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The association of cigarette smoking with self-reported disease
before middle age: the Coronary Artery Risk Development in Young
Adults (CARDIA) study.Prev
Med. 2006 Mar;42(3):193-9. Epub 2006
Feb 15.
BACKGROUND:
Evidence that demonstrates the harmful effect of cigarette smoking
during young adulthood is limited. Therefore, we assessed
associations between cigarette smoking and several self-reported
illnesses in a prospective cohort study in healthy young adults.
METHODS: Data were derived from 4472 adults aged 18 to 30 years at
baseline participants in the Coronary Artery Risk Development in
Young Adults (CARDIA) study and reexamined at least once after 7,
10, or 15 years. RESULTS: Cigarette smoking in 1985-86 was related
to self-reported smoking-related cancers, circulatory disease, and
peptic ulcer. Incidence of these diseases was 9.3/1000 person years
among current smokers vs. 4.5/1000 person years among never smokers
with no exposure to passive smoke, relative risk (adjusted for race,
sex, education, and center) 1.96 (1.42-2.70). Assuming causal
relationships, 32% of these premature incidents were attributable to
smoking. The relative risks of liver disease, migraine headache,
depression, being ill the day before the examination, and chronic
cough and phlegm production were also higher in smokers.
CONCLUSIONS: Smokers aged 18-30 followed for 7 to 15 years reported
an excess of both major and minor ailments related to earlier and
current smoking. Thus, prevention, cessation, and avoiding passive
smoking should remain strong goals among young people.
Smoking and
systemic disease.Clin
Occup Environ Med. 2006;5(1):173-92, x.
Cigarette
smoking is associated with a number of adverse health effects,
including well-established links to cardiopulmonary disease and
several cancers. Some of the other important systemic diseases
associated with smoking are the subjects of this article, such as
diabetes mellitus and insulin resistance, and thyroid diseases. Also
reviewed here is the impact of smoking on male and female
infertility, on selected dermatologic conditions, and on
gastrointestinal diseases including peptic ulcer and inflammatory
bowel diseases.
Helicobacter
pylori, non-steroidal anti-inflammatory drugs and smoking in risk
pattern of gastroduodenal ulcers.Scand
J Gastroenterol. 2003 Sep;38(9):923-30.
BACKGROUND: Helicobacter pylori, NSAID and cigarette smoking are
major risk factors for gastroduodenal ulcers. However, the results
of studies on the interaction between these factors on ulcerogenesis
are controversial. This study was designed to examine the
association between gastroduodenal ulcers and H. pylori infection,
NSAID use, smoking and age. METHODS: 5967 dyspeptic patients
underwent 13C-urea breath test (UBT) and upper endoscopy, while age
and dyspeptic symptoms were reported. RESULTS: Out of 5967 patients,
31.8% were ulcerated; 9.2% had gastric, 17.2% duodenal and 5.4% both
gastric and duodenal ulcers. H. pylori was found in 72.5% of gastric
ulcer patients, in 83.6% of duodenal ulcer patients, in 76.9% of
gastroduodenal ulcer patients and in 64.8% of dyspeptic patients.
The gastric, duodenal and gastroduodenal ulcers were related to H.
pylori significantly and the respective ORs were: 1.44, 2.77 and
1.81. NSAID alone was used by 6.2%-12.7% of ulcer patients, tending
to raise only the risk of gastric ulcer but reducing that of
duodenal and gastroduodenal ulcers. The H. pylori prevalence was
significantly higher in smokers (76%) than in non-smokers (67%) and
the ulcer risk was also significantly higher in smokers than in
non-smokers. About 20% of ulcers were 'idiopathic', i.e. without
NSAID and H. pylori and the ratio of these ulcers to all ulcers
significantly increased during the 5 years of the study.
CONCLUSIONS: Based on multivariable logistic regression analysis we
conclude that: 1) H. pylori infection, NSAID use, smoking and age
play major roles in the pathogenesis of peptic ulcerations; 2) there
is a negative interaction between H. pylori and NSAID on duodenal
ulcers, suggesting that H. pylori reduces the development of these
ulcers in NSAID users, and 3) about 20% of peptic ulcers in the
Polish population are unrelated to H. pylori and NSAID use
(idiopathic ulcers).
Cigarette
smoke-induced acute airway impairment.
Nihon Kokyuki Gakkai Zasshi. 2000 May;38(5):347-53.
Cigarette
smoking has been implicated in many pulmonary disorders, including
chronic bronchitis and chronic obstructive lung disease. Cigarette
smoking is associated with increased airway responsiveness. Acute
exposure to cigarette smoke increases airway responsiveness in a
dose-dependent manner. A superoxide is involved in airway
hyper-responsiveness induced by cigarette smoke, perhaps by direct
toxic action. Cigarette smokers have increased numbers of
neutrophils present in their lower respiratory tract. Acute exposure
to cigarette smoke initiates a superoxide-dependent mechanism that,
through NF-kappa B activation and IL-8 expression, induces
infiltration of neutrophils into the airways in vivo. The alveolar
macrophage is one potential source of NF-kappa B activation and IL-8
production after acute exposure to cigarette smoke. Manipulation of
NF-kappa B by antioxidants in vivo may be useful in limiting
biologic processes such as pro-inflammatory cytokine production,
which may lead to neutrophil accumulation in the lung.
Effect of acute cigarette smoking, alone or with
alcohol, on gastric barrier function in healthy volunteers.
Dig Liver Dis. 2002 Oct;34(10):702-6.
BACKGROUND:
Smoking is a risk factor for gastroduodenal ulcer and gastric
adenocarcinoma. However, the pathophysiological mechanisms induced
by acute cigarette smoking in the human gastric mucosa are poorly
understood. AIM: To evaluate the effect of acute cigarette smoking,
alone or with alcohol, on the gastric permeability to sucrose, a
specific marker of mucosal damage in the stomach. SUBJECTS AND
METHODS: Twenty healthy volunteers (8 smokers/12 non-smokers) were
studied. Each fasted subject ingested 500 ml of a 20% sucrose
solution and the amount of sucrose excreted in a 5-hour urine
collection was measured by gas chromatography Four sucrose
permeability tests were carried out: 1. basal, 2. while smoking 5
cigarettes, 3. after drinking 50 ml of a 40 degrees alcoholic
beverage, 4. a combination of 2+3. RESULTS: Sucrose excretion
increased after alcohol ingestion (40.5 +/- 6.0 mg vs 143.1 +/- 28.9
mg, p = 0.002), but was not modified by acute cigarette smoking
(34.4 +/- 5.9 mg). When alcohol and cigarettes were simultaneously
consumed, the increase in alcohol-induced sucrose excretion was
significantly reduced (73.1 +/- 16.6 mg, p = 0.03). Basal sucrose
excretion was similar in smokers and non-smokers. However, in acute
cigarette smoking, a decrease in sucrose excretion was observed in
smokers (p = 0.02) but not in non-smokers. CONCLUSIONS: These
results indicate that acute cigarette smoking may tighten the
gastric mucosa in habitual smokers and this is associated with a
smaller increase of gastric permeability induced by alcohol.
The
comparative analysis: the occurrence of acute respiratory system
infections and chronic diseases among active smokers and non-smokers.Przegl
Lek. 2006;63(10):858-63.
Cigarette
smoking is one of the factors causing a lot of health problems.
Breathing the smoke makes the development of arteriosclerosis and
ischemic heart disease faster and the risk of myocardial infarction
much higher. Toxic substances contained in the smoke induce
inflammatory processes in bronchial tree, which finally leads to the
destruction of lungs. One of the way of preventing complications in
the circulatory system and stopping the inflammatory process in
lungs is to give up the habit of smoking. Within the period of three
years the group of more than 1000 people (smokers and non-smokers)
was examined and the analysis of occurrence of acute respiratory
system infections and chronic diseases was conducted. In the studies
the questionnaire prepared by the author of the paper, some
specialistic studies and medical reports were used. The achieved
results show that more and more women smoke as many cigarettes as
men and for as many years as they do. Both men and women who
graduated either a grammar school or a university smoke more often
than with elementary level of education. People who smoke suffer
more often from numerous acute respiratory tract infections and must
more often pay a visit to general practitioner. Considering the sex
there are no statistically significant differences in the occurrence
of chronic pulmonary diseases and the cardiovascular system. The
achieved results show the changes of the attitude to smoking in
Polish society. The increase of the consumption of cigarettes among
women with high education is very worrying. It is a serious
challenge for the whole medical staff.
Goblet cell
hyperplasia and epithelial inflammation in peripheral airways of
smokers with both symptoms of chronic bronchitis and chronic airflow
limitation.Am
J Respir Crit Care Med. 2000 Mar;161(3 Pt 1):1016-21.
To quantify the
number of goblet cells and inflammatory cells in the epithelium of
peripheral airways in smokers with both symptoms of chronic
bronchitis and chronic airflow limitation, we examined surgical
specimens obtained from 25 subjects undergoing lung resection for
localized pulmonary lesions: 10 smokers with symptoms of chronic
bronchitis and chronic airflow limitation, six asymptomatic smokers
with normal lung function, and nine nonsmoking control subjects.
Peripheral airways were examined with histochemical methods to
identify goblet cells and with immunohistochemical methods to
identify total leukocytes (CD45(+) cells), neutrophils, macrophages,
CD4(+) and CD8(+) cells in the epithelium. When compared with
nonsmokers, smokers with both symptoms of chronic bronchitis and
chronic airflow limitation had an increased number of goblet cells
(p < 0.01), CD45(+) cells (p < 0. 01), macrophages (p < 0.05), and
CD8(+) cells (p < 0.01) in the epithelium of peripheral airways.
When all the smokers were grouped together, they showed an increased
number of neutrophils (p < 0.05) along with an increased number of
goblet cells, CD45(+) cells, macrophages and CD8(+) cells (p < 0.05)
compared with nonsmokers. In conclusion, smokers with both symptoms
of chronic bronchitis and chronic airflow limitation have an
increased number of goblet cells and inflammatory cells in the
epithelium of peripheral airways.
CD8+ve cells in the lungs of smokers with chronic obstructive
pulmonary disease.Am
J Respir Crit Care Med. 1999 Aug;160(2):711-7.
Previous
studies have shown an increased number of inflammatory cells and, in
particular, CD8+ve cells in the airways of smokers with chronic
obstructive pulmonary disease (COPD). In this study we investigated
whether a similar inflammatory process is also present in the lungs,
and particularly in lung parenchyma and pulmonary arteries. We
examined surgical specimens from three groups of subjects undergoing
lung resection for localized pulmonary lesions: nonsmokers (n = 8),
asymptomatic smokers with normal lung function (n = 6), and smokers
with COPD (n = 10). Alveolar walls and pulmonary arteries were
examined with immunohistochemical methods to identify neutrophils,
eosinophils, mast cells, macrophages, and CD4+ve and CD8+ve cells.
Smokers with COPD had an increased number of CD8+ve cells in both
lung parenchyma (p < 0.05) and pulmonary arteries (p < 0.001) as
compared with nonsmokers. CD8+ve cells were also increased in
pulmonary arteries of smokers with COPD as compared with smokers
with normal lung function (p < 0.01). Other inflammatory cells were
no different among the three groups. The number of CD8+ve cells in
both lung parenchyma and pulmonary arteries was significantly
correlated with the degree of airflow limitation in smokers. These
results show that an inflammatory process similar to that present in
the conducting airways is also present in lung parenchyma and
pulmonary arteries of smokers with COPD.
Effect of cigarette smoke on ethanol-induced
gastric mucosal lesions: the role of nitric oxide and neutrophils.
Eur J Pharmacol. 1998
Jan 26;342(2-3):253-60.
The roles of
neutrophil aggregation, inducible nitric oxide synthase activation
and chemoattractant, leukotriene B4, in potentiation of the
cigarette smoke effect on ethanol-induced gastric mucosal damage
were studied. Smoke exposure markedly increased gastric lesion
formation following ethanol administration and this was accompanied
by substantial increase in gastric mucosal leukotriene B4
concentration, myeloperoxidase and inducible nitric oxide synthase
activities. Antineutrophil serum or aminoguanidine pretreatment
significantly attenuated both gastric mucosal lesion formation and
inducible nitric oxide synthase activity. The increased
myeloperoxidase activity was abolished by antineutrophil serum but
not by aminoguanidine. These data indicated that both neutrophil
mobilization and inducible nitric oxide synthase activation in the
gastric mucosa play an important role in the potentiating action of
cigarette smoke on ethanol-induced gastric mucosal lesion formation.
Increased synthesis of nitric oxide from inducible nitric oxide
synthase during gastric damage may be secondary to neutrophil
infiltration in the gastric mucosa. Chemoattractant leukotriene B4
could also contribute to neutrophil recruitment in the tissue.
Smoking and
diseases of the gastrointestinal system: an epidemiological review
with special reference to sex differences.Can
J Gastroenterol. 1997
May-Jun;11(4):345-52.
Smoking
increases the risk of peptic ulcer disease and death from it.
Smoking delays peptic ulcer healing, with or without treatment, and
increases the risk of recurrence after healing. The effects of
smoking on this disease are similar and equally pervasive in women
and men. There is growing evidence that cigarette smoking is a risk
factor for Crohn's disease (CD) in both women and men. However,
women smokers appear to be at particular risk for this disease. In
studies that examined this risk separately in women and men. At each
level of smoking the excess risk in women smokers compared with
nonsmokers clearly exceeded the excess risk in men smokers compared
with nonsmokers. Smoking also appears to adversely affect the
clinical course of CD in both women and men, but more so in women.
The possible interaction between smoking and oral contraceptives
with regard to the risk of CD deserves further study. There is
growing evidence that current smoking protects against ulcerative
colitis in both men and women. Although there is some evidence that
smoking is a risk factor for gallstones, particularly in women,
evidence to support a causal relationship is inadequate. Further
studies, controlling for alcohol consumption in the analyses, are
needed. Smoking does not appear to be a risk factor for cirrhosis of
the liver.
Inflammatory cells
in the bronchial glands of smokers with chronic bronchitis.Am
J Respir Crit Care Med. 1997 Nov;156(5):1633-9.
To characterize
the inflammatory process in the bronchial glands of smokers with
chronic sputum production, we examined lobar bronchi from 18
subjects undergoing lung resection for localized pulmonary lesions,
all with a history of cigarette smoking. Nine of the subjects had
symptoms of chronic bronchitis and chronic airflow obstruction, and
nine were asymptomatic, with normal lung function. The number of
neutrophils, eosinophils, mast cells, macrophages, CD4+ and CD8+
T-lymphocytes, and the ratio of CD4+ to CD8+ cells were assessed in
the bronchial glands, epithelium, and submucosa. Cells were
identified through immunohistochemistry. Smokers with symptoms of
chronic bronchitis had an increased number of neutrophils (p = 0.01)
and macrophages (p = 0.03) and a decreased CD4+/CD8+ ratio (p =
0.01) in the bronchial glands as compared with asymptomatic smokers.
Chronic bronchitic smokers also had an increased number of
epithelial neutrophils (p = 0.04), whereas the numbers of
macrophages and CD4+ and CD8+ T-lymphocytes in the epithelium and
submucosa were similar in the two groups of smokers. No differences
in numbers of eosinophils or mast cells were observed between
bronchitic and asymptomatic smokers in any of the compartments
examined. In conclusion, smokers with chronic sputum production have
an increased infiltration of neutrophils and macrophages and an
increased proportion of CD8+ T-lymphocytes in their bronchial
glands, supporting the important role of bronchial-gland
inflammation in the pathogenesis of chronic bronchitis.
Airflow
limitation in chronic bronchitis is associated with T-lymphocyte and
macrophage infiltration of the bronchial mucosa.Am
J Respir Crit Care Med. 1996 Feb;153(2):629-32.
To investigate
whether the airway inflammatory process is different in patients
with chronic bronchitis with airflow limitation and those with
chronic bronchitis without airflow limitation, we obtained bronchial
biopsies from 14 subjects with chronic sputum production and fixed
airway obstruction, and from 10 subjects with chronic sputum
production and normal FEV1, all with a history of cigarette smoking.
Paraffin-embedded and frozen bronchial biopsies were examined by
immunohistochemistry to identify the number of neutrophils (neutrophil-elastase),
eosinophils (antieosinophil cationic protein [EG-2]), mast cells (tryptase),
T-lymphocytes (CD3), T-lymphocyte subpopulations (CD4 and CD8),
B-lymphocytes, and macrophages (CD68) in the submucosa. Subjects
with chronic bronchitis with airflow limitation had a greater number
of T-lymphocytes (p < 0.01) and macrophages (p < 0.05) than subjects
with chronic bronchitis without airflow limitation, whereas the
T-lymphocyte subpopulations and the numbers of B-lymphocytes,
neutrophils, eosinophils, and mast cells were similar in the two
groups. When all the subjects were considered together, the number
of T-lymphocytes correlated inversely with the values of FEV1 (r =
0.46, p < 0.02). In conclusion, airflow limitation in subjects with
chronic bronchitis is associated with an increased number of
T-lymphocytes and macrophages in the bronchial mucosa.
Effects of cigarette smoking on duodenal ulcer
healing and relapse rate.J
Med Assoc Thai. 1994 Nov;77(11):566-71.
104 duodenal
ulcer patients were classified into non-smokers (76) and smokers
(28). Their age range was between 14-72 years. They were randomly
treated with cimetidine (28 non-smokers and 8 smokers), colloidal
bismuth (27 non-smokers and 10 smokers) and sucralfate (21
non-smokers and 10 smokers). Follow-up endoscopic examination at 4,
6 and 8 weeks showed that overall healing rates were better in the
non-smokers than in the smokers (64.5% against 46.4% at 4 weeks and
92.1% against 67.8% at 6 weeks) and almost all ulcers had healed at
the end of 8 weeks (100% in non-smokers and 96.4% in smokers). Among
non-smokers, there were no statistically significant differences in
the healing rates by any medication at any period of time. Among
smokers, colloidal bismuth had significant better healing rate at 6
weeks over cimetidine and sucralfate. (p = 0.04 and p = 0.041
respectively). Overall relapse rates were higher among smokers
(32.1%) than non-smokers (10.5%). Of the 3 medications, sucralfate
had the lowest relapse rate in both smokers (20%) and non-smokers
(9.5%), while colloidal bismuth had the highest relapse rates (40%
for smokers and 11.1% for non-smokers).
Risk factors
of duodenal ulcer bleeding: the role of smoking and nicotine.
Ital J Gastroenterol.
1994 Oct-Nov;26(8):385-91.
Several
studies have shown that cigarette smoking affects duodenal ulcer (DU)
recurrence. To verify any correlation between smoking and
complications of ulcer disease, we studied 33 DU smokers, 16 DU
ex-smokers and 87 DU non-smokers for up to 48 months, recording age,
sex, family history of ulcer, ulcer symptoms, non-steroidal
anti-inflammatory drug use, length of DU history, alcohol
consumption, smoking habit, relapses and bleeding episodes. Nicotine
contents were also obtained for the type of cigarettes smoked.
Statistics used were: Analysis of variance with Bonferroni's test.
Pearson's chi-squared test and stepwise logistic regression
analysis. Smokers were found to have significantly more relapses but
fewer bleeding episodes than ex-smokers and non-smokers (63.3%,
31.2% and 34.5%, p = 0.029; 12.1%, 43.7% and 34.5%, p = 0.017).
Bleeders were significantly more often males than non-bleeders
(82.9% vs. 61.0%, p = 0.01) and had ulcer symptoms less frequently
(9.7% vs. 26.3%, p = 0.02). Multivariate analysis confirmed sex as a
risk factor (OR = 3.0) and smoking as a "protective" factor (OR =
0.4) for bleeding, while nicotine intake was found to be unrelated
to this complication. We concluded that smoking (but not nicotine
intake) and male sex are factors to take into account in evaluating
the risk of DU bleeding.
Acute
effects of smoking during modified sham feeding in duodenal ulcer
patients. An analysis of nicotine, acid secretion, gastrin,
catecholamines, epidermal growth factor, prostaglandin E2, and bile
acids.Scand
J Gastroenterol. 1993 Jun;28(6):487-94.
Smoking is
associated with an increased incidence of duodenal ulcer with a high
relapse rate, and smokers tend to be slow healers. The etiology
responsible for this remains unknown, and there is general
disagreement as to whether smoking affects gastric secretion. The
aim of the present study was to investigate both aggressive and
protective factors in response to vagal stimulation induced by
modified sham feeding (MSF) in duodenal ulcer patients when smoking
versus not smoking. On smoking days, nicotine concentrations in
plasma averaged about 15 ng/ml and were extremely high in saliva and
gastric juice (> 1300 and > 800 ng/ml, respectively). MSF induced a
significant decrease in intragastric pH during non-smoking (p =
0.01) but not during smoking. Acid output 1 h after MSF was lower on
smoking than on non-smoking days (p = 0.02), as was volume secretion
(p = 0.02). Plasma gastrin concentrations were significantly
increased during MSF on non-smoking days (p = 0.04) but not on
smoking days, the concentrations during the whole day being lower on
smoking days (p = 0.002). Plasma catecholamine levels were
unaffected by MSF, whether smoking or not. However, plasma
concentrations of noradrenaline decreased during the smoking of a
single cigarette (p = 0.03), whereas those of adrenaline were
increased on smoking days (p = 0.02). Epidermal growth factor
concentrations were decreased in gastric juice after MSF during
non-smoking (p = 0.01) but not during smoking. Although
prostaglandin E2 (PGE2) concentrations in gastric juice were
unaffected by MSF, PGE2 output increased after MSF whether smoking
or not, the increment being non-significantly less during smoking (p
= 0.09).
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