis‑testing.
Other limitations include left censorship, and the potential that
nonresponders are of different quality than the responders.
This hypothesis‑generating study suggests that there is a
signicant relation (with adjusted odds ratio of two and half)
between onset of gray hair before the age of 30 years and
cigarette smoking in a random sample of Jordanian people.
We think that the results of this study are important for young
smokers especially females and for policy makers in the elds
of public health and preventive medicine in their continuous
war against smoking.
1. Damon A, Roen JL. Aging in the Soloman Islands and the United States:
Tests of Pearl’s hypothesis. Hum Biol 1973;45:683‑93.
2. Morse HC 3rd, Yetter RA, Stimping JH, Pitts OM, Fredrickson TN,
Hartley JW. Greying with age in mice: Relation to expression of murine
leukemia viruses. Cell 1985;41:439‑48.
3. Trueb RM. Oxidative stress in ageing of hair. Int J Trichology
4. Mosley JG, Gibbs AC. Premature grey hair and hair loss among smokers:
A new opportunity for health education? BMJ 1996;313:1616.
5. Su LH, Chen TH. Association of androgenetic alopecia with smoking
and its prevalence among Asian men: A community‑based survey. Arch
6. Trueb RM. Association between smoking and hair loss: Another
opportunity for health education against smoking? Dermatology
7. Bulpitt CJ, Shipley MJ, Broughton PM, Fletcher AE, Markowe HL,
Marmot MG, et al. The assessment of biological age: A report from the
Department of Environment Study. Aging (Milano) 1994;6:181‑91.
8. Model D. Smoker’s face: An underrated clinical sign? Br Med J (Clin
Res Ed) 1985;291:1760‑2.
9. Gould L, Reddy CV, Oh KC, Kim SG, Becker W. Premature hair graying:
A probable coronary risk factor. Angiology 1978;29:800‑3.
10. Glasser M. Is early onset of gray hair a risk factor? Med Hypotheses
11. Morton DJ, Kritz‑Silverstein D, Riley DJ, Barrett‑Connor EL,
Wingard DL. Premature graying, balding, and low bone mineral density
in older women and men: The Rancho Bernardo study. J Aging Health
12. Rosen CJ, Holick MF, Millard PS. Premature graying of hair is a risk
marker for osteopenia. J Clin Endocrinol Metab 1994;79:854‑7.
13. Trueb RM. Pharmacologic interventions in aging hair. Clin Interv Aging
14. Quevedo WC, Szabo G, Virks J. Inuence of age and UV on the
populations of dopa‑positive melanocytes in human skin. J Invest
15. Whiteman DC, Parsons PG, Green AC. Determinants of melanocyte
density in adult human skin. Arch Dermatol Res 1999;291:511‑6.
Cite this article as: Zayed AA, Shahait AD, Ayoub MN, Yousef A. Smokers'
hair: Does smoking cause premature hair graying?. Indian Dermatol Online
Source of Support: Nil, Conict of Interest: None declared.