Here is an essay on ‘Tobacco and Cancer’ which states – How smoking or consuming tobacco can trigger the development of cancer.
Once the importance of environmental factors in triggering the development of cancer had been established, the question arose as to the identity of the agents involved. At the top of the list is tobacco smoke, now known to be responsible for roughly one of every three cancer deaths.
Tobacco smoke is responsible for approximately one-third of all cancer deaths.The first indication of the dangers posed by tobacco smoke came from the emergence of lung cancer as a major disease. Lung cancer was one of the rarest forms of cancer prior to the twentieth century, with only 140 cases reported in the entire world medical literature up until 1898.
As late as the 1920s, doctors were still being called in to observe any case that did arise because of the belief that they might never have an opportunity to see a patient with lung cancer again! Today lung cancer is among the most frequently encountered cancers, causing more deaths than any other type.
So what happened during the twentieth century to convert a rare cancer into the number one cancer killer? When doctors started asking questions of the increasing number of lung cancer patients that came to their offices in the early 1900s, it was discovered that virtually all individuals with lung cancer shared one thing in common: They smoked cigarettes. Moreover, cigarette smoking was a relatively new habit.
During the 1800s tobacco had been consumed in relatively small amounts, mainly in the form of pipe tobacco, chewing tobacco, and cigars. Habits began to change with the invention of the cigarette rolling machine in 1881, followed by the introduction of safety matches shortly thereafter.
Both developments encouraged the smoking of tobacco, and the number of cigarettes consumed per year went from a few dozen per person in 1900 to an average of more than 4000 per person in 1963, the year that smoking rates peaked in the United States.
Figure 7 illustrates the relationship between this explosive growth in cigarette smoking and the ensuing epidemic of lung cancer. Examination of this graph reveals that a time lag of about 25 years transpired between the increase in smoking rates and the subsequent increase in lung cancer rates. We now know that such a long delay is typical of the behavior of human cancers, which often require many years after carcinogen exposure to complete the steps involved in creating a malignant tumor.
When the link between cigarette smoking and lung cancer was first widely publicized in the 1960s, some scientists (and virtually all representatives of the tobacco industry) questioned whether epidemiological data pointing to events separated by 25 years could demonstrate that smoking and cancer risk were connected in any way.
After all, it could be easily argued that the epidemic of lung cancer that began in the 1940s was caused by some environmental factor that appeared at the same time, such as air pollution, rather than being triggered by cigarette smoking 25 years earlier.
As we saw earlier in this article, it is inherently difficult to infer cause-and-effect relationships from epidemiological data, and the problem is further magnified when the events being investigated are separated by long periods of time.
Caution in drawing conclusions about the linkage between smoking and lung cancer was appropriate in 1960 because of the limited amount of evidence available at the time. Hundreds of subsequent studies, however, have made it abundantly clear that smoking is the underlying cause of most lung cancers. Some of the additional evidence is seen in the portion of Figure 7 that covers the period after 1960, when two patterns emerged that had not been evident in the earlier data.
The first pattern is that smoking rates peaked during the 1960s and then began to slowly decrease. If the hypothesis that smoking causes lung cancer is correct, lung cancer rates should have started to decline about 25 years later, which is exactly what happened.
The second pattern involves the behavior of women, who did not begin to smoke in large numbers until the 1940s; about 20 years after smoking had become popular among men. If smoking causes lung cancer, we would expect lung cancer rates to start increasing in women later than it had in men. Again, this is exactly what the data in Figure 7 show.
The difference in timing between the onset of smoking as a common habit among men and women fostered a myth, often heard in the 1960s, which claimed that cigarettes cause lung cancer in men but not in women.
The origin of such a myth is easy to understand. Many men and women were smoking cigarettes on a regular basis by the early 1960s, but lung cancer was seen mainly in men because they had started smoking decades earlier and it takes about 25 years for lung cancer to develop.
The difference in lung cancer rates in men and women was relatively short lived. As expected, female lung cancer rates began to increase in the 1970s, and by 1987, lung cancer had surpassed breast cancer as the number one cancer killer in women (Figure 8).
A Dose-Response Relationship Exists between Exposure to Tobacco Smoke and the Risk of Developing Cancer:
Additional support for the conclusion that, smoking causes lung cancer has come from dose-response data relating cancer risk to how much people smoke. Such data have shown that lung cancer rates are directly proportional to the number of cigarettes smoked per day (Figure 9, left). A similar relationship has been demonstrated by analyzing the age at which people began smoking.
In this case, the data show that long-term smokers develop lung cancer more frequently than do short-term smokers (Figure 9, middle). Finally, people who inhale deeply develop lung cancer more frequently than smokers who do not inhale deeply, again revealing a dose-response relationship between tobacco smoke exposure and lung cancer (Figure 9, right).
Overall, a typical heavy smoker incurs roughly a 2500% increase in lung cancer risk, which is enormous compared with the risks posed by most of the other causes of cancer.
The carcinogenic properties of tobacco smoke can be traced to a specific group of chemical compounds. Tobacco smoke contains more than 4000 different chemicals, more than 40 of which are carcinogenic when administered to animals (Table 2). Laboratory studies have shown that many of these chemicals cause DNA damage and trigger gene mutations, which are early steps in the development of cancer.
The carcinogens benzo[a]pyrene and 2-naphthylamine are examples of the numerous potent carcinogens in tobacco smoke that cause mutations by forming chemical linkages to DNA. Ironically, strict safety regulations control the use of benzo[a]pyrene, 2-naphthylamine, and many of the other substances found in tobacco smoke when these chemicals are handled in the workplace, but the exact same chemicals can be freely inhaled in large concentration by anyone who chooses to smoke cigarettes.
Current evidence suggests that in addition to being responsible for about 85% of all lung cancers, cigarette smoking can also cause cancers of the mouth, pharynx, larynx, esophagus, stomach, pancreas, uterine cervix, kidney, bladder, and colon, as well as leukemias.
Depending on the particular cancer involved, smoking may be a major risk factor (e.g., cancer of the lung, mouth, pharynx, and larynx) or a smaller risk factor (e.g., colon cancer and leukemia). When the cancer risks associated with smoking are combined with other tobacco-related illnesses, such as stroke and heart disease, smoking accounts for at least 400,000 of the roughly two million deaths occurring in the United States each year. This statistic makes tobacco the number one cause of preventable death, killing close to half of all regular smokers.
Because tobacco smoke is carcinogenic, exposure of nonsmokers to secondhand smoke (tobacco smoke generated by others) is also a potential cancer hazard. Fortunately, the amount of secondhand smoke inhaled by nonsmokers is usually rather small. Current estimates suggest that secondhand smoke typically causes no more than a 30% increase in lung cancer risk, compared with the 2500% increase experienced by the average heavy smoker.
Nonetheless, secondhand smoke is thought to contribute to the 15% of lung cancer cases that occur in people who have never smoked. In addition, animal studies have shown that exposure to secondhand smoke increases the concentration of the angiogenesis stimulator VEGF in the bloodstream and speeds tumor growth in animals that had been previously injected with cancer cells. Such findings suggest that secondhand smoke may pose cancer-related risks that go beyond the carcinogenic chemicals it contains.