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Mortality in women and men in relation to smoking
Omissis
Summary
In this paper, pooled data from three prospective population studies in
Copenhagen are used to compare total and cause-specific mortality in relation
to smoking habits. A sample population, comprising more than 30 000 individuals
whose date and cause of death was recorded, was monitored between
1964 and 1994. Information was collected from individuals via a self-administered
questionnaire on smoking behaviour in never-smokers, ex-smokers,
those smoking fewer than 15 cigarettes a day, and those smoking more than
15 cigarettes a day. Data were also collected for those using other forms of
tobacco, and on inhalation.
Positive associations were confirmed for both men and women for smoking
and lung cancer (together with other causes of death). The authors noted
that while relative risks associated with smoking were higher for women in
relation to respiratory and vascular disease, there were no differences
between women and men in the relative risk of smoking-related cancers. The
authors cautiously concluded that although women may be more sensitive
than men in terms of some causes of death, lung cancer in not among them.
omissis
What Are the Known Key Factors
That Increase the Individual Risk
for Lung Cancer?
Smoking is the major risk factor, accounting
for about 90% of lung cancer incidence.
There are additional exogenous
and endogenous factors contributing to
the individual risk, such as the following:
Low consumption of fruit and vegetables
Genetic predisposition
Exposure to non-tobacco procarcinogens,
carcinogens, and tumor promoters
Previous lung disease such as chronic
obstructive pulmonary disease (COPD)
Previous tobacco-related cancer
Passive smoking
Omissis
Dr. Biesalski is Professor and Head, Department of
Biological Chemistry and Nutrition, University of
Hohenheim, Stuttgart, Germany.
Dr. Bueno de Mesquita is at the National Institute of
Public Health and the Environment, Bilthoven, The
Netherlands.
Dr. Chesson is at the Rowett Research Institute,
Aberdeen, Scotland.
Dr. Chytil is Professor, Department of Biochemistry,
Vanderbilt University, Nashville, TN.
Dr. Grimble is Professor, Institute of Human
Nutrition, Southampton, England.
Dr. Hermus is Professor, Strategy and Program
Department, Netherlands Organization for Applied
Scientific Research (TNO), Delft, The Netherlands.
Dr. Kφhrle is Professor, Department of Internal
Medicine, University of Wόrzburg, Wόrzburg,
Germany.
Dr. Lotan is Professor and Associate Vice President
for Cancer Prevention, Department of Tumor Biology,
M.D. Anderson Cancer Center, Houston, TX.
Dr. Norpoth is Professor Emeritus of Toxicology,
Institute of Hygiene and Occupational Medicine,
University of Essen, Essen, Germany.
Dr. Pastorino is at the Royal Brompton Hospital,
London, England.
Dr. Thurnham is in the Human Nutrition Research
Group, Department of Biology and Biomedical
Sciences, University of Ulster, Coleraine, Northern
Ireland.
Adapted with permission from European Journal of
Cancer Prevention, 1997;6:316-322.
This article is also available online at
www.ca-journal.org.
http://caonline.amcancersoc.org/cgi/reprint/48/3/167.pdf
Nature Reviews Cancer 3, 733-744 (October 2003) | doi:10.1038/nrc1190
There is a Correction (1 January 2004) associated with this article.
Tobacco carcinogens, their biomarkers and tobacco-induced cancer
Stephen S. Hecht1 About the author
Top of page
Abstract
The devastating link between tobacco products and human cancers results from a powerful alliance of two factors nicotine and carcinogens. Without either one of these, tobacco would be just another commodity, instead of being the single greatest cause of death due to preventable cancer. Nicotine is addictive and toxic, but it is not carcinogenic. This addiction, however, causes people to use tobacco products continually, and these products contain many carcinogens. What are the mechanisms by which this deadly combination leads to 30% of cancer-related deaths in developed countries, and how can carcinogen biomarkers help to reveal these mechanisms?
www.nature.com/nrc/journal/v3/n10/abs/nrc1190.html
Emerging tobacco hazards in China: 1. Retrospective
proportional mortality study of one million deaths
BoQi Liu, Richard Peto, ZhengMing Chen, Jillian Boreham, YaPing Wu, JunYao Li,
T Colin Campbell, JunShi Chen
Abstract
Objective To assess the hazards at an early phase of
the growing epidemic of deaths from tobacco in
China.
Design Smoking habits before 1980 (obtained from
family or other informants) of 0.7 million adults who
had died of neoplastic, respiratory, or vascular causes
were compared with those of a reference group of 0.2
million who had died of other causes.
Setting 24 urban and 74 rural areas of China.
Subjects One million people who had died during
19868 and whose families could be interviewed.
Main outcome measures Tobacco attributable
mortality in middle or old age from neoplastic,
respiratory, or vascular disease.
Results Among male smokers aged 3569 there was a
51% (SE 2) excess of neoplastic deaths, a 31% (2)
excess of respiratory deaths, and a 15% (2) excess of
vascular deaths. All three excesses were significant
(P < 0.0001). Among male smokers aged >70 there
was a 39% (3) excess of neoplastic deaths, a 54% (2)
excess of respiratory deaths, and a 6% (2) excess of
vascular deaths. Fewer women smoked, but those who
did had tobacco attributable risks of lung cancer and
respiratory disease about the same as men. For both
sexes, the lung cancer rates at ages 3569 were about
three times as great in smokers as in nonsmokers, but
because the rates among nonsmokers in different
parts of China varied widely the absolute excesses of
lung cancer in smokers also varied. Of all deaths
attributed to tobacco, 45% were due to chronic
obstructive pulmonary disease and 15% to lung
cancer; oesophageal cancer, stomach cancer, liver
cancer, tuberculosis, stroke, and ischaemic heart
disease each caused 58%. Tobacco caused about 0.6
million Chinese deaths in 1990 (0.5 million men).
This will rise to 0.8 million in 2000 (0.4 million at ages
3569) or to more if the tobacco attributed fractions
increase.
Conclusions At current age specific death rates in
smokers and nonsmokers one in four smokers would
be killed by tobacco, but as the epidemic grows this
proportion will roughly double. If current smoking
uptake rates persist in China (where about two thirds
of men but few women become smokers) tobacco will
kill about 100 million of the 0.3 billion males now
omissis
www.bmj.com/cgi/reprint/317/7170/1411.pdf
Lung Cancer in India
D. Behera and T. Balamugesh
Department of Pulmonary Medicine, Postgraduate Institute of Medical Education and Research,
Chandigarh, India
ABSTRACT
Background. Lung cancer is one of the commonest malignant neoplasms all over the world. It
accounts for more cancer deaths than any other cancer. It is increasingly being recognized in
India.
Methods. We did a systematic review of the published studies on epidemiology, diagnosis and
treatment of lung cancer in India. Literature from other countries was also reviewed.
Results. With increasing prevalence of smoking, lung cancer has reached epidemic proportions
in India. It has surpassed the earlier commonest form of cancer, that of oropharynx, and now
is the commonest malignancy in males in many hospitals. In addition to smoking, occupational
exposure to carcinogens, indoor air pollution and dietary factors have recently been implicated
in the causation of lung cancer. Squamous cell carcinoma is still the commonest histological
type in India in contrast to the Western countries, although adenocarcinoma is becoming more
common. Molecular genetics of lung cancer has opened up new vistas of research in
carcinogenesis. Various modalities for early detection through screening are being investigated.
Majority of the patients have locally advanced or disseminated disease at presentation and are
not candidates for surgery. Chemotherapy applied as an adjunct with radiation improves
survival and the quality of life. New anticancer drugs, which have emerged during the last
decade, have shown an improved efficacy- toxicity ratio.
Conclusions. In view of our large population, the burden of lung cancer will be quite enormous
in India. Drastic measures aimed at discouraging people from smoking must be taken to reduce
the morbidity and mortality due to lung cancer.
Omissis
SMOKING AND LUNG CANCER
IN INDIA
Smoking is the most important contributory
factor in the causation of lung cancer52.
Nota 52:
52. Hammond EC, Horn D. Smoking and death
rates: Report on 44 months of follow-up of 187,
783 men. II. Death rates by cause. JAMA 1958;
166 : 1294-04.
In patients with lung cancer a history of active
tobacco smoking is present in 87% of males and
in 85% of females. History of passive tobacco
exposure is found in only three per cent.
The relative risk of developing lung cancer is
2.64 for bidi smokers and 2.23 for cigarette
smokers with 2.45 as the overall relative risk35.
Bidi is more carcinogenic as has been shown in
studies by Jussawalla and Jain49 and Pakhale
et al51. Hooka smoking has also been associated
with lung cancer as reported by Nafae et al31.
In a recent study by Gupta et al45, 80% of men
and 33% of women among the patients were
ever-smokers as compared to 60% of men and
20% of women among controls. The odds ratio
(OR) for ever-smoking was 5.0 (95% CI=3.11-
8.04) among men and 2.47 (95% CI=0.79-7.75)
among women. Smoking of bidi and hooka as
well as cigarettes had similar ORs for
cumulative consumption. The risk increased
with both the duration and quantity of all
smoking products45.
Nota 45
45. Gupta D, Boffetta P, Gaborieau V, Jindal SK.
Risk factors of lung cancer in Chandigarh,
India. Indian J Med Res 2001; 113 : 142-50.
PASSIVE SMOKING AND LUNG
CANCER
Environmental tobacco smoke is a known
lung carcinogen. A meta-analysis of 41 studies
showed that environmental tobacco exposure
carries a relative risk of development of lung
cancer of 1.48 (1.13-1.92) in males and 1.2 (1.12-
1.29) in females53. Risk increases with increase in
exposure. Exposure at work place results in a
relative risk of 1.16. In a study on non-smoking
lung cancer patients, environmental tobacco
exposure during childhood carried an OR of 3.9
(95% CI-1.9-8.2). There was an increasing risk
with increase in number of smokers in the
household and the duration of exposure.
Women had a higher OR of 5.1. Work place, and
vehicular pollutant exposure have shown a
weak association. Another study by Rapiti
et al54 has shown that environmental tobacco
smoke exposure during childhood is strongly
associated with the risk of later development of
lung cancer (OR 3.9, 95% CI=1.9-8.2).
Omissis
www.vpci.org.in/upload/Journals/pic130.pdf
Declining Incidence Rate of Lung Adenocarcinoma in the United States*
1. Fan Chen, DrPH,
2. William F. Bina, MD, MPH, and
3. Philip Cole, MD, DrPH
+ Author Affiliations
1. *From the Department of Community Medicine (Drs. Chen and Bina), School of Medicine, Mercer University, Macon, GA; and School of Public Health (Dr. Cole), University of Alabama at Birmingham, Birmingham, AL.
Next Section
Abstract
Background: Adenocarcinoma of the lung (ADL) increased worldwide during the last half century. We now report that a continuous decline of ADL began in the United States in 1999.
Method: Incidence rates of ADL and squamous cell carcinoma of the lung (SQL) from The Surveillance Epidemiology and End Results Program were reviewed for the 31-year period beginning in 1973. The low-tar cigarette (tar ≤ 15 mg) consumption/per capita by year was estimated based on cigarette consumption/capita data and the market share of low-tar cigarette of the same year in the United States.
Results: From 1973 to 1998, the age-adjusted incidence rate of ADL increased 83% in men, and > 200% in women. From 1999 through 2003, the rate declined 14% in men and 8% in women. An analysis of age-specific incidence rates of ADL according to birth cohort demonstrates that rates declined progressively among persons born after 1934 for both genders. The increase in low-tar cigarette consumption did not precede the increase in ADL incidence rates, and the decline of ADL incidence after 1998 occurred without a preceding decline of low-tar cigarette consumption.
Conclusion: Since 1999, the ADL incidence has declined. The temporal trend of ADL incidence may suggest that air pollution could be the possible determining cause for the trend. Increasing use of low-tar cigarettes in the United States and the decline in environmental tobacco smoke may be contributors but are less likely to be the driving force.
adenocarcinoma
air pollution
incidence rate
low-tar cigarette
lung cancer
Incidence rates of squamous cell carcinoma of the lung (SQL) have declined over the past 24 years. The decline in SQL is attributable to the decline in smoking that started during the 1960s. In contrast, numerous studies1234567 report that adenocarcinoma of the lung (ADL) has been increasing over the past several decades. The age-adjusted incidence of ADL in Connecticut increased nearly 17-fold in women (from 0.9 to 15.2 cases per 100 000 person-years) and nearly tenfold in men (from 2.4 to 23.2 cases per 100 000 person-years) from 1950 through 1991.8 Devesa et al9 reported that, through 1997, ADL incidence rose in virtually all areas of the world, with the increases among men exceeding 50% in many parts of Europe. It has been hypothesized that the trend of increase in ADL is mainly due to the dissemination of low-tar filter cigarettes.101112 It has been pointed out that low-yield, filter-tipped cigarettes, introduced since the 1950s, are inhaled more deeply than smoke from earlier unfiltered cigarettes. Inhalation transports tobacco-specific carcinogens more distally toward the bronchoalveolar junction where adenocarcinomas often arise. Second, blended reconstituted tobacco, introduced in the 1950s, releases higher concentrations of nitrosamines from tobacco stems. Nitrosamines from tobacco are known to induce lung adenocarcinomas in rodents when injected systemically.8 Air pollution is another concern when trying to understand the trend of lung cancer. Vineis and colleagues13 reported a significantly higher odds ratio (1.30) of lung cancer for those exposed to nitrogen dioxide (NO2) at levels ≥ 30 μg/m3 compared to those who were exposed to NO2 at levels < 30 μg/m3. In this article, we report that the 50 years increasing trend has stopped, and a declining incidence rates of ADL after 1998 appears in the United States.
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Materials and Methods
Lung cancer incidence rates from the Surveillance Epidemiology and End Results (SEER) Program were reviewed for the available 31-year period from 1973 to 2003. The SEER database provides information on persons with cancer in diverse geographic areas, which constitute approximately 10% of the US population. The nine standard SEER regions include the states of Connecticut, Hawaii, Iowa, New Mexico, and Utah, as well as the metropolitan areas of Atlanta, GA, Detroit, MI, San Francisco/Oakland, CA, and Seattle/Puget Sound, WA. We describe time trends in the age-adjusted incidence rates of ADL (International Classification of Diseases for Oncology codes 8140, 8211, 82308231, 82508260, 8323, 84808490, 85508560, 85708572) and SQL (International Classification of Diseases for Oncology codes 80508076). Birth cohort-specific rates for both genders are also presented.
To assess whether the patterns of ADL incidence are associated with the use of low-tar cigarettes (tar ≤ 15 mg per cigarette) in the United States, we describe per capita total cigarette consumption as well as per capita low-tar cigarette consumption by years. This consumption was based on the market share of low-tar cigarettes and total cigarette sales in each year. These data were obtained from the Federal Trade Commission.14
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Results
Figure 1 shows that the incidence rates of ADL for men and women are parallel to one another. Since 1973, the rates of ADL increased and then leveled off from 1993 to 1998, followed by a declining trend since 1999 for both genders. This fact of similarity may suggest the major cause has similar impact on both men and women despite the different smoking behavior between the two genders. In contrast, the age-adjusted incidence rate of SQL peaked in 1982 for men but peaked in 1991 for women. The SQL incidence in 2003 compared to their peak declined 52% for men and 18% for women. These facts may reflect the difference in smoking behavior for men and women. The incidence rate of ADL in men surpassed that of SQL in 1992. The age-adjusted incidence rate of ADL in women is approximately twofold higher than that of SQL for all years. For the period 1998 to 2003, the incidence rate of ADL declined 14% for men and 8% for women.
Figure 2 describes the age-specific incidence rates of ADL for men according to birth cohort. It shows that, compared to the birth cohort 1890, incidence rates for all subsequent cohorts increased progressively with peak rates for the 1930 to 1934 birth cohort. The incidence rates for all subsequent cohorts declined at nearly all ages. A very similar pattern is demonstrated in Figure 3 for female subjects. For women, the highest age-specific incidence rates also were seen for the 1930 to 1934 birth cohort.
Figure 4 shows the temporal patterns of lung cancer incidence rate by histologic types and the temporal trend of cigarette consumption in the United States. Peak cigarette consumption occurred approximately 15 years earlier than the peak in SQL incidence rates, reflecting the induction period. The peak in ADL occurred > 30 years later than the peak of cigarette consumption, suggesting that causes other than cigarettes may play a major role in the sharp increase in ADL incidence, or the induction time for ADL is much longer than 30 years. While the sharp increase of low-tar cigarette consumption began in 1973, the sharp increase in ADL incidence rate had by then existed for approximately 20 years. From 1973 to 1981, the consumption of low-tar cigarettes increased 584% and the incidence rate of ADL increased 55%. Low-tar cigarette consumption leveled off from 1981 to 2000. However, the age-adjusted incidence rate of ADL declined consistently after 1998. In 1973, the ADL and SQL cases counted for 17.3% and 31.0% of all lung cancer cases, respectively; but in 2000, ADL and SQL accounted for 29.8% and 22.8% of the lung cancer cases.
Previous SectionNext Section
Discussion
The increase of ADL incidence rates, especially in women, was first observed in 1950 and confirmed in 1956.15 The incidence rate of ADL among men surpassed that of SQL in 1992. These increases may be due in part to diagnostic advances that make it easier to perform biopsies on tumors in small, distal airways where these tumors often arise. However, the increase in ADL started in the 1950s, > 2 decades prior to the major diagnostic advances that occurred in 1980s. Moreover, the male to female ratio was 2.5 in 1973, and decreased to 1.3 by 2002. There is no reason to believe that diagnostic advances were greater for women than for men; therefore, the rapid increase is likely to be a real increase rather than artifact. Of course, diagnostic advances cannot explain the considerable decrease after 1998.
The similarity of the ADL incidence curves of men and women, over time, is much greater than the similarity of SQL incidence curves of men and women. The turning points of ADL incidence, ending increase and beginning decline, occurred in 1999 for both genders. This suggests that the major cause of ADL is a more general phenomenon and has impacts on men and women in the same way, such as air pollution. Different behaviors between genders, such as smoking, are less likely to be the major cause, because it cannot explain why the peaks of ADL in both genders are on the same year. In contrast, smoking is the major cause of SQL. The incidence rates of SQL peaked in 1982 for men but peaked in 1991 for women, which could be explained by different smoking behaviors between men and women. The substantial decline in SQL started in 1982 for men, approximately 18 years later than the substantial decline of cigarette consumption. This indicates that the induction period for SQL is approximately 18 years. If the induction period for ADL is similar to that for SQL, we can assume that the possible determining factor for ADL started to increase around 1940 or even earlier, and then it started to decrease in 1980. It is not clear what is the possible determining factor, ie, the major cause of ADL, that can fully explain the temporal trend of 50 years increase and the recent 5 years declining. The possible speculated factors include air pollution caused by industrialization and urbanization. The remarkable increase in automobile density as an indicator of industrialization and air pollution started in 1945 in the United States.16 The substantial decline of national air pollutant emissions started in 1980.17 This coincidence with a reasonable induction period for both increase and decline suggests the necessity for further studies in the air pollution hypothesis. Vineis et al13 conducted a nested case-control study in 10 European countries and found a 30% statistically significant increase in the risk of lung cancer developing for those who were exposed to NO2 levels ≥ 30 μg/m3 compared to those who were exposed to NO2 levels < 30 μg/m3. Nyberg et al18 reported a result of a population-based case-control study covering the lung cancer cases in Stockholm County, from 1950 to 1990. They found that those with the highest exposure to NO2 had an estimated 44% statistically significant increase in risk for lung cancer compared to those who had the lowest levels, adjusting for age, year, smoking habits, radon exposure, and occupational exposures known to be associated with lung cancer. These studies suggest a need for further studies to test whether air pollution is the major cause of ADL.
Another possible cause that is the effect of increased consumption of low-tar cigarettes since 1970s. Although the low-tar cigarette (tar ≤ 15 mg) was developed in 1955, Figure 4 demonstrated that its sales did not rise sharply until 1972. This result is similar to the results reported by Giovino et al.19 However, the increase in ADL predated this by approximately 20 years. The rapid increase of ADL incidence rate was evident by the 1950s or 1960s.20 Between 1981 and 1998, both low-tar cigarette sales and ADL incidence fluctuated at high levels, but a remarkable decline in ADL started in 1999 and continued thereafter. This decline is not preceded by a decline in consumption of low-tar cigarette. The lack of temporal association between ADL and the low-tar cigarette consumption in either rise or decline argues against the hypothesis that the use of low-tar cigarettes is the major cause of the increase in ADL incidence rate, although it is one of the causes of the ADL.
Another possible explanation for the ADL trend may be environmental tobacco smoke (ETS). In recent years, more strict regulations have been enacted that reduced ETS exposure. These changes may partially explain the recent down trend of ADL incidence. However, based on the nationwide Current Population Survey,21 only 4 states reported smoke-free public areas in 1992, but 32 states in 1995. If the policies restricting ETS were enacted in most states during 1990s, it is then less likely to be the cause of down trend of ADL that started in 1999, because the years between the policies and the down trends are too short for the expected induction period. Moreover, the total lung cancer cases attributed to ETS is approximately 3,000/yr in the United States, which accounts for < 2% of the 172,570 new lung cancer cases a year.22 If the decline in the number of people who were exposed to ETS is 10%/yr, we would expect < 0.2% changes in number of lung cancer cases. This number is therefore too small to explain the remarkable change in ADL incidence. In fact, for the period 1998 to 2003, the incidence rate of ADL declined 14% for men and 8% for women. Such large reductions could not be explained by a decline in the number of people who were exposed to ETS.
The recent 5-year decline in the age-adjusted incidence rate of ADL, especially in men, is further explained by birth cohort patterns. Both genders show the same pattern, with persons born after 1930 having progressive declines in age-specific incidence rate of ADL. This suggests that incidence rates in both genders will continue to decrease in coming years. It is not clear why the highest age-specific incidence rate for all ages occurred in 1930 to 1934 birth cohorts, and after that the age-specific incidence rates start to decline.
Limitation
This study is a descriptive study. The estimation of consumption of low-tar cigarettes is based on the average level in the whole United States. In fact, the consumption of low-tar cigarettes may vary by areas (rural vs metropolitan), race/ethnicity, gender, age, and education. The increase of consumption of low-tar cigarettes after 1973 may play some role in the increase of ADL incidence in some areas or some populations, but is not sensitive enough to be detected by this study, in which the average level of the United States was used.
In summary, this study described the fact that ADL incidence has declined since 1999. The driving force for its long period increase, and subsequent decline in recent years is not clear. The possible causes may include air pollution, low-tar cigarette consumption, and ETS.
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Figure 1.
Incidence rates according to histologic type and gender. Rates are age adjusted to the 2000 standard population.
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Figure 2.
Incidence rates of ADL among men according to birth cohort.
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Figure 3.
Incidence rates of ADL among women according to birth cohort,
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Figure 4.
Incidence rates of lung cancer among men by histologic type and cigarette consumption.
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Footnotes
Abbreviations: ADL = adenocarcinoma of the lung; ETS = environmental tobacco smoke; NO2 = nitrogen dioxide; SEER = Surveillance, Epidemiology, and End Results; SQL = squamous cell carcinoma of the lung
The authors have no conflicts of interest to disclose.
o Accepted November 22, 2006.
o Received July 6, 2006.
Previous Section
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The Increasing Incidence of Lung
Adenocarcinoma: Reality or Artefact?
A Review of the Epidemiology of
Lung Adenocarcinoma
ANNE CHARLOUX,* ELISABETH QUOIX,** NORMAN WOLKOVE,* DAVID SMALL,* GABRIELLE PAULI**
AND HARVEY KREISMAN*
Charloux A (Pavillon Laennec, Hτpitaux Universitaires de Strasbourg, 1 place de lhτpital, BP 426, 67091 Strasbourg
Cedex, France), Quoix E, Wolkove N, Small D, Pauli G and Kreisman H. The increasing incidence of lung adenocarcinoma:
Reality or artefact? A review of the epidemiology of lung adenocarcinoma. International Journal of Epidemiology
1997; 26: 1423.
Lung adenocarcinoma is the most common cell type in females (smokers or non-smokers) and in non-smoking males. Its
incidence has been increasing in younger cohorts of males and females until very recent years. Changes in classification
and in pathological techniques account for some of this increase. In females and non-smoker males, the increase could
be partly due to a detection bias in former studies. Nevertheless, successive cohorts over time seem more likely to
develop adenocarcinoma and less likely to develop squamous cell carcinoma. These differences between birth cohorts
suggest that the increasing incidence of adenocarcinoma is not only due to changes in pathological diagnosis.
Geographical differences are also observed: in Europe, the squamous cell type still predominates and an increase in
incidence of adenocarcinoma has only been reported in the Netherlands. In Asia, in the 1960s and 1970s, the proportion
of adenocarcinoma was higher than in North America or Europe and seems to be increasing. To what extent these
differences are due to differences in establishing diagnosis remains unknown.
Despite these biases in temporal and geographical trends detailed in this review, there has probably been a true
increase in incidence of adenocarcinoma. An explanation for this should be sought in studies on detailed smoking history
and passive smoking exposure, occupational exposure, diet and cooking, pollution and other environmental factors.
omissis
Adenocarcinoma and Tobacco Consumption
The increase in incidence of adenocarcinoma could be
partly explained by an increase in tobacco smoking.
Several authors have found a dose-response relationship
between adenocarcinoma and cigarette smoking,
however this was weaker than that between squamous
cell carcinoma and smoking.2730 This risk increased
with both number of cigarettes per day and duration of
smoking.27,28 Reduction of tobacco consumption in the
1960s in males has been followed by a recent decrease
in incidence of squamous cell carcinoma, but not by a
decrease in incidence of adenocarcinoma. Some factors
could partly explain these differences in temporal
trends between subtypes. Relative risk for adenocarcinoma
has been found to decrease more slowly
after smoking cessation than that for squamous cell carcinoma.
27,31 Variations in composition of cigarette
tobacco with time could have played an important role.
These variations could have favoured the development
of adenocarcinomas at the expense of squamous cell
carcinomas. This could explain too why differences in
incidence patterns between squamous cell carcinoma
and adenocarcinoma are less pronounced in women,
who started smoking 1020 years later than men. For
example, introduction of filter cigarettes in the 1950s
has been incriminated in the increase in incidence of
adenocarcinoma which occurred 20 years later, in the
1970s.25 Filters remove larger particles in cigarette
smoke, thus reducing deposition of those particles in
central airways where squamous cell carcinoma
develop preferentially. This could lead to a reduction
in incidence of the squamous cell type, but not of the
adenocarcinoma subtype which primarily occurs in
peripheral areas of the lung.32 Moreover, smokers,
especially women, who switched from non-filter to filter
cigarettes increased the number of cigarettes smoked
per day, which increases the risk of lung cancer.33
Smokers of filter cigarettes take larger puffs and inhale
more deeply than smokers of plain cigarettes. Consequently,
an increased deposition of smoking particles in
the small airways could result in an increased risk of
adenocarcinoma.34 In France, smokers decreased their
consumption of plain cigarettes and black tobacco
much later than in the USA. These particularities may
explain why no increase in the incidence of adenocarcinoma
has yet been described.34 Impact of tar and
nicotine level, additives and their variations with time
on lung cancer differentiation deserve to be analysed.
NNK, a tobacco specific N nitrosamine, preferentially
causes adenocarcinoma in rodents. This carcinogen,
which increased in cigarette smoke between 1978 and
1992 by about 45%, could be one factor responsible for
the increase in incidence of adenocarcinoma.34
http://ije.oxfordjournals.org/cgi/reprint/26/1/14.pdf
Second hand smoke, age of exposure and lung cancer risk
Kofi Asomaning, MB ChB MS,1 David P. Miller, ScD,1 Geoffrey Liu, MD,1 John C. Wain, MD,2 Thomas J. Lynch, MD,3 Li Su, BS,1 and David C. Christiani, MD1,4
1 Department of Environmental Heath, [Environmental and Occupational Medicine and Epidemiology Program] (D.P.M., K.A., G.L., L.S., D.C.C.), Harvard School of Public Health, Boston MA 02115
2 Thoracic Surgery Unit, Department of Surgery (J.C.W.), Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston MA 02114
3Oncology Unit (T.J.L), Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston MA 02114
4Pulmonary and Critical Care Unit (D.C.C.), Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston MA 02114
Address correspondence to Dr. David C. Christiani, Harvard School of Public Health, 665 Huntington Avenue Bldg 1 Room 1402, Boston, MA 02115. Tel. 617-432-3323, Fax. 617-432-3441, Email: [email protected]
Kofi Asomaning and David Miller contributed equally to this work.
The publisher's final edited version of this article is available at Lung Cancer.
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o AbstractIntroductionMaterials and MethodsResultsDiscussionReferencesAbstract
Background
Exposure to second hand smoke (SHS) has been identified as a risk factor for lung cancer for three decades. It is also known that the lung continues to grow from birth to adulthood, when lung growth stops. We hypothesize that after adjusting for active cigarette smoking, if SHS exposure took place during the period of growth i.e. in the earlier part of life (0 to 25 years of age) the risk of lung cancer is greater compared to an exposure occurring after age 25.
Method
Second hand smoke exposure was self-reported for three different activities (leisure, work and at home) for this study population of 1669 cases and 1263 controls. We created variables that captured location of exposure and timing of first exposure with respect to a study participant's age (0 - 25, >25 years of age). Multiple logistic regressions were used to study the association between SHS exposure and lung cancer, adjusting for age, gender and active smoking variables.
Result
For study participants that were exposed to SHS at both activities (work and leisure) and compared to one or no activity, the adjusted odds ratio (AOR) for lung cancer was 1.30(1.08-1.57) when exposure occurred between birth and age 25 and 0.66(0.21-1.57) if exposure occurred after age 25 years. Respective results for nonsmokers were: 1.29 (0.82-2.02) and 0.87 (0.22-3.38), and current and ex smokers combined 1.28 (1.04-1.58) and 0.66 (0.15-2.85).
Conclusion
All individuals exposed to SHS have a higher risk of risk of lung cancer. Furthermore, this study suggests that subjects first exposed before age 25 have a higher lung cancer risk compared to those for whom first exposure occurred after age 25 years.
Keywords: Second hand smoke, age of exposure, lung cancer risk
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o AbstractIntroductionMaterials and MethodsResultsDiscussionReferencesIntroduction
Lung cancer is the leading cause of cancer death for both men and women in the United States. Past studies have demonstrated the association between active cigarette smoking (mainstream smoke, MSS) or second hand smoke (SHS) exposure and the risk of adult non-small cell lung cancer (NSCLC). However, less is known about the effect of the age of exposure, particularly to SHS, on the risk of NSCLC (1-3). Most studies (4-18) have focused on paternal and maternal smoking during pregnancy and the effect on childhood illnesses and cancers in general or more recently the risk of lung cancer for non-smoking women exposed to tobacco smoke during childhood (19-28). Very few studies (19, 22, 29, 30) have focused on the effect of the period of exposure relevant for lung cancer development while also assessing the significance of lifetime exposure by location.
The lung continues to grow from birth to adulthood (31) and most lung growth is over by age 18 (32-34), but lung volume continues to expand to 25, suggesting additional growth may occur (35-39). Exposure of target organs to carcinogens during periods of rapid cell division or childhood is known to increase the risk of cancer and elevated exposure to carcinogens has been associated with higher levels of both DNA-adducts and somatic aberrations in cancer cells and may lead to genetic abnormalities that result in the development into cancer (40, 41).
SHS consists of emissions from cigarettes, pipes and cigars, as well as exhaled materials from MSS, which contains several chemicals including over 50 known carcinogens (40, 42, 43). The concentrations of benzol(a)pyrene, toluene, dimethylnitrosamines in SHS is much higher than in MSS, and the smaller particles in SHS are more likely to be deposited in the lung. SHS may induce DNA adducts, sister chromosome exchange (44), oxidative DNA damage (45, 46), and increased number of p53 mutations in lung cancer (47, 48), suggesting a similar etiologic mechanism for cases exposed to SHS and to MSS.
SHS exposure may occur at home (including childhood exposure from parents/other family members and exposure from spouse/family members in adulthood), at work (occupational exposure), and at leisure (exposure at public places other than work). Due to public health education and as a result of legislation in several developed countries, exposure to second hand smoke is declining at work and public places but direct marketing to younger populations by tobacco companies has contributed to continued high exposure among youths (49-52). The intensity or frequency of exposure in work places has been noted to be generally higher than that of at home or leisure places (53), and results from a previous study has suggested that SHS exposure at work places may have a stronger effect on NSCLC risk than exposure at home or at leisure places (54).
We hypothesize that after adjusting for active cigarette smoking, if the SHS exposure took place during the critical period of growth i.e. in the earlier part of life (0 to 25 years of age) the risk of lung cancer is greater compared to an exposure occurring after age 25.
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o AbstractIntroductionMaterials and MethodsResultsDiscussionReferencesMaterials and Methods
Study Population
This study was reviewed and approved by the Institutional Review Boards of the Massachusetts General Hospital and the Harvard School of Public Health. The study population of 1669 cases and 1263 controls is derived from a large case control study evaluating the molecular epidemiology of lung cancer, which began in 1992 at the Massachusetts General Hospital (MGH). Eligible cases included any person over the age of 18 years, with a diagnosis of primary lung cancer. An MGH lung pathologist confirmed all cases. The controls were the friends or spouses of cancer patients or the friends or spouses of other surgery patients in the same hospital. Potential controls that carried a previous diagnosis of any cancer (other than non-melanoma skin cancer) were excluded from participation. Controls were recruited among friends and non-blood related family members of the cases (usually spouses) (41%). If friends of lung cancer patients were not available, controls were recruited from friends and family of patients either receiving thoracic surgery, chemotherapy or radiation treatment for a condition other than lung cancer (59%).
Data collection
Interviewer-administered questionnaires (a modified version of the detailed American Thoracic Society health questionnaire) collected information on demographics, occupational exposures, and detailed smoking histories from each subject. Some participants chose to complete the questionnaire at home, and return it by mail in a self-addressed stamped envelope. Participants were contacted by telephone when there was missing data. Age, gender, race, weight, education, medical history, smoking history, family history of cancer, work history, exposure to various substances, participation in many activities, and food preparation and consumption data were collected. Smoking status was defined as non-smoker (smoked less than one cigarette per day for less than a year), ex-smoker (quit smoking at least one month prior to diagnosis) and current smoker (at time of diagnosis). Pack-years were calculated to estimate the cumulative exposure to smoking by multiplying the number of packs smoked per day by the number of years smoked. Second hand smoke exposure was self-reported for three different activities (leisure, work and at home) and determined from information obtained in the health questionnaire. Exposure for each location was categorized as an indicator variable equal to 1 if the participant reported exposure to SHS and equal to 0 otherwise. We created a similar indicator variable that captured timing of first exposure with respect to a study participant's age (0 - 25, >25 years of age).
Population characteristics were tabulated, and significant differences in the distribution of the principal covariates were tested using the chi square, Fisher exact, and student t tests, where appropriate. Multiple logistic regressions was used to assess the association between second hand smoke and lung cancer risk, adjusting for age, gender, indicator variables for smoking status (non-smoker, ex-smoker and current smoker) and a continuous variable for cumulative smoking exposure (pack-years).
Statistical Analysis
Demographic and clinical information were compared across smoking and SHS locations for both cases and controls. Multiple logistic regression was used to assess the association between SHS and lung cancer risk, adjusting for age (continuous variable), gender, indicator variables for smoking status (non-smoker, ex-smoker and current smoker), a continuous variable for cumulative smoking exposure (pack-years) and an indicator variable for alcohol intake (yes, no). Where indicated, the odds ratio (OR) and 95 % confidence intervals (CI) for the risk of lung cancer was calculated from these models. All statistical testing was done at the two-sided 0.05 level, and SAS software version 9.1 (SAS Institute, Cary, NC) was used.
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o AbstractIntroductionMaterials and MethodsResultsDiscussionReferencesResults
Patient characteristics
There were a total of 1669 cases and 1263 controls. The distribution of demographic and clinical characteristics by smoking status is summarized in Table1. Overall median age (standard deviation) was 62 (12) years, males were 49%; 604 (21%) non smokers, 1464 (50%) ex smokers, 864 (29%) current smokers; median packyears (standard deviation) for ex and current smokers 39 (37). Patients with early stage (stages I an II) numbered 803 (50%), with adenocarcinoma 698 (42%), squamous 339 (21%), others 615 (37%).
Table I
Table 2 shows the distribution of SHS exposure by location and age at exposure. No exposure to SHS at work or leisure 212 (7%), one activity 727 (25%), or both 1993 (68%). Persons with exposure to SHS between birth and age 25 numbered 403 (14%), and after age 25, 2529 (86%). Exposure at home was excluded from further analysis since there was little variability by outcome status (most subjects reported exposure from birth).
Table II
Distribution of SHS variables for all subjects
Adjusted odds ratios of SHS at work and leisure are shown in table 3. For study participants who were exposed to SHS at both activities and compared to one or no activity, the adjusted odds ratio (AOR) for lung cancer was 1.30(1.08-1.57) when exposure occurred between birth and age 25 and 0.66(0.21-1.57) if exposure occurred after age 25 years. Respective results for nonsmokers were: 1.29 (0.82-2.02) and 0.87 (0.22-3.38), and for current and ex smokers combined: 1.28 (1.04-1.58) and 0.66 (0.15-2.85).
Table III
Adjusted Odds Ratio (95%CI) of SHS duration at Work and Leisure places and lung cancer risk*
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o AbstractIntroductionMaterials and MethodsResultsDiscussionReferencesDiscussion
Previous studies of biochemical markers of exposure and toxicological studies, confirm that there is a causal association between the risk of NSLC and exposure to SHS(2). Similar conclusions have been reached by past summary scientific reports (43, 55). We suggest further that subjects first exposed before age 25 have a higher lung cancer risk compared to those for whom first exposure occurred after age 25 years. Consistent results are seen in our study for different smoking categories, i.e. current, past and non smokers. Our results go to further support the hypothesis that SHS has a similar harmful effect as for cases exposed to MSS.
Growing evidence (19, 22, 29, 30) suggests that exposure to SHS in childhood increases the risk of lung cancer in adulthood. With the decline of adult smoking in public and work places in the United States and Europe but still very prevalent in other regions around the world, SHS exposure and associated risks are still a major source of uncontrolled exposure in younger individuals, especially in children without the ability to negotiate a smoke free environment at home, work or leisure. Most lung cancers occur in smokers but still a significant proportion (approximately 10%) develops in lifetime nonsmokers (56) and approximately 3,000 lung cancer deaths occur each year among adult nonsmokers in the United States as a result of exposure to SHS (57). No risk-free level of exposure to SHS exists(43) and exposure to SHS has also been linked with slowed lung growth in children (58). In a study that investigated the effects of SHS exposure in childhood and the subsequent risk of lung cancer among female primary lung cancer cases and their hospital based controls (matched on age, residential area and lifetime smoking status), Wang and colleagues (30) showed that passive smoking from household exposure to tobacco smoke significantly increased the risk of lung cancer for both smoking and non smoking pairs when exposed under the age of 15 years (p<0.05). In a similar study in Taiwan, Lee et al (22) found that environmental tobacco smoke exposure occurring in childhood increased the effect of high doses of exposure in adult life in the development of lung cancer. In women exposed to greater than 20 smoker-years, compared to never exposed, the risk of lung cancer was 1.8 (1.2-2.9). When the exposure was greater than 40 years the risk was 2.2 (1.4-3.7). In addition, when smoker-years was treated as a continuous variable, the increased risk associated with a one unit increase larger for childhood exposure compared to adulthood (1.35 vs.1.27). In a population-based case-control study of lung cancer among lifetime nonsmoking women and with measured lifetime residential and workplace environmental tobacco smoke, the odds ratio for women with passive exposure as a child and as an adult was 1.63 (0.8-3.5) and for those exposed only as an adult 1.20 (0.5-3.0). Although no increase was observed with childhood exposure only, there were just 2 cases in that category.
SHS exposure and associated risks are increasingly becoming a major source of uncontrolled exposure in younger individuals, especially in children without the ability to negotiate a smoke free environment at home, work or leisure. A worldwide study among students aged 13-15 years (58), showed that nearly half of never smokers were exposed to SHS at home (46.8%), and a similar percentage were exposed in places other than the home (47.8%). Never smokers exposed to SHS at home were 1.4-2.1 times more likely to be susceptible to initiating smoking than those not exposed. Students exposed to SHS in places other than the home were 1.3-1.8 times more likely to be susceptible to initiating smoking than those not exposed, especially for SHS exposure at home.
The strengths of this study include large sample size, relatively homogeneous population, and almost complete demographic and smoking information. However, we acknowledge several limitations to our study. As expected of a case control study, recall bias may have affected our results. Smoking and SHS exposure history were collected by questionnaire and patients' recall and are not validated biochemically. However, given the nature of controls (friends and non blood related family) the impetus to recall would be similar (non differential) across case status, with controls possibly as affected by diagnosis of friend or family member. Nondifferential misclassification biases to the null making the odds ratio a conservative estimate of the actual magnitude of association
We also observed similar and consistent results in different smoking categories. To ensure that control selection was representative we compared the smoking habits of our controls to the smoking habits of the general Massachusetts population and found no significance differences. It is most likely that these controls would have been referred to MGH for treatment, if they were to become cases as they were either their spouses or friends. Residual confounding may be another limitation that exists for the results in our study. We observed a slightly stronger effect of SHS exposure among smokers as compared to non smokers, which may be explained partly by residual confounding. However, the associations were consistent in different subgroups of smoking status (past, current and non smokers), and we adjusted for pack-years of smoking and years since cessation (for past smokers) in all of the analysis. Residual confounding may bias the magnitude of the association but it is unlikely to change the direction of the association. In our analysis we did not adjust for the duration or the amount of SHS exposure.
To conclude, results from this epidemiological study support the evidence that individuals first exposed to SHS before age 25 have a higher lung cancer risk compared to those for whom first exposure occurred after age 25 years. These results need to be confirmed by other independent studies and further studies are needed to more accurately assess the SHS exposure and fully investigate the SHS-age of exposure interaction and to what extent this is influenced by the duration or the amount of SHS exposure.
Acknowledgments
The authors gratefully acknowledge the assistance of Linda Lineback, Barbara Bean, Andrea Shafer, Jessica Shin, Jeanne Jackson and Andrea Solomon for patient recruitment and data collection; Lucy Ann Principe, Salvatore V. Mucci, and Richard Rivera-Massa for data entry.
Grant Support NIH Grants: CA74386 and ES00002, Flight Attendant Medical Research Institute
Footnotes
Conflict of Interest Statement None declared.
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58. Exposure to secondhand smoke among students aged 13-15 years--worldwide, 2000-2007. MMWR Morb Mortal Wkly Rep. 2007;56:497500. [PubMed]
www.ncbi.nlm.nih.gov/pmc/articles/PMC2515267/
OMISSIS
One such disease is lung cancer, the most common
cause of cancer death in both men and women. The risk of dying from lung cancer is
22 times hither among male smohers and 12 times higher among female smokers
compared with people u ho have never smoked.The risk of lung cancer declines steadil)
in people who quit smoking; after IO years of abstinence, the risk of lung cancer is about
3) to 50 percent of the risk for continuing smokers,. Smoking cessation also reduces
the risk of cancers of the larynx. oral cavity. esophagus. pancreas. and urinary bladder.
Coronary heart disease (CHD) is the leading cause of death in the United States.
Smokers have about twice the risk of dying from CHD compared with lifetime
nonsmokers. This excess risk is reduced by about half among ex-smokers after only 1
year of smoking abstinence and declines gradually thereafter. After 15 years ot
abstinence the risk of CHD is similar to that of persons who have never smoked.
Compared with lifetime nonsmokers. smokers have about twice the risk ofdying from
stroke, the third leading cause of death in the United States. After quitting smoking.
the risk of stroke returns to the level of people who have never smoked: in some studies
this reduction in risk has occurred within 5 years. but in others as long as IS years of
abstinence were required.
Cigarette smoking is the ma.jor cause of chronic obstructive pulmonary disease
(COPD). the fifth leading cause of death in the United States. Smoking increases the
risk of COPD by accelerating the ape-related decline in lung function. With sustained
abstinence from smoking. the rate of decline in lung function among former smokers
returns to that of never smokers. thus reducing the risk of developing COPD.
Influenza and pneumonia represent the sixth leading cause of death in the United
States. Cigarette smohing increases the risk of respiratory infections such as intluenla.
pneumonia. and bronchitis. and smoking cessation reduces the rish.
Cigarette smohing is a major cause of peripheral artery occlusive disease. This
condition causes substantial mortality and morbidity: complications may include intermittent
claudication. tissue ischemiu and gangrene. and ultimately. loss of limb.
Smoking cessation substantially reduces the risk of peripheral arter) occlusive disease
compared with continued smoking.
The mortalit> rate from abdominal aortic aneurysm is two to fi\,e times higher in
current smokers than in never smohers. Former smohers ha\e half the excess rish of
dying from this condition relative to current smohcrs.
About 20 million Americans currently ha\,e. or ha\c had. an ulcer of the stomach 01
duodenum. Smohers have an increased rish of developin g gastric or duodenal ulcers.
and this increased rish is reduced h> quitting smohing.
OMISSIS
http://profiles.nlm.nih.gov/NN/B/B/C/T/_/nnbbct.pdf
OMISSIS
1.34 Smoking causes increased risk of cancers in several sites, pre-eminently the lung, but also several others such as the oral cavity, pharynx, larynx, oesophagus, pancreas and bladder. The association between smoking and certain cancers of the head and neck is discussed in Part Six.
OMISSIS
www.archive.official-documents.co.u...part-1.htm#1.31
Cancro
Il rischio di morire di cancro ai polmoni θ 22 volte maggiore negli uomini che fumano sigarette e 12 volte nelle donne fumatrici, rispetto ai non fumatori.
Il fumo della sigaretta incrementa il rischio di molti tipi di cancro inclusi i cancri: delle labbra, del cavo orale, della faringe, della laringe, dell'esofago, del pancreas, della cervice uterina, delle vie urinarie e dei reni.
Prima causa di morte nei soggetti maschi, il cancro ai polmoni θ sempre piω frequente nelle donne. Il tabagismo θ il fattore di rischio principale: il 90% dei casi θ attribuito al fumo di sigaretta! I primi sintomi della malattia si presentano solo ad uno stadio giΰ avanzato (tosse, difficoltΰ respiratorie, espettorazioni con sangue); le cure variano in base al tipo di malattia (chirurgiche, radioterapiche, chemioterapiche) e le possibilitΰ di guarigione sono limitate.
Il fumo θ il responsabile di 9 casi di tumore ai polmoni su 10!
Confronto tra i polmoni di un fumatore (a sinistra) e di un non fumatore (a destra)
Nella figura a fianco, la superficie del polmone θ di colore grigio-scuro a causa delle particelle di catrame inalate per un lungo periodo da un fumatore. I noduli bianchi sono il carcinoma tipico del polmone, chiamato a piccole cellule. Questi tumori sono tra i piω veloci a diffondersi.
Una persona che fuma un pacchetto di sigarette al giorno ne consumerΰ in vita sua 500.000! Sapendo che una sigaretta rilascia circa 1/100 di grammo di particelle, alla fine saranno piω di 5 kg di sostanze tossiche rilasciate nei polmoni!
Il fumo caldo del tabacco altera progressivamente il rivestimento mucoso dei bronchi e paralizza le piccole ciglia protettive. Continuando a fumare, le piccole ciglia polmonari - che rivestono le cellule dei bronchi e che servono a respingere il pulviscolo, i microbi e le secrezioni - si alterano fino a scomparire. L'evacuazione delle secrezioni e di tutte le particelle e pulviscolo contenuti nell'aria che si respira diventa impossibile. La tosse diventa il solo modo per eliminare parzialmente muco e particelle. Infine, allo stadio finale, il progredire dell'infiammazione trasforma profondamente il rivestimento mucoso dei bronchi e provoca una "metaplasia della mucosa", che farΰ da terreno al cancro: le cellule invece di rimanere su un solo strato si sovrapporranno. La metaplasia ci impiega oltre un anno a scomparire dopo che si θ smesso di fumare completamente.
www.unitab.it/cancro.htm
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