Around the world tobacco consumption among young adults has reached epidemic levels, negatively impacting the health of populations and increasing financial burden on the healthcare systems [1,2,3]. The majority of young smokers tend to continue smoking later into their adulthoods. Half of adult smokers die prematurely from a smoking-associated pathology [4,5,6,7,8,9].

Though numerous programs have been implemented to curb smoking and thousands of articles have been written to warn against the use of tobacco, a substantial number of individuals across generations continue using this hazardous product. The use of tobacco usually begins during childhood and adolescence [10,11], with 88% of grown-ups reporting to have initiated smoking before the age of 18 years [12]. Owing to immaturity, college students are considered impressionable, increasing their likelihood of being influenced by the media showing advertisements on tobacco use, which often feature attractive models/movie actors portraying smoking as “cool”. Tobacco dependence remains a serious problem on a global scale. Among the individuals that once tried to smoke, approximately a third will become daily smokers [11]. Smokers trying to stop will succeed around 5% of the time. Even though not all smokers will become addicted to nicotine, the proportion of people diagnosed with nicotine addiction is higher than for any other substance [13,14]. Nicotine belongs to a large class of substances called alkaloids which contain an amine nucleus.

The chemical name of nicotine is (S)-3-(1-Methyl-2-pyrrolidinyl) pyridine, which reflects the existence of two cycles of carbon atoms that also contain nitrogen. In pure form, nicotine is a colorless or slightly yellowish oily fluid. Chemically, nicotine is a base that combines with acids to form water-soluble stable salts. Nicotine is absorbed fastest by cigarette smoke inhalation and the highest arterial blood values are reached within 20 s of inhalation. In body fluids, such as blood, most nicotine molecules are positively charged and that is why they cannot cross cell membranes by themselves. The positive charge is the result of nicotine’s chemical composition—a weak base with a pH of approximately 8.0 [15]. There is, however, a significant proportion of nicotine, about 30%, which travels without any electrical charge, and this form reaches the brain and other target tissues easily. Apart from nicotine, tobacco and cigarette smoke contain certain other ingredients such as Nornicotine and Acetylaldehyde. These ingredients either exert synergistic effects or potentiate the effect of nicotine. Certain active metabolites of nicotine have been noticed to exert strong effects on the central nervous system after acute nicotine administration [16].

Nornicotine is both a metabolite of nicotine and a minor alkaloid in tobacco. At low nornicotine concentrations, nicotine receptor antagonists, such as mecamylamine and [3H]-dihydro-β-eritroidine (DHβE) inhibit S (-)-nornicotine-triggered dopamine release. At high nornicotine doses, this inhibition is absent, indicating that high doses of dopamine release can be triggered by non-selective mechanisms. S (-)-nornicotine, R (+)-nornicotine, and nicotine are all involved in activating the neuronal mechanisms responsible for behavior sensitization [17].

Nicotine is extensively metabolized in the body, mainly in the liver. In humans, there are six primary metabolites [15]. Nicotine is the major component of tobacco and cigarette smoke (approximately 7–8 mg/cigarette). Nicotine can be measured, both in active and passive smokers, in several body fluids including serum, urine, and saliva.

Cotinine, formed as a result of nicotine oxidation by P450 cytochrome, is one of nicotine’s primary metabolites. Having a blood half-life of fewer than two hours, the levels of nicotine concentration in biological fluids can help determine the recentness of exposure. By contrast, Cotinine has a blood or plasma half-life of 15–19 h. An international study, conducted across six countries by Biber et al. [18], compared the analytical results of urine and serum cotinine. The results of the study indicated that both gas chromatography (GC) and RIA (radioimmunoassay) accurately assess the quantities of cotinine in serum and blood samples.

In cancer, a common assessment of the biologically effective dose of nicotine is obtained by measuring the DNA adducts’ levels. Several mutagens and carcinogens are metabolically activated in vivo to electrophilic forms capable of interacting with cellular macromolecules. One of the mechanisms used by the body to fight the electrophilic attack is to conjugate reactive chemical residues with reduced glutathione, which is a nucleophile. This reaction induces an increase in polar thioether conjugates which are excreted from the body through urine and bile. Thioether urine concentrations are used as an unspecific indicator of exposure to alkylating agents. Smoking has been noticed to induce a dose-dependent increase in thioether urine excretion. Chemical substances found in cigarette smoke, excreted in urine as thioethers, include benzene, styrene, and vinyl chloride [19]. High concentrations of alkyl adenines and alkyl guanines from the reaction of alkylating agents with DNA have also been found in the urine of smokers. All three types of carcinogens (thioethers, alkyl adenines, alkyl guanines) reflect the ratio and balance between activation and detoxification [20].

The chemical structure and pharmacology of nicotine qualify it as the drug that creates the strongest addiction. Tobacco products are created to enable nicotine’s fast extraction, absorption, and distribution to the central nervous system. This drug is 5 to 10 times more potent than cocaine or morphine in generating physical and behavioral signs associated with addiction, including pleasure and preference [21]. The development of nicotine addiction depends on the quantity of nicotine that enters the body and its mode of delivery; rapid intake, absorption, and attainment of high plasma concentration increase the potential of creating addiction [22].

The understanding of the consequences of health statuses and pathologies induced by smoking has prompted the scientific foundations to increase awareness on prevention and cessation of both active and passive smoking. In this context, this study aimed at exploring the predictive behaviors/habits suggestive of the degree of tobacco use among young college students, and other elements in their immediate environment that may influence not only the smoker/nonsmoker status but also the smoking intensity.