Epidemiological studies have played multiple roles in verifying the causality between smoking and lung cancer and quantifying the extent of harmfulness of smoking. However, in establishing the evidence for the causality between smoking and lung cancer, other observational and experimental results (i.e., individual observations, animal studies, and laboratory chemical analyses) have also contributed significantly [20].
First, there are the results of animal experiments. These include studies that demonstrated cancer development when ‘tobacco juice’ was administered to animals. Wynder and colleagues induced carcinogenesis by applying cigarette tar to mice [21].
Second, there are observational studies of cellular pathology. Since the 1930s, pathologists determined that smoking impairs the movement of cilia (a cellular organelle in the human body that sweeps foreign materials out of the lungs) in the upper airway causing ciliostasis [20]. Cellular pathologic studies have found that upon ciliostasis, the cigarette contents inhaled become trapped in the lungs, which can cause cancer.
Third, carcinogenic chemicals have been found in cigarette smoke. In the 1930s, Angel Roffo identified polycyclic aromatic hydrocarbons present in cigarette smoke [20], and in 1952 researchers in the tobacco company Brown and Williamson, identified benzpyrene [22]. Afterwards, numerous carcinogens were identified through chemical analysis. Indeed, approximately 7,000 chemicals are produced during smoking, which may have harmful effects on human [23].
Scientific evidence for the causality between smoking and lung cancer is based on data from individuals and groups, studies in animals and humans, observational and experimental studies, studies in laboratories and communities, and studies in both underdeveloped and developed countries. Therefore, the denial of the causality between smoking and lung cancer cannot help but be considered denial of the current scientific knowledge system.
