Adverse Effects Of Cigarette Smoking Research Articles

Smoking habits and health-related quality of life in a rural Japanese population

To investigate the association between smoking and health-related quality of life (HRQOL) in a rural Japanese population. A cross-sectional study of data from 823 subjects in Iwaki area of Hirosaki City, Japan. SF-36 scores between non-smokers and smokers were compared. To test the sensitivity of SF-36 scores in detecting health deterioration, effects of having diseases and having deviations from normal thresholds in health check-up were analyzed by adding them into covariates in ANCOVA. There was no significant difference in SF-36 scores between non-smokers and smokers. Presence of diseases significantly decreased the physical components of SF-36 scores while the results of health check-up had no significant influence on SF-36 scores. The results suggested the possibility that in Japan, where smoking prevalence is still relatively high, smokers may be less sensitive to sub-clinical deterioration in their own health status than smokers in Western countries that already have experienced the major decline in their smoking rate. The importance of having the smoker become more sensitive to the sub-clinical adverse effects of cigarette smoking should be stressed for the success of smoking control programs.

Adverse Effects of Cigarette Smoke and Induction of Oxidative Stress in Cardiomyocytes and Vascular Endothelium

Active and passive exposure to cigarette smoke (CS) increases the risk of, and has deleterious effects in, ischaemic heart disease. Exposure to CS increases infarct size in experimental models of coronary occlusion and reperfusion. Among many possible mechanisms for these deleterious effects in intact animals and humans three have more substantial evidence: 1) functional alterations of endothelial cells, neutrophils and platelets; 2) impaired mitochondrial function and energy metabolism caused by toxins in CS, including oxidative free radicals; 3) increased arterial stiffness and vulnerability of the atherosclerotic plaque. In addition to the various pro-mitogenic, carcinogenic and apoptotic pathways thought to be affected and upregulated by CS, a direct necrotic action on cardiomyocytes is also believed to exist. Many, if not all, of these alterations are caused by oxidative stress, either as a direct consequence of inhalation of free radicals, or by induction from the vast range of chemicals present in both the gas and solid phase of tobacco smoke. Here, some of the proposed mechanisms will be reviewed and their impact on the cardiomyocytes and peripheral vasculature discussed.

Adverse Effects of Cigarette Smoke and Induction of Oxidative Stress in Cardiomyocytes and Vascular Endothelium

Adverse Effects of Cigarette Smoke and Induction of Oxidative Stress in Cardiomyocytes and Vascular Endothelium

Clearing the Smoke in Chronic Liver Diseases

In the 1930s, serious concerns about the health risks of cigarette smoking (CS) began to surface. During subsequent decades, scientific reports linking CS and specific ailments rapidly accumulated [1,2], but it was not until 1964 that the Surgeon General’s Advisory Committee on Smoking and Health finally acknowledged that CS was linked to specific diseases and to increased mortality. Today, the evidence is robust: The adverse effects of CS on several cancer outcomes as well as on cardiovascular and respiratory disease are established [3, 4]. Although in the US the prevalence of CS has been decreasing [5], the overall worldwide prevalence is steadily rising. Independent of prevalence rates, the absolute number of smokers everywhere keeps increasing due to population growth.

Abstract B118: Modifiable correlates of low testosterone in U.S. men

Abstract Background: In some studies, men with low total, free, or SHBG-adjusted testosterone possibly had a higher risk of cancer death. Because testosterone replacement therapy for men with clinically low testosterone has an uncertain risk versus benefit ratio, identifying modifiable factors that influence testosterone level and that are public health targets is needed. Obesity (lower testosterone) and cigarette smoking (higher testosterone) are two behavioral factors that are recognized to influence testosterone levels; given the great magnitude of the adverse effects of cigarette smoking, it is not a prevention strategy. Thus, in this study we investigated obesity as well as dietary and lifestyle factors in association with low total and free testosterone. Methods: The Third National Health and Nutrition Examination Survey (NHANES III), conducted 1988–1994, was a cross-sectional study of the U.S. civilian non-institutionalized population. Subjects participated in an interview, underwent a physical examination, and provided a blood specimen. Serum was available for 1470 men who participated in the morning session of Phase I (1988–1991) and were ≥20 years old. Testosterone and sex hormone binding globulin (SHBG) were measured by competitive electrochemiluminescence immunoassay. Free testosterone was estimated by mass action. We excluded men whose testosterone level was ≤2nd percentile because these men may have had congenital hypogonadism. We defined low total and free testosterone as ≤ 3.0 ng/mL and ≤ 0.07 ng/mL, respectively. We estimated the associations of the modifiable factors with low total and free testosterone using logistic regression adjusting for age and race/ethnicity. Results: Measures of overall and central adiposity were positively associated with low total and free testosterone. After mutual adjustment, men with high waist circumference (ethnic specific cutpoints; vs. low) were 2.59 (95% CI: 1.12–6.00) times more likely to have low total testosterone and 2.65 (95% CI: 1.44–4.89) times more likely to have low free testosterone, whereas body mass index and percent body fat did not remain statistically significantly associated. Independent of waist circumference, percent of calories from protein, fruit and vegetable intake, alcoholic beverage consumption, and physical activity were not statistically significantly associated with low total and free testosterone. These results were similar in men who did not have comorbidities at time of blood draw and in non-smokers. Discussion: Cross-sectionally, high waist circumference was the most consistent correlate of low total and free testosterone. These findings suggest that avoiding or reducing central adiposity may be one way to prevent clinically low androgen levels. Given that men with low androgens may have a higher risk of cancer death, our results may have import for cancer prevention and/or survival. Citation Information: Cancer Prev Res 2010;3(1 Suppl):B118.

Effects of tobacco exposure on lung health and pulmonary biomarkers in young, healthy smokers aged 12–25 years: a systematic review

Chronic obstructive pulmonary disease (COPD) is associated with high personal and societal burden and mortality. COPD is usually diagnosed during middle or late adult life, but the starting point for a ‘COPD career’ may be found earlier in life, during adolescence: first, because of smoking initiation and subsequent accumulation of risk, and second, because of the adverse effects of cigarette smoking on lung-function development. The objective of this paper is to systematically review the literature on the effects of active smoking on lung health in 12–25-year-old healthy boys and girls, measured with simple and noninvasive methods: lung function by spirometry, exhaled gases (including nitric oxide, carbon monoxide and hydrocarbons) and exhaled breath condensate. The identification of biomarkers may be useful for early detection of tobacco-related respiratory disease in this population, for targeted smoking prevention or smoking-cessation programs and, in the long term, for a reduction of personal and societal impact of COPD and other smoking-related diseases.

Quantification of benzo[a]pyrene and other PAHs in the serum and follicular fluid of smokers versus non-smokers

Cigarette smoking is a well-established reproductive hazard that has been linked with decreased fertility in both smokers and those exposed to second hand smoke. The chemical components responsible for the reproductive toxic effects of cigarette smoke are unknown. Moreover, exposure of reproductive tissues to the chemical constituents of cigarette smoke is largely unknown. Therefore, we measured the levels of benzo[a]pyrene (B[a]P), and other polycyclic aromatic hydrocarbons (PAH) present in cigarette smoke, in the serum and follicular fluid of women exposed to mainstream ( n = 19) and side stream smoke ( n = 7) compared to non-smokers ( n = 10). Women exposed to mainstream smoke had significantly higher levels of B[a]P (1.32 ± 0.68 ng/ml) in their follicular fluid compared to side stream exposed (0.05 ± 0.01 ng/ml) or their non-smoking (0.03 ± 0.01 ng/ml) counterparts. More importantly we found significantly higher ( p < 0.001) levels of B[a]P in the follicular fluid of women who did not conceive (1.79 ± 0.03 ng/ml) compared to those that achieved a pregnancy (0.08 ± 0.03 ng/ml). Other PAHs known to be present in cigarette smoke were also detectable in both serum and follicular fluid of study subjects studied but with lower frequency compared to B[a]P and no differences in serum or follicular fluid levels between the groups could be demonstrated. The important finding that B[a]P reaches the follicular fluid and the fact that it is found at much higher levels in women who smoke provides further evidence that of the many toxicants present in cigarette smoke, B[a]P may be a key compound that is central to the documented adverse effects of cigarette smoke on follicular development and subsequent fertility.

Beyond Our Pages

Beyond Our Pages

IL13 Promoter Polymorphism –1112C/T Modulates the Adverse Effect of Tobacco Smoking on Lung Function

Although the duration and amount of cigarette smoking correlate with reduction in pulmonary function, there is still variation among individual responses. IL-13 is involved in pulmonary inflammation, remodeling, and susceptibility to chronic obstructive pulmonary disease (COPD). We investigated whether the relationships between smoking and the lung function measures FEV(1) and FEV(1)/FVC ratio are modulated by IL13 polymorphisms. Smokers (>or=20 pack-years), aged at least 40 years old (n = 1,073), were genotyped for three single nucleotide polymorphisms (SNPs; -1112C/T [rs1800925], +2044G/A [rs20541, R130Q], and +2525G/A [rs1295685]) in the IL13 gene. Linear, quantile, and logistic regression methods were used to assess the effect of cigarette smoking (pack-years), IL13 polymorphisms, and their interaction on %predicted FEV(1) and FEV(1)/FVC ratio. Age, sex, and current smoking status were included as confounders. The number of pack-years smoked was associated with a lower value for both %predicted FEV(1) and FEV(1)/FVC (P < 0.001). The three SNPs were not associated with lung function measures; however, there was a significant combined effect between smoking and the promoter polymorphism -1112C/T on %predicted FEV(1) (P for interaction < 0.03 for mean %predicted FEV(1) and < 0.0001 for 90th percentile %predicted FEV(1)). Every 20-pack-year increment in smoking was associated with a 2.4% reduction in mean %predicted FEV(1) in the common homozygous (CC) or heterozygous (CT) promoter genotypes, and an 8.2% reduction in mean %predicted FEV(1) in minor allele homozygotes (TT, recessive model). An IL13 polymorphism in the promoter region may modulate the adverse effects of cigarette smoking on pulmonary function in long-term cigarette smokers.

Response to Selection Bias, Confounding, or Information Bias?

Kabir’s1 comments highlight the differences between epidemiology in theory and in practice. The recruitment procedures were stated clearly. The subjects consisted of consecutive new referrals suspected to have elevated blood pressure to a hypertension unit that provides confirmatory ambulatory blood pressure monitoring. Not on treatment at the time of clinical and hemodynamic assessment is not the same as “left untreated,” because it is important to establish the diagnosis of hypertension before lifelong treatment. However desirable in epidemiological terms, it would be unethical to leave patients untreated. Kabir1 argues that we have used a selected cohort of patients with hypertension, which is …

Follicle growth is inhibited by benzo-[a]-pyrene, at concentrations representative of human exposure, in an isolated rat follicle culture assay

The adverse effects of cigarette smoking on human fertility have been well documented. However, the mechanism(s) underlying the detrimental effects of cigarette smoking are unknown. Using a novel isolated rat follicle culture assay, we tested the hypothesis that benzo-[a]-pyrene (B[a]P), a constituent of cigarette smoke, can inhibit follicle growth. B[a]P levels were quantified in the serum and follicular fluid (FF) of women undergoing in vitro fertilization (IVF) treatment exposed to mainstream smoke (n = 19) and non-smokers (n = 10) by gas chromatography mass spectrometry. Isolated rat follicles were cultured with increasing concentrations of B[a]P (1.5-300 ng ml(-1)) and follicle diameter was measured daily. Mean ( +/- Standard error of the mean) B[a]P) was quantified in the serum (0.40 +/- 0.13 ng ml(-1)) and FF (1.32 +/- 0.68 ng ml(-1)) of women who smoke. IVF stimulation and outcome measures were similar between female smokers and non-smokers with the exception of implantation rate and pregnancy rate, which were both significantly lower (P < 0.05) in the MS group. B[a]P treatment significantly reduced rat follicle diameter and attenuated FSH stimulated growth in a dose-dependent manner, beginning at 1.5 ng ml(-1). Our data suggest that B[a]P, at levels representative of those measured in human FF, may adversely affect follicle development and be an ovarian toxicant.

Early postnatal exposure to cigarette smoke impairs the antigen-specific T-cell responses in the spleen

Annually, approximately two million babies are exposed to cigarette smoke in utero and postnatally through cigarette smoking of their mothers. Exposure to mainstream cigarette smoke is known to impair both innate and adaptive immunities, and it has been hypothesized that the effects of in utero exposure to cigarette smoke on children's health might primarily stem from the adverse effects of cigarette smoke on the immune system. To simulate the environment that babies from smoking mothers encounter, we examined the effects of prenatal mainstream and postnatal sidestream cigarette smoke on spleen cell responses. Results show that postnatal exposure of newborn Balb/c mouse pups to sidestream cigarette smoke through the first 6 weeks of life strongly suppresses the antibody response of spleen cells to the T-cell-dependent antigen, sheep red blood cells. The reduction in the antibody response seen within 6 weeks of postnatal smoke exposure is much quicker than the published data on the time 25 weeks) required to establish reproducible immunosuppression in adult rats and mice. Moreover, the immunosuppression is not associated with significant changes in T-cell numbers or subset distribution. While the postnatal exposure to cigarette smoke did not affect the mitogenic response of T and B cells, the exposure inhibited the T cell receptor-mediated rise in the intracellular calcium concentration. These results suggest that the early postnatal period is highly sensitive to the immunosuppressive effects of environmental tobacco smoke, and the effects are causally associated with impaired antigen-mediated signaling in T cells.

Response to Cigarettes and ADMA: The Smoke Hasn’t Cleared Yet

As acknowledged by Kielstein and coauthors, our recent study1 sought to investigate in detail the complex nature of the adverse effects of cigarette smoking on endothelial function. Using both in vivo and in vitro methodology we demonstrated that components of cigarette smoke, most likely reactive oxygen species, exerted inhibitory effects on several elements of the L-arginine:NO pathway, which cumulatively resulted in …

Adverse effects of cigarette smoking during pregnancy : review article

Extracted from text ... REVIEW Obstetrics & Gynaecology Forum - 12 Adverse effects of cigarette smoking during pregnancy Smoking of cigarettes is a major health problem. This habit is causing the death of about 5 million people per year.1 More than 4000 chemicals, of which at least 60 are known carcinogens, are contained in the smoke from tobacco in cigarettes. The most harmful components are nicotine and carbon monoxide. Nicotine is highly addictive, since it can cause both stimulation and euphoria. 2-4 Outside pregnancy the most common general adverse health effects of cigarette smoking are lung cancer, heart disease, atherosclerotic vascular disease, ..

Factors influencing hip joint space in asymptomatic subjects: A survey of 4151 subjects of the Copenhagen City Heart Study: The Osteoarthritis Substudy

Objective The aims of the study were to investigate the distribution of hip joint space width (JSW) in asymptomatic subjects without radiologic evidence of degeneration, and investigate the influence of age, sex, physical parameters, occupational activity, and smoking on JSW. Materials and methods The distribution of minimum JSW was determined in hip joints in standardized, weight-bearing pelvic radiographs of the Copenhagen City Heart Study: The Osteoarthritis Substudy cohort of 4151 subjects. Asymptomatic subjects without radiologic osteoarthritis were included (1018M/1554F). Occupational exposure to repeated daily lifting, smoking, and physical parameters were registered for each individual. Results Overall, female minimum JSW was significantly smaller compared with male JSW ( P<0.0001). Female minimum JSW decreased significantly with age ( P<0.0001), while male minimum JSW remained relatively unaltered throughout life ( P right=0.19; P left=0.18). Minimum JSW correlated positively with height, weight, and BMI, as did femoral head radius. Multiple logistic regression analysis revealed significant influence of sex and age on minimum JSW in females only. Positive or adverse effects of cigarette smoking on hip JSW were not documented. Type and duration of occupational exposure to repeated daily lifting did not affect hip JSW significantly. Conclusion Minimum JSW decreased progressively with age in women, while it was unaltered in men. A history of smoking or different occupational exposure to repeated daily lifting did not influence minimum hip JSW significantly. Differences in body mass index, height or weight did not significantly influence minimum hip joint JSW.

A period of increased susceptibility to cigarette smoking among high school students.

Cross-sectional surveys of randomly selected high school students were conducted in October 1999 and in May 2000 to measure awareness of youth-led tobacco prevention efforts. A secondary goal of the surveys was to learn about tobacco use and attitudes. Respondents who never smoked cigarettes were asked if they had made a firm commitment to not smoke, and respondents who had not made such a commitment were considered susceptible. Among ninth graders, susceptibility increased from 31% in October to 47% in May, while susceptibility decreased from October to May for students in more advanced grades (p = 0.03, interaction of linear trends). Susceptibility was more common among students who felt smoking produced social benefits (OR 1.59, 95% CI 1.22-2.08) or who were tolerant of tobacco company behavior (OR 1.65, 95% CI 1.23-2.21), and less common among students who felt short-term adverse effects of cigarette smoking on health or hygiene were important to them (OR 0.74, 95% CI 0.56-0.97). Further studies should confirm the increase in susceptibility and its underlying mechanisms. Whether associated with ninth grade or with the first year in a new school, this previously unrecognized period of heightened susceptibility might represent an important opportunity for prevention.

In vivo evaluation of leucocyte dynamics in cremaster muscle in rats after exposure to cigarette smoke.

This experiment was designed to examine the effects of chronic cigarette smoking on the microcirculation immediately after exposure to smoke for two, four, and six weeks and after withholding smoke for two weeks from those previously exposed for four weeks. The mean (SD) rolling leucocytes at two, four, and six weeks were 11.10 (1.8), 23.7 (2.3), 40.2 (3.9) (p < 0.001). The rolling leucocytes after smoking for four weeks and then having smoke withheld for two weeks was 9.6 (1.4). The mean adherent leucocytes were 5.0 (0.7), 7.5 (1.1), 12.6 (1.8) (p < 0.001). The adherent leucocytes after smoking for four weeks and then having smoke withheld for two weeks was 3.5 (0.5). Our results confirm those of many previous studies of the adverse effects of cigarette smoking, and also that those deleterious effects are time-dependent. The reversibility of the deleterious effect of cigarette smoking after cessation of cigarette smoking before face-lift or flap reconstruction is at least two weeks. This information is also important for clinical management of patients who smoke and who are scheduled for face-lift and flap reconstruction. Two weeks without cigarettes is a necessary period for successful elective plastic surgery.

Prevalence of bronchial hyperresponsiveness among HIV-infected men.

HIV infection is associated with immune dysregulation primarily affecting T-cell function, whereas asthma is related to excessive T-cell activity. We compared the prevalence of asthma and related conditions among adult seropositive men with the prevalence among men of similar age drawn from the general population. Seropositive men had a significantly more frequent occurrence of wheezing (54.4 versus 21.2%), bronchial hyperresponsiveness (BHR) to methacholine (26.2 versus 14.4%), and an elevated total serum IgE (37.8 versus 25.7%). Differences in BHR were significant only among smokers. Among the seropositive men, FEV(1)/FVC and an elevated IgE were the principal determinants of BHR. Our results suggest that the frequency of asthma may be underestimated in HIV disease. Furthermore, the frequent occurrence of BHR in HIV-infected men who smoke (30.1%) suggests this group may be especially susceptible to the adverse effects of cigarette smoke.

Substitution of asparagine for aspartic acid at residue 9 (D9N) of lipoprotein lipase markedly augments risk of ischaemic heart disease in male smokers

Genetic variants of lipoprotein lipase (LPL), a key enzyme in the hydrolysis of triglyceride (TG)-rich particles, may contribute to ischaemic heart disease (IHD) risk. We have examined the risk of IHD in carriers of two common LPL variants, asparagine substitution for aspartic acid at residue 9 (D9N) and serine for asparagine at residue 291 (N291S) in 2708 middle-aged healthy European men, followed for over 6 years. The carrier frequencies were 2.6% for N9, and 3.9% for S291. Both variants were associated with higher plasma TG at baseline of 9% and 14%, respectively. At baseline, 28% of men were current smokers and smoking was unrelated to genotype. Associations between LPL variants and disease outcome, according to smoking status, were assessed by Cox’s proportional hazards analysis. S291 carriers showed no increased risk of IHD compared to non-carriers, while there was strong evidence of interaction between D9N genotype and smoking status ( P=0.0003) in determining the risk of IHD. In 2248 non-carriers of N9, smoking increased the risk of an IHD event by 1.6 (95% CI: 1.1–2.4%) times. Among 58 N9 carriers, no IHD events occurred in 42 who were non-smokers, whereas five events were reported in 16 who smoked. The combined effect of smoking and N9 allele was to increase the risk of an IHD event by 10.4 (95% CI: 4.7–22.8%) times compared with D9 non-smokers. These findings could not be explained by confounding effects of baseline TG. Carriers of N9 appear to be especially vulnerable to the adverse effects of cigarette smoking on IHD risk, but this susceptibility is unrelated to the influence of this variant on plasma TG levels.

Normal Patterns of Angiogenesis and Extracellular Matrix Deposition in Chick Chorioallantoic Membranes Are Disrupted by Mainstream and Sidestream Cigarette Smoke

The adverse effects of cigarette smoke on mature blood vessels are well established, whereas little is known about the influence of smoke on blood vessel development. To determine if cigarette smoke alters angiogenesis, chick chorioallantoic membranes (CAMs) were exposed for 4 days to culture medium (control) or to mainstream (MS) or sidestream (SS) smoke solution, and then blood vessel patterns were compared in blind tests. In contrast to the normal tree-like branching of control blood vessels, smoke-treated CAMs often had vessels that ran parallel to each other without much branching. A significant increase in the number of fibroblasts was observed in histological sections of treated CAMs, and this increase correlated with alterations in extracellular matrix components. Many more matrix fibrils were observed in treated CAMs than in controls using scanning electron microscopy. Immunohistochemistry showed that type III collagen was distributed in a tight band adjacent to the endoderm in controls but was distributed throughout the mesoderm in both treatment groups. Western blots confirmed that both type I and type III collagen were more abundant in treated CAMs than in controls. Fibronectin, which was localized immunohistochemically in the basal laminae and mesodermal matrix of controls, increased in abundance in CAMs treated with SS smoke solutions. Hyaluronic acid, which was present in a dense band subjacent to the capillary plexus of control CAMs, was greatly reduced in MS-treated CAMs and was absent in SS-treated CAMs. These observations demonstrate that both MS and SS cigarette smoke solutions caused abnormal pattern formation of CAM blood vessels and altered the composition of the extracellular matrix in the CAM mesoderm.