Key words:
Environmental tobacco smoke - gingiva - melanin - passive smoking - young adults
INTRODUCTION
The World Health Organization has indicated that chronic environmental tobacco smoke
(ETS) exposure, especially among young adults increases the risk of serious health
hazards such as impaired lung function and increased incidence of subsequent lung
cancer.[1] Brownish or black pigmentation in human gingiva has been reported in several countries.[2] The prevalence rate of gingival pigmentation is diverse according to race and country.[3] Physiological gingival pigmentation is more in dark skinned individuals compared
to light-skinned patients.[4] About 15% of Europeans have oral pigmentation, and this rate reaches 80% in the
Asian population.[5] Pigmentation in human gingiva derives from melanin granules, which are synthesized
in melanosomes of melanocytes.[6]
The prevalence of gingival pigmentation in smokers increases and reaches maximum levels
even on slight exposure to smoking in minimal categories of duration of smoking and
number of cigarettes smoked.[7] The increase in gingival pigmentation was reported in 21.5% of smokers and intensity
of pigmentation was related to a number of cigarettes consumed.[8] Various studies have observed a positive association of ETS exposure from parents
on gingival pigmentation in children.[9]
[10]
[11] Further, the extent of gingival pigmentation has been observed to be higher in adolescents
who are exposed to ETS at home compared to those who are not exposed.[12] A relationship between second-hand smoke and gingival pigmentation in women has
been observed, and this effect was magnified when residing in smaller houses.[13] These findings are significant when applied to India; since the majority of the
urban population are from a lower socio-economic status and reside in small households.
Apart from that, the other sources of ETS for young adults could be workplace and
vehicles. There remains a need to quantify the dose from passive smoking in more representative
samples of the population to estimate the burden that passive smoking may impose on
the whole community. Human whole saliva is an important body fluid that contains a
highly complex mixture of substances similar to other body fluids in many aspects.[14] It has been observed that salivary alpha-amylase levels may be influenced by smoking
and exposure to ETS in children.[15] Gingival pigmentation could be an easy method to assess as well as educate patients
in terms of their oral health.[12] There have been no studies assessing the effect of ETS exposure from various environmental
sources, its relationship with gingival pigmentation and salivary amylase activity
in young adults. Thus, the aim of this study was to assess the effects of ETS exposure
from various sources and its relationship to gingival pigmentation in young adults.
In addition, to correlate a number of years of exposure with extent, the intensity
of gingival pigmentation and salivary alpha amylase activity.
MATERIALS AND METHODS
A total of 200 nonsmoking systemically healthy subjects aged 18–35 years were randomly
selected from patients reporting to Department of Periodontics, SRM Dental College,
Ramapuram, Chennai. The inclusion criteria were subjects with a positive history of
exposure to ETS. Subjects with long-term use of minocycline, naevi, antimalarial drugs,
Kaposi’s sarcoma, melanomas, Addison’s disease, or amalgam tattoos were excluded from
the study. Informed consent from all patients was obtained and the study was approved
by the ethical committee of the institute. All the measurements were carried out by
a single examiner who had been calibrated. ETS exposure was assessed through a questionnaire
regarding ETS exposure at home from parents, spouse for married individuals and cohabitants
for unmarried individuals. Environmental sources included college, workplace, and
vehicles. Unstimulated whole saliva samples were collected from all subjects 1 h after
breakfast. The collected samples were immediately centrifuged at 3000 rpm for 10 min
at 4°C to remove cell debris and stored frozen until time of assay. The Quantichrom™
α-amylase kit DAMY 100 (Bioassay Systems San Francisco, California, USA) was used
for the assessment of salivary α-amylase. The quantitative alpha-amylase activity
was assessed by a colorimeter assay (595 nm). The intensity of color produced was
proportional to the activity of the enzyme in the saliva samples.[16]
The subjects were then examined for the presence of melanin pigmentation on the gingiva
clinically, and the extent of pigmentation was correlated with digital photographs
which were then reproduced on a computer display. The extent of brownish or black
pigmentation units on the gingiva of labial aspect of anterior teeth was classified
according to a modification of melanin index categories - gingival pigmentation index
(GPI)[17] as follows: 0 = no pigmentation; 1 = solitary units of pigmentation in papillary
gingiva without the formation of a continuous ribbon between solitary units; and 2
= 1 unit of formation of a continuous ribbon extending from two neighboring solitary
units.
The intensity of pigmentation was recorded using the Dummett oral pigmentation index
(DOPI)[18] as follows 0 = Pink tissue (no clinical pigmentation); 1 = Mild, light brown tissue
(mild clinical pigmentation); 2 = Medium brown or mixed pink and brown tissue (moderate
clinical pigmentation); 3 = deep brown or blue/black tissue (heavy clinical pigmentation).
To compare three or more mean values one-way ANOVA was applied and to compare proportions.
Chi-square test was applied. SPSS version 22.0 (IBM, United States) was used to analyze
the data. Significance level was fixed as 5% (α = 0.05).
RESULTS
The mean age of participants was 23.7 ± 3.1 years. 78% were females, and 22% were
males. None of the participants was active smokers and the average years of exposure
to ETS were 4.31 ± 2.8 years with a maximum of 15 years. The mean exposure to passive
smoke per day was 13.1 ± 14.4 min. The extent of gingival pigmentation according to
GPI index; 51.5% of patients exhibited a continuous ribbon extending from neighboring
solitary units (score 2). The intensity of pigmentation was found to be medium brown
in 53% and deep brown in 8.5% of patients as assessed by DOPI [Figure 1]. The number of years of exposure to passive smoking was highly significant when
compared to the extent and intensity of gingival pigmentation (P < 0.001) [Tables 1] and [2]. The intensity of pigmentation was highly significant to skin color as well (P = 0.001). ETS exposure from home was assessed in this study, and it was observed
that 39% of patients reported to have at least 1 smoking parent and out of that 69%
exhibited formation of continuous ribbon [Table 3]. The ETS exposure from parents and spouse was not significant to the extent of the
pigmentation (P> = 0.375) and (P = 0.062), respectively [Figures 2] and [3]. However, the intensity of pigmentation exhibited a moderate significance when the
source was from parents (P = 0.003) and highly significant when the source was a spouse (P < 0.001). In the present study, 99% of patients reported positive exposure to ETS
from environmental sources, namely, vehicles and workplace. The intensity of pigmentation
was highly significant to ETS exposure from workplace, namely, colleagues and co-workers
(P = 0.018).
Figure 1: Depicting the intensity of gingival pigmentation (dummett oral pigmentation index)
compared to years of exposure (a) no clinical pigmentation in <1 year of environmental
tobacco smoke. (b) Mild clinical pigmentation in 5 years of environmental tobacco
smoke. (c) Moderate clinical pigmentation in 10 years of environmental tobacco smoke.
(d) Heavy clinical pigmentation in 15 years of environmental tobacco smoke
Figure 2: Representation of correlation of environmental tobacco smoke from parent to gingival
pigmentation index (extent of gingival pigmentation)
Figure 3: Representation of correlation between environmental tobacco smoke exposure from spouse
to gingival pigmentation index (extent of gingival pigmentation)
Table 1:
Comparison of number of years of environmental tobacco smoke exposure to gingival
pigmentation index (extent of gingival pigmentation)
|
GPI
|
n
|
Mean number of years of exposure
|
SD
|
F
|
P
|
|
**P<0.05 is considered statistically significant. SD: Standard deviation, GPI: Gingival
pigmentation index
|
|
No pigmentation
|
14
|
2.21
|
1.477
|
7.944
|
<0.001**
|
|
Solitary units
|
83
|
3.84
|
2.861
|
|
|
|
Formation of continuous ribbon
|
103
|
4.97
|
2.878
|
|
|
|
Total
|
200
|
4.31
|
2.896
|
|
|
Table 2:
Comparison of number of years of environmental tobacco smoke exposure to Dummett oral
pigmentation index (intensity of gingival pigmentation)
|
DOPI
|
n
|
Mean number of years of exposure
|
SD
|
F
|
P
|
|
**P<0.05 is considered statistically significant. DOPI: Dummett oral pigmentation index,
SD: Standard deviation
|
|
Pink
|
8
|
4.25
|
3.536
|
8.104
|
<0.001**
|
|
Light brown
|
69
|
3.30
|
2.692
|
|
|
|
Medium brown
|
106
|
4.57
|
2.346
|
|
|
|
Deep brown
|
17
|
6.82
|
4.517
|
|
|
|
Total
|
200
|
4.31
|
2.896
|
|
|
Table 3:
Comparison of environmental tobacco smoke from parent to Dummett oral pigmentation
index (intensity of gingival pigmentation)
|
DOPI
|
n
|
Mean duration of smoking (years)
|
SD
|
F
|
P
|
|
**P<0.05 is considered statistically significant. DOPI: Dummett oral pigmentation index,
SD: Standard deviation
|
|
Light brown
|
20
|
11.2042
|
10.62838
|
6.383
|
0.003**
|
|
Medium brown
|
48
|
6.6094
|
5.53260
|
|
|
|
Deep brown
|
10
|
14.8417
|
8.10633
|
|
|
|
Total
|
78
|
8.8430
|
7.96679
|
|
|
Salivary alpha-amylase activity was assessed in all 200 patients. The levels were
assessed in three subgroups according to number of years of exposure to ETS. Group
1 (1–5 years), Group 2 (6–10 years), and Group 3 (11–15 years). Amylase activity was
expressed as mol maltose/mg protein. It was observed that subjects in Group 3 had
a mean value of 10.07 (7.1–12.62), Group 2 had 11.10 (7.42–12.66), and Group 1 had
the highest value of 14.40 (9.45–22.04). The amylase levels when compared between
group 1 and 3 were highly significant (P < 0.05).
DISCUSSION
The results of this study revealed that prevalence of gingival pigmentation in young
adults was directly proportional to the amount of ETS exposure. The previous studies
did not take into consideration the environmental sources of ETS which add to the
ETS burden. Apart from that the exact amount of time perday patients were exposed
to passive smoking was also not assessed.[3]
[9]
[10]
[11]
[12] This study was unique in this aspect since it evaluated the ETS exposure from home
and environmental sources while also accounting for the time exposed to passive smoking
per day. The association between a number of years of exposure to ETS with extent
and intensity of gingival pigmentation was highly significant. The greater the number
of smoking years, the more was the extent of pigmentation in the present study. Madhani
and Thomas, similarly observed that ETS from smoker parents causes more prevalence
of gingival pigmentation in children which was statistically significant to a number
of years exposed to ETS.[12]
It has been established that skin color is associated with the intensity of gingival
pigmentation.[19] The extent of gingival pigmentation was more in fair skin patients. These findings
are similar to a study done by Hajifattahi et al., in 2010 who observed that passive smoking leads to more pigmentation in the fair
skin than patients with dark skin color.[10]
In the present study, the ETS exposure from parents was highly significant to the
intensity of gingival pigmentation. Studies evaluating, association of melanin pigmentation
of gingiva in children with parents who smoke observed a positive correlation to ETS
exposure from parents to the prevalence of gingival pigmentation. Further, it was
seen that percentage of smoking parents was higher in children who exhibited greater
pigmentation than those who did not.[8]
[9] Similarly, Sreeja et al. 2015, observed that gingival pigmentation in children has been linked to passive
smoking from parents and other adults who smoke.[20]
In the present study, the extent of gingival pigmentation was not significant to the
severity of exposure from spouse, but the intensity of pigmentation was highly significant
(P < 0.001). These findings are similar to a recent study in which relationship of gingival
pigmentation in women exposed to second-hand smoke from their husbands was observed.
The odds ratio of gingival pigmentation in women exposed to second-hand smoke from
husbands was 3 and this effect was magnified in smaller houses.[14]
A factor that can skew the determination of true effects of ETS from parents and spouse
is the impact of ETS from additional environmental sources. The ETS exposure from
environmental sources such as vehicles and workplace was also assessed, and it was
seen that 99% of patients reported positive ETS exposure from vehicles. Similarly,
Aurrekoetxea et al. 2016 observed exposure to second-hand tobacco smoke in 4-year-old children in Spain
and found that based on parental reports, more than half of children were exposed
to ETS out of which 21.6% were exposed at home, whereas 41.7% were exposed elsewhere.
Highlighting the environmental sources contributing to ETS exposure. They also found
that children whose parents were from a lower educational level had a higher odds
of exposure to ETS.[21]
In this study, ETS exposure from workplace was highly significant to the intensity
of gingival pigmentation with 37.5% of subjects having positive exposure from workplace
exhibiting medium brown and deep brown color (P = 0.018). The gingival pigmentation due to ETS exposure can be used as a visible
tool for patient education to inform the ill effects of passive smoking on oral health
and developing precancerous lesions. Cicciù et al., 2017 studied the use of an autofluorescence examination handheld device the Visually
Enhanced Lesion Scope (VEL scope) system to delineate between benign, dysplastic,
and malignant oral mucosa lesions and found it to be noninvasive. They noted that
it can be used as a screening tool to educate patients since any pigmented or precancerous
oral and gingival lesions can be screened easily and aid in the detection and diagnosis.[22]
The activity of amylase was decreased in patients with the highest exposure to ETS
(11–15 years) compared to least exposure (1–5 years) which was statistically significant
(P < 0.05). Similarly, Granger et al. 2007 reported lower salivary amylase activity for mothers, but not for infants as
a result of exposure to tobacco smoke.[14] However, this is in contrast to Avsar et al., 2009 who observed higher salivary amylase activity in children with passive smoking.[15] This could be attributed to differences in age of subjects. In the present study,
the low levels of amylase in subjects with high exposure to ETS can be explained by
inhibition of salivary amylase by cigarette smoke may be due to the interaction between
smoke aldehydes and–SH groups of the enzyme molecules.[15]
CONCLUSION
There is a correlation between ETS and gingival melanin pigmentation. Duration of
ETS exposure is highly significant to both extent and intensity of pigmentation. Environmental
sources of ETS significantly contributed to the gingival pigmentation.
The salivary amylase levels were inversely proportional to the duration of exposure.
The findings of the present study are helpful in understanding the impact of ETS exposure
from various sources in the environment. In a country like India where no stringent
smoke-free legislation exists, the social norm from smoking in home or car will shift
to formal smoking restrictions or bans once the awareness about the impact of ETS
exposure on oral health is educated to the general population. In addition, gingival
pigmentation can be used as a visible tool for patient education.
Financial support and sponsorship
Nil.
