General Presentation: Exposure to second hand smoking is considered as one of the most encountered health problems especially for prenatal and childhood age group [1]. A study tackling effects caused by tobacco exposure showed that prenatal smoking exposure and environment tobacco smoking result in menarche at an earlier age [2]. Tobacco smoke contains known hormonally active chemical and reproductive toxicants and has a positive and independent effect on testosterone level [3,4]. Several studies showed that second hand smoking during pregnancy has been linked to decreased fertility in women, sudden infant death syndrome; prematurity and low birth weight [5]. Despite being linked to these morbid outcomes there has been limited information concerning the correlation between second hand smoking exposure and early pubertal events in girls [6]. Puberty is a complex process leading to sexual maturation, controlled by the multiple different hormones, yet not completely understood [7]. It is associated with two related processes, the maturation of the hypothalamic–pituitary–gonadal (HPG) system, or gonadarche and the maturation of the hypothalamic-pituitary-adrenal system, or adrenarche [2]. Although the exact mechanisms triggering the onset of puberty are subtle, the first known biochemical change during puberty is the elevated production of kisspeptin in the hypothalamus. Stimulatory and inhibitory signals of kisspeptin are not yet clearly elucidated; however, the increase in kisspeptin production results in increased gonadotropin-releasing hormone (GnRH) releases [8]. Thus, a rise in kisspeptin is widely acknowledged as the initiative event in HPG axis activation during puberty [9]. Inhibition of the GnRH pulse generator decreases first during sleep which causes an increase of luteinizing hormone (LH) pulse amplitude in the nighttime during early and mid-puberty. As puberty progresses, the pulse amplitude of LH increases during daytime hours as well, thus, resulting in rise of estrogen and testosterone levels accordingly [8].Puberty is a key mechanism because it is associated with major psychological changes including cognitive, affective and social relationship skills. Knowing that early puberty has been linked to diseases later on in life, identification of modifiable causes of early puberty is of interest [10]. Noting that; trends in Lebanon are in line with the global pattern of decreasing age at menarche. As worldwide, studies showed, dose dependent associations between maternal smoking during pregnancy and earlier timing of puberty in both sons and daughters [5]. Data from the Middle East is scarce and the only studies available in Lebanon was an observational study done in the American University in Beirut in 2018-2019 confirming that trends in Lebanon are in line with the global pattern of decreasing age at menarche.

Review of Literature

Precocious puberty: Precocious puberty (PP) is the development of pubertal changes before the lower accepted limits of age of onset of puberty; these limits are mainly before the age of 8 years for girls and before 9 years for boys. The onset of sexual symptoms suggestive of Tanner stage 2 before 8 years of age in girls and 9 years of age in boys is considered PP. However, some studies, mainly in the United States of America, suggested that the onset of puberty may be as early as 7.7 years in girls and 7.6 years in boys. PP causes many modifications in the human body such as early progression of sexual characteristics, rapid bone malnutrition, reduced final height and psychological behavioral abnormalities [11]. The recent data concerning earlier pubertal development in girls living in developed countries is well-established and is of concern because of the possible effects on later health outcomes, particularly breast and other reproductive system cancers [12,14]. In addition, a young pubertal age can cause increased risks on behaviors and adverse health effects including depression, anxiety, early sexual activity, substance abuse, and smoking [15].

Classification of Precocious Puberty

Classification of PP is as follows: gonadotropin dependent (central/true PP) or gonadotropin independent (peripheral/pseudo PP). In true PP, the process is dependent on the hypothalamus, pituitary, and gonad axis unlike the pseudo PP where no activation of the axis occurs [11].

Central Precocious Puberty (CPP)

It is characterized by the same biochemical and physical features as normally timed puberty but occurs pathologically at an earlier age [8]. The occurrence of CPP is due to early maturation of HPG axis with a frequency ranging from 1/5000 to 1/10000 [11,16]. The reported female/male ratio varies between 3/1 and 23/1 indicating a female predominance [17]. One of the earliest symptoms of central puberty in girls is usually breast development (Thelarche), followed by pubic hair growth (Pubarche) [8]. This spurt of the pubertal growth generally occurs during Tanner stage II–III, with the first menstrual period, known as menarche, usually occurring at Tanner stage IV. On the other hand, the initial clinical sign of central puberty in boys is testicular enlargement and the pubertal growth spurt happens later than it does in girls [9,18]. Risk factors for CPP include a history of international adoption, congenital or acquired central nervous system insults, such as hypothalamic hamartomas, septo-optic dysplasia, tumor, trauma, infection, or ischemia. In addition, several genetic syndromes, including neurofibromatosis type 1, tuberous sclerosis and Sturge–Weber syndrome, are associated with CPP [9]. Furthermore, 5.2% to 27.5% of the cases have been reported to be familial [19, 20]. The large proportion of CPP is idiopathic in girls; however, approximately 50% of the boys have an identifiable cause [8]. Environmental factors and some hormonal mimickers (endocrine disrupting chemicals) may have some estrogenic properties or act as stimulants for estrogen secretion. For example, cosmetic products, foods, and some pharmacological insecticides may cause some disruption in the HPG axis causing PP [21,22]. Cerebral lesions are found in a small minority of CPP cases. Individuals with neurofibromatosis type 1, hydrocephaly, meningomyelocele, neonatal encephalopathy and exposure to low-dose cranial radiation show an increased risk for CPP. Furthermore, one of the most common observed pathologies is hypothalamic hamartoma which may pose a diagnostic challenge due to the difficulty in detecting it by radiological imaging [11]. Hypothalamic hamartomas are congenital, non-neoplastic, and tumor-like lesions leading to gelastic seizures resistant to anticonvulsant treatment [23]. The suspicious symptoms for hypothalamic hamartoma are: PP onset before 2 years (generally 4 years) of age that is gonadotropin dependent, presence of isointense tumor on magnetic resonance imaging (MRI) with gadolinium enhancement and negative tumor markers (to rule out for pseudo PP) [24]. GnRH neurons are present in the hamartoma tissue and are functional and secrete GnRH episodically. The prevalence of hypothalamic hamartomas in patients with CPP before 4 years of age is 10% [11]. Recent data described specific genetic causes of CPP. For example, a substitution mutation was found in a patient with CPP in the G-protein coupled kisspeptin receptor gene KISS1R (formerly known as GPR54) and was linked to delayed degradation of the ligand–receptor complex within the cell membrane which was further associated with an extended period of downstream signaling, postulated to result in increased amplitude of GnRH pulsatility [8]. Another example is a mutation in KISS1, encoding the ligand kisspeptin, which has also been seen within an amino-terminal sequence associated with protein degradation [25]. This mutated ligand–receptor complex shows resistance to degradation too. But it is a relatively uncommon cause of CPP [8]. Newly found ten heterozygous mutations in MKRN3, encoding for makorin RING-finger protein 3, have been linked to both sporadic and familial CPP [26,27]. Other molecular defects have been identified with less clear or weaker associations, like single nucleotide polymorphisms in the FSHB gene and the LHB gene [28]. Cases of CPP may not be evident if growth hormone deficiency is associated with it because of the delay of the growth caused by the deficiency, and sometimes CPP may be the presenting symptom of a multisystem disease such as neurofibromatosis type 1. In a child with optic glioma, if it is not detected early it can lead to complete blindness [11]. Untreated, CPP causes early epiphyseal fusion and a significant compromise in adult height. This is why; the main goal of therapy is preservation of height potential with GnRH analogs being the gold-standard treatment for CPP [8].

Combined Secondary and Central Precocious Puberty When a patient is exposed to high levels of sex steroids for a long period of time, he can have an increase in somatic development and advancement in bone age resulting in an earlier puberty and HPG axis maturation depending on the somatic development and ignoring the chronological age [11]. Congenital adrenal hyperplasia is the most common etiology. Rare causes of this condition include testotoxicosis and McCune-Albright syndromes [24]. An untreated peripheral pseudo PP can become complicated when CPP is superimposed. The onset of CPP is evident when the bone age reaches 10-13 years (29).

Peripheral Precocious Puberty (PPP)

The definition of PPP, or GnRH-independent precocious puberty, is an early pubertal maturation that is not a result of central activation of the HPG axis [30]. The etiology can be categorized into either genetic or acquired disorders. Congenital or genetic causes include McCune-Albright syndrome, familial male-limited precocious puberty, and congenital adrenal hyperplasia whereas acquired causes include hormone-secreting tumors or cysts, exogenous hormone exposure, and the pseudoprecocious puberty seen in patients with profound primary hypothyroidism [30,31]. In girls, one of the most common etiologies is ovarian follicular cysts which may cause vaginal bleeding. Pelvic ultrasonography evaluation is very useful in the diagnosis. In some case spontaneous regression ensues with time, and estrogen levels decrease. McCune-Albright syndrome occurs by the presence of a mutation that activates the gene encoding Gs protein-alpha subunit. This causes the classical triad of café-au-lait spots, poliostatic fibrous dysplasia and PPP. It should be kept in the differential diagnosis of children who have recurrent follicular cysts and irregular vaginal bleeding even without other signs. However, in addition to the triad, endocrine organ hyper-functioning (hyperthyroidism, Cushing syndrome, acromegaly, and hypophosphatemic rickets) should also be investigated with the necessity for a bone scintigraphy in the diagnosis. McCune-Albright Syndrome is rare in males [11]. The LH receptor activating mutations (familial testotoxicosis) are autosomal dominant rare diseases in male children characterized by symmetrical testicular enlargement. A human chorionic gonadotropin secreting tumor is another cause of PPP in boys. It can exist in organs other than gonads, such as the liver (due to a hepatoblastoma), pineal region, brain or mediastinum. It causes testicular enlargement and an increase in serum testosterone levels [11]. Leydig cell tumors are mostly benign and result in unilateral testicular enlargements [32]. Adrenal gland diseases that cause visualization, especially congenital adrenal hyperplasia, are the most common cause of PPP in childhood and causes iso-sexual PPP in boys and heterosexual PPP in girls [11]. Thyroid-stimulating hormone levels have also a role in puberty. A significant TSH increase in some prepubertal children results in elevation of follicular-stimulating hormone (FSH) level and the occurrence of early pubertal signs. These can be early breast development in girls and mild testicular enlargement in boys. However, acceleration in somatic development is not seen and an elevated prolactin level with galactorrhea may be observed. The treatment of hypothyroidism results in a recovery of the PPP [11]. 

Premature Thelarche

An isolated breast development before the age of 2 years in girls may be unilateral with no acceleration in somatic development and no increase in bone age. The development of the breast may be cyclical and related to blood estrogen levels. This situation regresses with time. On the other hand, the premature Thelarche that starts after 2 years of age with a significant glandular structure necessitates a follow up for PP since it may progress to CPP with advancement in bone age, ovarian enlargement and higher estrogen levels [11]. The increase in FSH level is the physiologic event that causes premature Thelarche. It causes inhibin B to be secreted from granulosa cells. GnRH stimulus is the cause of the FSH response [33]. However, in premature Thelarche that begins before 2 years of age, the LH response together with the FSH may increase to higher levels than those values seen after 2 years suggesting some interference in the development of CPP naming this phenomenon “mini-puberty [34]. To note that some patients with premature Thelarche could have some estrogenic environmental pollution [21].

Premature Adrenarche and Pubarche

Adrenarche is the increase of pubertal adrenal androgens and it may be seen in both sexes in normal children between 6-8 years of age. On the other hand, pubarche is the genital and axillary hair growth. Adrenarche is associated with pubarche in some children which is the most innocent form of the premature pubarche and it is important to distinguish this situation from pathologic etiologies. Adrenarche occurs as a result of increased secretion of androgens from the zona reticularis of the adrenal cortex which causes increase of serum dehydroepiadnrosterone and its metabolite sulfate, dehydroepiandrosterone sulfate (DHEA-S), due to an increase in 17, 20 liyase and 17 alpha hydroxylase activities. An increase in serum level of DHEA-S over 40μg/dl indicates adrenarche. Congenital adrenal hyperplasia or adrenal tumors should be ruled out initially in premature pubarche. Also, some partial enzyme deficiencies such as 21-hydroxylase and 3β-hydroxylase deficiencies can initially present with premature pubarche. In both cases the somatic growth and advancement in bone age are accelerated. Therefore, DHEA-S measurement should be performed in addition to testosterone and 17-hydroxyprogesterone to assist in the diagnosis. Although DHEA-S is increased in isolated premature pubarche, testosterone and 17-hydroxyprogesterone levels are in normal ranges and sometimes, an adrenocorticotropic hormone stimulation test is necessary when borderline results are present. Onset of puberty is expected to be in normal time (you mean on time?) in cases with premature adrenarche and the final heights must be compatible with their genetics [11]. Recently, some data suggested the association of polycystic ovary syndrome, hyperinsulinism and dyslipidemia with premature pubarche which may be the earlier sign of metabolic syndrome in childhood [35,36].

Evaluation of Precocious Puberty

It is very important to define the etiologic cause for the management of the underlying disease and the prevention of irreversible damage. History of the onset of the symptoms, progression rate, and growth tempo in the last 6-12 months, appearance of secondary sex characteristics (acne, oily skin, vaginal bleeding) should be sought. In addition, any presence of PP in the family suggests the diagnosis of familial forms. The Tanner-Marshel method is the method of choice for staging puberty. Anthropometric evaluation should be defined by measurement of the weight, height and body proportions. Growth velocity per year must be calculated; patients with CPP generally score more than the 75th percentile. In addition, bone age should be determined by left hand and wrist x-ray, and whenever it is higher than 2 standard deviations for the chronological age, it is not suggestive of a normal variant of pubertal development [24]. If the change in bone age/change in chronological age over a period of time is greater than 1.2, it is in favor of progressive CPP. The volume of the testis should be measured, a volume less than 4 ml in the presence of secondary sex characteristics is probably due to adrenal pathologies, whereas, asymmetric testicular enlargement is observed in McCune-Albright syndrome and Leydig cell tumor cases. Any bilateral testicular enlargement is probably due to testotoxicosis, human choriogonadotropic hormone secreting tumors and CPP cases. Cases without accelerated growth and advanced bone age with only one of the pubertal signs can be normal variants, but a close follow-up is recommended [11]. The initial evaluation of the patient includes the measurement of gonadotropins (LH, FSH), related sex steroids, and a GnRH stimulation test. In the stimulation test, the FSH response is dominant in premature Thelarche; however, the LH response is the dominant gonadotropin in CPP patients [11]. On the other hand, LH and FSH are suppressed or at prepubertal levels in PPP cases. In premature Thelarche cases younger than 2 years of age, the stimulation test causes LH to increase along with FSH, but the dominant response is still for FSH [24]. The organic/idiopathic etiological assessment needs investigations beyond hormone levels [37]. Pelvic ultrasonography should be performed in girls to assess the ovarian and uterine sizes noting that any increase in ovarian volumes is important especially seen in CPP cases [11]. Bilateral enlarged ovaries can be seen in CPP patients and the uterine volume is pubertal in all CPP cases [37]. Cranial and pituitary MRI should be performed when suspecting organic CPP. Although there has been a suggestion to perform MRI in only male CPP cases or in girls below 6 years old, today it is accepted that MRI should be done for all cases because intracranial tumors may cause CPP at any age; follow up images are recommended periodically in patients below 4 years of age or those reported to be normal [24,38,39].

Smoking and Early Pubertal Symptoms

Tobacco smoke contains reproductive and developmental toxicants and other carcinogenic toxins associated with hormonal changes in women. These include anti-estrogen and progesterone effects [40,41]. Several studies discussed the prenatal maternal smoking in relation to age at menarche. There was an inconsistency between the results: some showing an earlier onset while others did not [42]. In addition, women who smoke during pregnancy are also likely to smoke post-delivery, so that the offspring continues to be exposed. Few studies examined the secondhand smoke exposure in relation to age at menarche, also showing with inconsistent results [43,44]. One study showed that a longer prenatal and childhood secondhand smoke exposure time was associated with an earlier onset of pubic hair growth. However, this was not true for breast development [2]. In addition, a recent meta-analysis showed an effect estimated by 1-month earlier age at menarche among girls with prenatal smoke exposure [42]. Smoking can alter adrenal androgen secretion, causing increases in cortisol, DHEA-S, dehydroepiandrosterone (which increases prior to, or early, in puberty and is a precursor of other androgens), adrenaline, and catecholamine [45]. Some theories suggest that the smoke effects on adrenal hormones may be the cause of early pubic hair development, however the absence of earlier breast development by its anti-estrogenic effects leads to delayed breast development [41]. Furthermore, prenatal exposure to smoking is associated with low birth weight or intra-uterine growth retardation [46].

Objectives

Primary objective

To determine if a correlation exists between secondhand smoking during childhood and maternal smoking during pregnancy and early pubertal events in the Lebanese population. 

Secondary objectives

• To determine the prevalence of early pubertal events in Lebanese boys and girls and 

• To evaluate the contribution of the socio-economic status on second hand smoke exposure

Study Design and Population

A cross-sectional retrospective study is conducted to identify correlation between second hand smoking and onset of pubertal events in Lebanese boys and girls aged between 14-16 years. A questionnaire is used to ask about their previous pubertal events onset (ejaculation, menarche, pubic hair development, breast development, voice change, axillary hair development, acne and increase in sweating). The study population includes teenagers from two different regions Mount Lebanon and Saida. It is composed of 180 adolescents divided into the following groups: Group A: includes 50 girls who are exposed to secondhand smoking. Group B: includes 50 girls who are not exposed to any source of smoking. Group C: includes 40 boys who are exposed to secondhand smoking. Group D: includes 40 boys who are not exposed to any source of smoking.

Inclusion criteria

Lebanese boys and girls, People living in Mount Lebanon and Saida, age 14-16 and clinically and physically healthy. 

Exclusion criteria

Presence of mental problems, non-Lebanese people and Hermaphrodism.

Sample size: The number of interviewed individuals is 180

Methods: Procedure of Data Collection

The questionnaire is divided into 2 parts. The first part includes general information about sex age and residence and socioeconomic status in addition of questions about second hand smoking (type of smoking, number of cigarettes, area of smoking, household active smokers, if the smoking occurs in prenatal or postnatal period). The second part includes specific information about time of onset of pubertal events. An early pubertal event is defined as an event relating to puberty and occurring below the age 8 years for girls and below the age 9 years for boys. The questionnaire was translated to a validated Arabic version. It was filled by medical students during interview sessions.

Statistical Analysis

Data analysis was performed using the SPSS software for Windows, version 20 (IBM, Armonk, USA). The association of secondhand smoking and prenatal maternal smoking with early pubertal events was determined using a chi-square test. The test also served in checking the association between the educational level of the parents and the smoking behaviors as well as the association between the intervals of duration of hubble-bubble smoking and early puberty. An independent-sample t-test was used to determine if any differences exist between the average number of cigarettes to which a child was exposed and the occurrence of early puberty. A P- value of < 0.05 is considered significant.

General Description of the Population

The study included 180 teenagers. Girls were 55.6% (100 participants) and boys represented 44.4% (80 participants). All participants were aged between 14 and 16 years. Half of them were living in Beirut and the other half in Saida. Only 9 participants (5%) suffered from chronic diseases.

Second Hand Smoking in Childhood and Early Pubertal Events

The participants were asked if they were exposed to smoking during their childhood and 12.8% (23 participants) said that they were. On the other hand, 37.2% (67 participants) answered “rarely” and 50% (90 participants) answered “never”. Among the studied population, 11.1% (20 participants) had early pubertal events. A chi-square test was performed to check for a correlation between the childhood exposure to smoke and early pubertal events. Among those exposed frequently to smoke, only 1 participant had an early pubertal event (4.3%). Among those rarely exposed, 10 participants had early puberty (14.9%) and in the group that was never exposed, 9 had early puberty (10%). These observed differences in the frequency of early puberty were not found to be statistically significant (P-Value = 0.39). The results are presented in (Table 1).

Table 1: Correlation between childhood exposure to smoke and early puberty

^ns: non-significant

The Table 1 shows that no correlation was seen between exposure to smoke in childhood and an early puberty. Notably, most of the early puberty events occurred in the population with rare or absent exposure to smoke. Fischer’s exact test is reported since some categories had an expected count less than 5. Among the population exposed to smoke during childhood (90 participants), after exclusion of hubble-bubble smoking (remains 67 participants), the average number of cigarettes to which the child was exposed per day was 10.81. An independent-sample t-test was performed to check if a significant difference in this value exists between the group who had an early puberty and the one who hadn’t. The group with early puberty was exposed to an average of 6.83 cigarettes per day (±10.20), while the group without early puberty was exposed to an average of 11.2 cigarettes per day (±12.12). This difference was not found to be statistically significant, indicating that the number of cigarettes the child is exposed to does not correlate with early puberty. The results are shown in (Table 2). 

Table 2: Difference in the average exposure to cigarettes between the two groups

^ns: non-significant

The Table 2 shows that the difference between the average numbers of cigarette exposure per day is not statistically significant between the group with and without early puberty. For the hubble bubble smoking, the time of daily exposure was also not significantly linked to early puberty. The results are presented in (Table 3).

Table 3: Correlation between hubble-bubble daily exposure time and early puberty

^ns: non-significant

The Table 3 shows no significant association between the duration of exposure to hubble-bubble smoke every day and the onset of early puberty. Second Hand Smoking in Pregnancy and Early Pubertal Events: In the studied population, 21.1% of the teenager’s mothers were exposed to smoke during pregnancy (38 participants’ mothers), while 78.9% had no such exposure (142 participants’ mothers). A chi-square test was performed to check if an association exists between such exposure and an early onset of puberty. In the group without this exposure, the prevalence of early puberty was 10.6% (15 participants) while in the group with the exposure, this prevalence was 13.2% (5 participants). This difference was, however, not statistically significant (P-Value = 0.77). This indicates that exposure of the mother to smoke during pregnancy is not associated with an early puberty. The results are shown in (Table 4). 

Table 4: Correlation between maternal exposure to smoke during pregnancy and early puberty

^ns: non-significant

The Table 4 shows no significant association between the exposure of the mother to smoke during pregnancy and early puberty. Prevalence of Early Pubertal Events in Lebanese Teenagers: Pre-pubertal events occurred in 11.1% of our studied population (20 participants). Half of these events occurred in boys and the other half occurred in girls. The results are shown in (Figure 1).

Figure 1: Distribution of early pubertal events between the sexes

For the girls, the most common early pubertal event was the growth spurt and pubic hair development, both of which occurred in 4% of the girls before the age of 8 years. This was followed, in order of frequency, by breast development and skin changes, which were observed in 2% of the girls before the age of 8 years. Excess sweating, growth of axillary hair and menstruation occurred each in 1% of the girls before the age of 8 years. These results are shown in (Figure 2). 

Figure 2: Frequency of early pubertal events in girls

For the boys, the most common events that occurred before the age of 9 years were ejaculation and axillary hair growth (5%), excessive sweating (3.8%), growth spurt (2.5%), increase in testicular and penile size, change in voice and skin changes (1.3%). The results are shown in (Figure 3). 

Figure 3: Frequency of early pubertal events in boys

Effect of Smoking in Pregnancy on Birth Events: The participants were asked if they had a normal birth weight and if they were delivered on term, preterm or late term. Their answers were tabulated with the history of maternal smoking during pregnancy and a chi-square test was run to check for significant associations. No significant association was seen in either case. For birth weight, 1 had a problem in the smoking group while 7 had a problem in the non-smoking group (2.6% and 4.9% respectively). For the term of delivery, most of the population was born at term; 92.1% in the smoking group and 92.3% in the non-smoking group. These small differences are not of statistical significance. The results are presented in (Table 5). 

Table 5: Effects of mother smoking during pregnancy on birth weight and term delivery

^ns: non-significant

The Table 5 shows no significant association between the exposure of the mother to smoke during pregnancy and abnormal birth weight or disturbances in the term of delivery. Correlation between the Level of Education of the Parents and the Exposure of the Child to Smoke: The level of education of the parents was determined according to the following classification: “did not reach high school”, “started high school”, “finished high school”, and “graduated from university”. A chi-square test was performed to check for association between the level of education of each parent and the exposure of their child to smoke. Here, again, no association was observed, neither in the pre-natal nor the childhood phases. The results are shown in (Table 6).

Table 6: Effects of the parent’s education level on smoke exposure

^ns: non-significant

The Table 6 shows no significant association between the parent’s level of education and exposure of the mother to smoke during pregnancy or exposure of the child to smoke. Difference in Early Puberty Rates between Mount Lebanon and Saida: Using the chi-square test, the predilection of precocious puberty to a certain geographic area was checked. In those who live in Mount Lebanon, the prevalence of early puberty was 10%, whereas in those living in Saida, the prevalence was 12.2%. This difference was not found to be statistically significant (χ2 = 0.22; P-Value = 0.63).

We found that the pre-pubertal events among the population occurred in 11.1%. Half of these events occurred in boys and the other half occurred in girls. For the girls, the most common early pubertal event was the growth spurt and pubic hair development, both of which occurred in 4% of the girls before the age of 8 years. This was followed, in order of frequency, by breast development and skin changes, which were observed in 2% of the girls before the age of 8 years. Excess sweating, growth of axillary hair and menstruation occurred each in 1% of the girls before the age of 8 years. However, For the boys, the most common events that occurred before the age of 9 years were ejaculation and axillary hair growth (5%), excessive sweating (3.8%), growth spurt (2.5%), increase in testicular and penile size, change in voice and skin changes (1.3%). Our results show no statically significant correlation between smoking exposure and with any early pubertal symptoms. In addition, no correlation is seen between the number of cigarettes the child is exposed to and the early pubertal signs. Same is seen with hubble-bubble smoking, the time of daily exposure was also not significantly linked to early puberty. Also, the results of our study found that the exposure of the mother to smoke during pregnancy is not associated with neither an early pubertal signs nor abnormal birth weight or disturbances in the term of delivery. Moreover, our study shows again no significant correlation between the parent’s level of education and exposure of the mother to smoke during pregnancy and exposure of the child to smoke. Concerning the absence of statically significant association between smoking exposure and early pubertal signs, many studies have addressed this issue revealing contradictory results. For example, a study done in the United States of America found that the greater the prenatal and childhood secondhand smoke exposure the earlier the onset of pubic hair development; however, this was not the case for the breast development. There were also some variations according to the race concerning breast development in some studies. White girls exhibited earlier breast development, unlike black girls, with higher prenatal smoking exposure [2]. The reasons for this are unclear; some suggested differences in nicotine metabolism in different races [47]. In contrast, a small study reported no association of breast development (or menarche) with prenatal smoking [48]. Furthermore, a study mentioned that menarche started 2 months earlier in girls with high secondhand smoke exposures; and in those with the highest exposures to both prenatal and postnatal smoke, menarche started even earlier (by 4 months) [49]. A cohort study on Danish population reported the presence of association between prenatal smoke exposure and early pubertal age; however, this was not the case with postnatal exposure [44]. Two other studies reported that prenatal smoke exposure was associated with earlier age of menstrual onset, but a third study reported higher risk of later age at menstrual onset [50,51]. How smoking exposure affects puberty timing is not understood yet. Over 4000 chemicals are present in cigarettes. Nicotine was found to decrease blood flow to the placenta and fetus in pregnant smokers [52]. In addition, retardation of trophoblastic outgrowth and evolution of placenta was caused by the heavy metal cadmium [53]. Prenatal smoke exposure affects the secretion and production of sex hormones and gonadotropins. This was suggested in several studies on animals and humans [51,54,55]. Furthermore, males show reduced testis size and sperm count in adulthood by 20–40% when exposed to moderate or heavy smoking in pregnancy. The data concerning any associations between secondhand smoking and menarche are inconsistent in the literature. This could be due to exposure definition differences between the articles present and limited separation of prenatal exposure [2]. No study has assessed the association between the hubble-bubble smoking and any early pubertal symptoms. There are few studies describing the prevalence of precocious puberty. The very first study done was from the epidemiologic Danish national registry and reported that 0.2% of the females had some form of precocious puberty (CPP, PPP or benign variants). The prevalence was less than 0.05% in males. This number much lower than that in our population because prevalence and incidence vary significantly among different populations making it difficult to estimate definitive numbers. In addition, our results show higher number because even if 1 early pubertal symptom was present it was considered in the definition of early puberty, ignoring the possibility of isolated premature Thelarche or pubarche. This may overestimate the prevalence.

Limitations

The sample included consisted of teenagers of 2 regions in Lebanon and is, therefore, not representative of the Lebanese population. Future studies ought to perform a better sampling strategy including individuals from all over the country. In addition, the design included segregation of groups based on the presence or absence of exposure to smoking, which was the studied factor. We recommend, however, that subsequent studies have a case-control design, in which the groups are separated on the basis of presence or absence of early puberty, which is the studied outcome. Such design would allow better evaluation of the contribution of secondhand smoke on puberty by increasing the number of individuals suffering from this condition. It would also allow an estimation of the prevalence of secondhand smoking and prenatal maternal smoking in the population. A recall bias is also present in the study since the teenagers were asked to remember the timing of their pubertal events, some of which are not always easy to date. On the other hand, such events represent major changes in the lives of children that they can most of the time; accurately place them on the timescale. However, this bias can be overcome by planning prospective studies with a follow-up of pre-pubertal children for few years.

In conclusion, no correlation was seen between childhood secondhand smoking and early puberty. No correlation was observed between prenatal maternal smoking and early puberty. No correlation between the average number of cigarettes to which the child is exposed or the average interval of time during which he was exposed to hubble-bubble and early puberty was seen. The prevalence of early pubertal events in the studied population was 11.1%. This rate did not differ significantly between Mount Lebanon and Saida. The most frequent events being growth spurt and pubic hair growth in girls and ejaculation and axillary hair growth in boys. The educational level of the parents did not affect the rates of exposure of the children to secondhand smoking. It did not affect either the prevalence of maternal smoking in pregnancy.

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