PUBLICATIONS

Prof. Geoffrey Onyemelukwe

Professor of Medicine and Immunology, The Ahmadu Bello University Teaching Hospital, Zaria, Nigeria

Dr Ashraf A. Amir

Consultant, Family Medicine Center

International Medical Center, P.O. Box: 2172

Jeddah: 21451, Saudi Arabia

Introduction

The World Health Organization (WHO) estimates that tobacco caused 5.4 million deaths in 2004 and that annual tobacco-attributable deaths will rise to 8.3 million by 2030, at which point these will represent almost 10% of all deaths globally [6]. By 2030, more than 80% of tobacco deaths will be in developing countries [3]. The scale of the epidemic and its growth is apparent in the contrast between the estimated death toll of 100 million for the 20th century and the current estimated death toll for the 21st century of 1 billion [3]. Nations least prepared to deal with the financial, social and political consequences of this global public health issue, including the countries of Africa and the Middle East region, will bear particularly high burdens [7].

As at 2000, 1.22 billion people worldwide were estimated to be tobacco users, and assuming a modest increase in income per capita this was predicted to reach 1.45 billion by 2010 and between 1.5 and 1.9 billion by 2025 [8]. Tobacco use is almost five times higher in men than women, and rates for women have begun to climb in developing countries [8].

Tobacco usage, in smoked and smokeless forms, occurs in all cultures worldwide [1]. Tobacco smoke contains more than 4,000 chemicals, more than 50 known or suspected carcinogens, and many potent irritants. Chemical carcinogens present in tobacco smoke include tobacco-specific nitrosamines (TSNAs), polyaromatic hydrocarbons (PAHs), and

volatile organic compounds (VOCs) [1]. Carcinogenic nitrosamines are also present in smokeless tobacco products [9]. Despite the well-known adverse health effects of tobacco, people continue to use this, and once started, find it difficult to quit, due to addiction [10]. The pharmacologic and behavioral processes that determine tobacco addiction are similar to those that determine addiction to drugs such as heroin and cocaine. Human and animal studies have shown that the powerful pharmacologic agent nicotine is the main psychoactive compound in tobacco that leads to addiction. The beta-carbolines harmane and norharmane which are present in cigarette smoke may also play a role in tobacco addiction by activating the firing and/or burst activity of dopamine neurons [11]. Smoking initiation and persistence are also influenced by genetic factors. Among the candidate genes predisposing to tobacco use are several genes involved in nicotine metabolism and dopamine catabolism, including genes encoding the nicotinic receptor, the dopamine D1, D2, D4 and D5 receptors, the serotonin transporter (SERT), dopamine beta‑hydroxylase, and Cytochrome P450[12–14].

Understanding the tobacco epidemic: the WHO/Lopez model

The WHO/Lopez model of the four stages of the evolving tobacco epidemic provides a conceptual framework to link the stages of the epidemic into a continuum, rather than a series of isolated events (Figure 1) [15]. This model, originally proposed by Lopez et al. [16], allows virtually any country to identify where it is in relation to the larger epidemic.