The cigarette controversy.
Cancer Epidemiol Biomarkers Prev. 2007
Jun;16(6):1070-6.
This study
examines the history of the cigarette controversy using the tobacco
documents as a roadmap to explore the following four questions: (a)
What did tobacco companies know about the health risks of smoking and
when did they know it? (b) What evidence is there that tobacco
companies conspired to deliberately mislead the public about the
health risks of smoking? (c) How were scientists involved in the
cigarette controversy? (d) Have tobacco companies changed the way they
do business since signing the 1998 Master Settlement Agreement? The
tobacco companies knew and for most part accepted the evidence that
cigarette smoking was a cause of cancer by the late 1950s. The
documents also reveal that the tobacco companies helped manufacture
the smoking controversy by funding scientific research that was
intended to obfuscate and prolong the debate about smoking and health.
Today, the tobacco companies acknowledge that smoking is a cause of
disease, but they have not materially altered the way they do
business. In our opinion, it is not sufficient for the tobacco
industry to merely concede the obvious point that smoking is a cause
of disease when it is evident that decades of misinformation has
resulted in a public that is massively ignorant about the risks of
smoking low-tar cigarettes, nicotine addiction, and secondhand smoke
exposure. Public education efforts are still needed to correct these
misperceptions along with government oversight to ensure that the
industry is not permitted to mislead the public further. If the past
50 years have taught us anything, it is that the tobacco industry
cannot be trusted to put the public's interest above their profits no
matter what they say.
Health
consequences of reduced daily cigarette consumption.Tob
Control. 2006 Dec;15(6): 472-80.
OBJECTIVE:
To determine the risk of dying from specified smoking-related diseases
and from any cause in heavy smoking men and women (> or =15
cigarettes/day), who reduced their daily cigarette consumption by
>50%. DESIGN: A prospective cohort study. SETTING: Three counties in
Norway. PARTICIPANTS: 24,959 men and 26,251 women, aged 20-49 years,
screened for risk factors of cardiovascular disease in the mid-1970s,
screened again after 3-13 years, and followed up throughout 2003.
Outcomes: Absolute mortality and relative risks adjusted for
confounding variables, of dying from all causes, cardiovascular
disease, ischaemic heart disease, all smoking-related cancer and lung
cancer. RESULTS: With sustained heavy smokers as reference, the
smokers of both sexes who reduced their daily consumption (reducers)
had the following adjusted relative risks (95% confidence interval
(CI)): of dying from any cause, 1.02 (0.84 to 1.22); cardiovascular
disease, 1.02 (0.75 to 1.39); ischaemic heart disease, 0.96 (0.65 to
1.41); smoking-related cancer, 0.86 (0.57 to 1.29); and lung cancer,
0.66 (0.36 to 1.21). The difference in cigarette consumption between
two examinations was not a significant predictor of death from any of
the causes. A follow-up from a third screening of the subgroup who
were reducers at both second and third examinations (sustained
reducers) did not have a lower risk than those who were heavy smokers
at all three examinations. CONCLUSIONS: Long-term follow-up provides
no evidence that heavy smokers who cut down their daily cigarette
consumption by >50% reduce their risk of premature death
significantly. In health education and patient counselling, it may
give people false expectations to advise that reduction in consumption
is associated with reduction in harm.
Health
consequences of smoking 1-4 cigarettes per day.Tob
Control. 2005 Oct;14(5):315-20.
OBJECTIVES: To
determine the risk in men and women smoking 1-4 cigarettes per day of
dying from specified smoking related diseases and from any cause.
DESIGN: Prospective study. SETTING: Oslo city and three counties in
Norway. PARTICIPANTS: 23,521 men and 19,201 women, aged 35-49 years,
screened for cardiovascular disease risk factors in the mid 1970s and
followed throughout 2002. OUTCOMES: Absolute mortality and relative
risks adjusted for confounding variables, of dying from ischaemic
heart disease, all cancer, lung cancer, and from all causes. RESULTS:
Adjusted relative risk (95% confidence interval) in smokers of 1-4
cigarettes per day, with never smokers as reference, of dying from
ischaemic heart disease was 2.74 (2.07 to 3.61) in men and 2.94 (1.75
to 4.95) in women. The corresponding figures for all cancer were 1.08
(0.78 to 1.49) and 1.14 (0.84 to 1.55), for lung cancer 2.79 (0.94 to
8.28) and 5.03 (1.81 to 13.98), and for any cause 1.57 (1.33 to 1.85)
and 1.47 (1.19 to 1.82). CONCLUSIONS: In both sexes, smoking 1-4
cigarettes per day was associated with a significantly higher risk of
dying from ischaemic heart disease and from all causes, and from lung
cancer in women. Smoking control policymakers and health educators
should emphasise more strongly that light smokers also endanger their
health.
Impact of tobacco-smoke on key signaling pathways in the innate immune
response in lung macrophages.
J Cell Physiol. 2007 May
31;
Many of the
healthcare consequences of cigarette smoking could be due to its
ability to compromise the immune system, and in respiratory diseases
like chronic obstructive pulmonary disease (COPD), a constant low
level of infection could be responsible for some of the
symptoms/pathology. The aim was to assess the impact of cigarette
smoke (CS) on the release of innate effector cytokines in THP-1 cells
and human lung macrophages, and to determine the molecular mechanism
behind the altered response. Cells were exposed to CS with and without
endotoxin stimulus, cytokines, glutathione, mitogen-activated protein
kinase (MAPK) phosphorylation, IkappaB kinase-2 (IKK-2) activity,
nuclear factor kappa B (NF-kappaB), and activator protein-1 (AP-1)
pathway activation was measured. Attempts were made to mimic or block
the effect of CS by using nicotine, nitric oxide donors/inhibitors,
prostanoid inhibitors, and anti-oxidants. Results showed that CS
initially delayed the production of "innate" cytokines (e.g., IL-1beta
and IL-6) and reduced glutathione levels. This was associated with a
reduction in NF-kappaB pathway activation, which suggested a causative
link. CS also increased the phosphorylation of MAPK's and the
production of IL-8 but interestingly only in stimulated cells.
Exogenous glutathione treatment reversed both these effects of CS,
which suggests that this molecule may play a central role. In
conclusion, this data provides a novel mechanistic explanation for why
smokers have increased prevalence/severity of respiratory infections.
In addition, the suppression of the innate response is accompanied by
an increase in the neutrophil chemoattractant, IL-8, which may suggest
a link to the pathogenesis of smoking-related inflammatory disease.
Effect of
cigarette smoking on the oxidant/antioxidant balance in healthy
subjects. Am
J Ther. 2007 Mar-Apr;14(2):189-93.
BACKGROUND AND
PURPOSE: Cigarette smoking has been associated with the development of
cardiovascular disease and cancer. Even though the molecular
mechanism(s) are not clear, the pathology has been related to oxygen
free radicals present in cigarette smoke. Thus, the main objective of
this study was to establish the changes in the oxidation/antioxidation
balance induced by cigarette smoking. METHODS: Thirty healthy subjects
(15 smokers and 15 nonsmokers) of both sexes were studied. The smokers
group had smoked a mean of 14 cigarettes per day for an average of 4.5
years. Fasting serum levels of malondialdehyde (MDA), a marker of
oxidative stress, nitric oxide (NO), reduced glutathione (GSH), and
vitamin C (ascorbic and dehydroascorbic acids) were measured. RESULTS:
Fasting NO concentration was significantly higher in smokers (51.3 +/-
5.3 microM) than in nonsmokers (35.2 +/- 4.8 microM, P < 0.05). The
smokers had significantly higher serum dehydroascorbic acid levels
(2.4 +/- 0.5 mg/dL, P < 0.03) than the nonsmokers (1.08 +/- 0.08 mg/dL).
No significant differences were observed in the levels of ascorbic
acid, MDA, and GSH between the smokers and nonsmokers. CONCLUSIONS:
Our results suggest that exposure to cigarette smoke increases NO
synthesis, such that NO may act in a compensatory way as an inhibitor
of lipid peroxidation. Smoking also activates other antioxidative
mechanisms such as involving vitamin C. These protective mechanisms
appear to be enough in preventing accumulation of oxidative products
such as MDA and avoiding oxidative damage.
Alcohol drinking
and cigarette smoking: a "partner" for gastric ulceration.Zhonghua
Yi Xue Za Zhi (Taipei). 2000
Dec;63(12):845-54.
Alcohol
consumption and cigarette smoking are two etiologic factors that have
a close relationship with peptic ulcer diseases. Chronic active
gastritis is reportedly associated with chronic alcohol ingestion.
Nonetheless, the inflammatory changes are likely to be related to
concurrent Helicobacter pylori infection that is common among
alcoholics. Moreover, chronic alcoholism is also correlated with the
presence of gastric metaplasia. Both clinically and experimentally,
alcohol had been shown to affect the mucosal barrier and histology.
These ulcerogenic effects play a crucial role in altering gastric
mucosal defense mechanisms. Cigarette smoking is coupled with the
initiation and prolongation of gastric ulcers. Epidemiologic data show
that cigarette smoking increases both the incidence and relapse rate
of peptic ulcer diseases and also delays ulcer healing in humans.
Retrospective studies also indicate that cigarette smoking is a key
factor in inducing ulcer diseases rather than a linked behavior. The
general detrimental effects of cigarette smoking in the gastric mucosa
include reduction of circulating epidermal growth factor, increase in
tissue free radical production and the presence of free radicals in
smoke, together with reduction of mucosal constitutive nitric oxide
synthase activity. Furthermore, the alteration of normal gastric
mucosal blood flow and angiogenesis and the suppression of cell
proliferation contribute largely to the delay in ulcer healing in
cigarette smokers. Concurrent consumption of alcohol and cigarette
smoking significantly increases the risk of gastric ulcers. In animal
experiments, cigarette smoking potentiated ethanol-induced gastric
mucosal damage. The reduction of mucus secretion, increase in
leukotriene B4 level, increased activities of inducible nitric oxide
synthase, xanthine oxidase and myeloperoxidase, and the expression of
adhesion molecules in the gastric mucosa accompanied such potentiating
effects. Substances other than nicotine in cigarette smoke may also
contribute to the above effects.
Cigarette smoking
and mortality risk: twenty-five-year follow-up of the Seven Countries
Study.
Arch Intern Med. 1999 Apr
12;159(7):733-40 .
BACKGROUND:
Although most observations in the Seven Countries Study suggest that
cigarette smoking is harmful for health, universality of this
conclusion remains controversial. SUBJECTS AND METHODS:
Cohort-specific and pooled smoking habits at baseline (1957-1964) in
12 763 men aged 40 through 59 years living in Europe, the United
States, and Japan in relation to 25-year mortality follow-up. Pooled
hazard ratios for smokers vs never smokers were calculated by the Cox
proportional hazards model, adjusting for baseline country of
residence, age, body mass index, serum cholesterol, systolic blood
pressure, and clinical cardiovascular disease. RESULTS: Adjusted
hazard ratios for all-causes death in smokers compared with never
smokers were 1.3 (95% confidence interval, 1.2-1.4) for smokers of
less than 10 cigarettes per day and 1.8 (95% confidence interval,
1.7-1.9) for smokers of 10 cigarettes per day or more. Hazard ratios
were elevated for death due to coronary heart disease, all stroke,
other arterial disease, lung cancer, other cancer, chronic obstructive
pulmonary disease, and other disease in smokers compared with never
smokers. Within country, a few instances in which never smokers had a
higher cause-specific death rate than smokers of 10 cigarettes per day
or more were attributable to random variation associated with low
prevalence of never smokers and multiple comparisons. CONCLUSIONS:
These findings confirm the association of cigarette smoking with
elevated risk of mortality from all causes, several cardiovascular
diseases, cancer, and chronic obstructive pulmonary disease. Risk
associated with cigarette smoking is independent of culture.
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