Prevention of smoking behaviors in middle school students: student nurse interventions

This article examines the use of the Tar Wars curriculum with the public health problem of preteen smoking and outlines interventions with a middle school population by community health student nurses from a state university. Smoking is the single most preventable cause of death and disability. Three million people die worldwide each year as a result of smoking. Cigarette smoking has now been labeled a pediatric disease. Estimates are that 3,000 children will begin a lifelong addiction to cigarettes every day. They will face a life of poor quality based on the medical consequences of smoking cigarettes. Mortality from tobacco use is annually greater than that from drug abuse, AIDS, suicide, homicide, and motor vehicle accidents combined. Preteen and teenage smoking is now a public health problem, therefore implications for service learning, nursing advocacy, and interventions with this health problem are discussed.     

Increased respiratory symptoms following surgery in children exposed to environmental tobacco smoke

OBJECTIVE: The aim of this study was to determine if children exposed to environmental tobacco smoke (ETS) via parental smoking (ETS+) developed more respiratory symptoms resulting in longer recovery times following surgical outpatient procedures compared with children of nonsmoking parents (ETS-). METHODS: One hundred and forty six children (4.9 +/- 3 years) undergoing inguinal hernia repair were prospectively studied. Parental smoking behaviour was determined by survey and urine analysis. Seven respiratory symptoms were evaluated during induction and emergence from anaesthesia and during the recovery room (RR) stay. RESULTS: Fifty-seven (39%) families admitted a smoking history while 89 (61%) denied it. This strongly correlated with the cotinine/creatinine ratio (Pearson correlation coefficient = 0.76; P = 0.01). ETS exposure was associated with an increased frequency of RR symptoms (ETS+: 56%; ETS-: 31%; P = 0.007). CONCLUSIONS: In children undergoing general anaesthesia for inguinal hernia repair, ETS exposure was associated with an increased frequency of respiratory symptoms during emergence from anaesthesia and during postoperative recovery.     

Cigarette smoke impairs neutrophil respiratory burst activation by aldehyde-induced thiol modifications

Exposure to airborne pollutants such as tobacco smoke is associated with increased activation of inflammatory-immune processes and is thought to contribute to the incidence of respiratory tract disease. We hypothezised that cigarette smoke (CS) could synergize with activated inflammatory/immune cells to cause oxidative injury or result in the formation of unique reactive oxidants. Isolated human neutrophils were exposed to gas-phase CS, and the production of nitrating and chlorinating oxidants following neutrophil stimulation was monitored using the substrate 4-hydroxyphenylacetate (HPA). Stimulation of neutrophils in the presence of CS resulted in a reduced oxidation and chlorination of HPA, suggesting inhibition of NADPH oxidase or myeloperoxidase (MPO), the two major enzymes involved in inflammatory oxidant formation. Peroxidase assays demonstrated that neutrophil MPO activity was not significantly affected after CS-exposure, leaving the NADPH oxidase as a likely target. The inhibition of neutrophil oxidant formation was found to coincide with depletion of cellular GSH, and a similar modification of critical cysteine residues, such as those in NADPH oxidase components, might be involved in reduced respiratory burst activity. As ,β-unsaturated aldehydes such as acrolein have been implicated in thiol modifications by CS, we exposed neutrophils to acrolein prior to stimulation, and observed inhibition of NADPH oxidase activation in relation to GSH depletion. Additionally, translocation of the cytosolic components of NADPH oxidase to the membrane, a necessary requirement for enzyme activation, was inhibited. Protein adducts of acrolein (or related aldehydes) could be detected in several neutrophil proteins, including NADPH oxidase components, following neutrophil exposure to either CS or acrolein. Alterations in neutrophil function by exposure to (environmental) tobacco smoke may affect inflammatory/infectious conditions and thereby contribute to tobacco-related disease.     

Dietary intake and microsatellite instability in colon tumors

Microsatellite instability (MSI) occurs in approximately 15% of colon tumors. Other than relatively rare mutations in mismatch repair genes, the causes of MSI are not generally known. The purpose of this study was to determine if dietary intake of nutrients previously reported as being associated with colon cancer relate specifically to the MSI disease pathway. Data from a population-based case-control study of adenocarcinoma of the colon were used to evaluate associations between dietary intake and MSI. Participants were between 30 and 79 years of age at time of diagnosis and included both men and women. Dietary intake data were obtained from a computerized diet history questionnaire. MSI was evaluated in several ways: by a panel of 10 tetranucleotide repeats, and by 2 mononucleotide repeats, BAT-26 and TGFbetaRII. A total of 1,510 cases had valid study data and tumor DNA on which we were able to obtain MSI status. Cases with and without MSI were compared with dietary data reported by 2,410 population-based controls to determine dietary associations that may be different for these 2 subsets of cases. We compared dietary intake for cases with and without MSI to further determine associations that are specific to the MSI disease pathway. When comparing MSI+ to MSI- tumors we observed that long-term alcohol consumption, especially intake of liquor, increased the probability of having a tumor with MSI [odds ratio (OR) for MSI+ vs. MSI- tumors for alcohol 1.6, 95% confidence interval (CI) 1.0-2.5; OR for liquor 1.6, 95% CI 1.1-2.4]. The likelihood of having MSI in the tumor from the combined effects of high alcohol consumption and smoking cigarettes showed a 70% excess in risk from the additive model. There were some suggestions that high intakes of refined grain might also be associated with MSI+ tumors, although associations were less consistent. Risk estimates for most other dietary factors did not differ substantially by MSI status. Data from this large population-based case-control study of colon cancer indicate that alcohol consumption, especially consumption of liquor, may increase the odds of an MSI+ tumor. Most other dietary factors do not appear operate exclusively in the MSI+ disease pathway.     

Lifetime residential and workplace exposure to environmental tobacco smoke and lung cancer in never-smoking women, Canada 1994-97

Although the risk of lung cancer among never-smokers living with a spouse who smokes has been extensively studied, the impact of lifetime residential and workplace environmental tobacco smoke has received less attention. As part of a large population-based case-control study of lung cancer, we collected lifetime residential and occupational passive smoking information from 71 women with lung cancer and 761 healthy control subjects, all of whom reported being lifetime nonsmokers. The adjusted odds ratio (OR) for lung cancer associated with residential passive exposure only was 1.21 (95% confidence interval [CI] 0.5-2.8). Although more years of and more intense residential passive smoke exposure tended to be associated with higher risk estimates, no clear dose-response relationship was evident. The OR for women with passive exposure as a child and as an adult was 1.63 (95% CI 0.8-3.5) and for those only exposed as an adult 1.20 (95%CI 0.5-3.0). Exposure to environmental tobacco smoke only in the workplace was associated with an adjusted OR of 1.27 (95% CI 0.4-4.0). Risks associated with increasing occupational exposure year tertiles were 1.24, 1.71 and 1.71. Total smoker-years of residential and occupational exposure combined resulted in a statistically significant trend (linear test for trend p = 0.05) with ORs for tertiles of exposure of 0.83, 1.54 and 1.82. Our results are consistent with the literature suggesting that long-term, regular exposure to either residential or occupational environmental tobacco smoke is associated with increased lung cancer risk in never-smoking women.     

Exposure to environmental tobacco smoke: association with personal characteristics and self reported health conditions

STUDY OBJECTIVE: To examine the association between exposure to environmental tobacco smoke (ETS) and demographic, lifestyle, occupational characteristics and self reported health conditions. DESIGN: Cross sectional study, using data from multiphasic health checkups between 1979 and 1985. SETTING: Large health plan in Northern California, USA. PARTICIPANTS: 16 524 men aged 15-89 years and 26 197 women aged 15-105 years who never smoked. RESULTS: Sixty eight per cent of men and 64 per cent of women reported any current ETS exposure (at home, in small spaces other than home or in large indoor areas). The exposure time from all three sources of ETS exposure correlated negatively with age. Men and women reporting high level ETS exposure were more likely to be black and never married or separated/divorced, to have no college or partial college education, to consume three alcoholic drink/day or more and to report exposure to several occupational hazards. Consistent independent relations across sexes were found between any current exposure to ETS and a positive history of hay fever/asthma (odds ratio (OR)=1.22 in men, 1.14 in women), hearing loss (OR=1.30 in men, 1.27 in women), severe headache (OR=1.22 in men, 1.17 in women), and cold/flu symptoms (OR=1.52 in men, 1.57 in women). Any current ETS exposure was also associated with chronic cough (OR=1.22) in men and with heart disease (OR=1.10) in women. Self reported stroke was inversely associated with any current ETS exposure in men (OR=0.27). No associations were noted for cancer or tumour and for migraine. CONCLUSION: ETS exposure correlated with several personal characteristics potentially associated with adverse health outcomes. Although the study design precluded causal inference, ETS exposure was associated with several self reported acute and chronic medical conditions.     

Cigarette smoking, endothelial injury and cardiovascular disease

Despite the fact that the epidemiological evidence linking cigarette smoking with cardiovascular disease is overwhelming, the precise components of cigarette smoke responsible for this relationship and the mechanisms by which they exert their effect have not yet been elucidated. There are however, some promising pointers as a result of recent developments and this review concentrates on new evidence since earlier reviews of this topic. It is now known that the endothelium has a vastly more important role than was ever thought to be the case a decade ago. Its role in health and disease is increasingly understood, as is the relationship between endothelial injury and the development of atherosclerosis. There is considerable evidence that cigarette smoking can result in both morphological and biochemical disturbances to the endothelium both in vivo and in cell culture systems. Cigarette smoke is a complex mixture and only a few components have been extensively studied. Nicotine and carbon monoxide are much less damaging than is whole smoke. However the free radical components of cigarette smoke have been shown to cause damage in model systems. Further work will be necessary to consolidate the evidence base but the data reported in this review suggest that the free radical components of cigarette smoke may be responsible for the morphological and functional damage to endothelium that has been observed in model systems.     

The comet assay of nasal epithelia: measurement of DNA damage for the assessment of genotoxic air pollution

OBJECTIVES: The alkaline single cell gel electrophoresis or "comet" assay allows measurement of DNA damage in single cells with a high degree of sensitivity, e.g., for investigations of the effect of environmental agents with DNA-damaging potential. This study aimed to adapt this test to respiratory cells of the human nasal mucosa to examine the genotoxic effect of air pollution (cigarette smoke). STUDY DESIGN: In a prospective study, nasal epithelia of 16 cigarette smokers were examined by the adapted comet assay and the results were correlated with the results of the Papanicolaou-stained nasal cytology, carried out in a blinded fashion. The control group comprised 20 non-smoking men. All subjects under investigation were healthy office workers. METHODS: Nasal epithelia were harvested from the maxilloturbinates. One part of cells was Papanicolaou stained and evaluated by cytopathologists. The comet assay was performed on the other part of the cells. The examiners were blinded to the study and control groups. RESULTS: Among cigarette smokers, a significant correlation between cytopathological cell nucleus changes (metaplasia and dysplasia) and the DNA migration (tail lengths) in the comet assay was found as a sign of DNA damage. This was not found in nonsmoking control persons. CONCLUSIONS: These results confirm the sensitivity of the comet assay and the hypothesis that cell nucleus changes in conventional nasal cytology are associated with DNA damage.     

Increased burden of respiratory disease in the first six months of life due to prenatal environmental tobacco smoke: Krakow birth cohort study

The main purpose of our study was to assess the effects of prenatal tobacco smoke on respiratory symptoms and on doctor consultations in a birth cohort of 445 infants who had no smoking mothers and who had no postnatal exposure to environmental tobacco smoke (ETS). Before and after delivery, questionnaires and interviews with mothers were administered to solicit information on prenatal and postnatal ETS exposure. Newborns were followed-up over six months of life, and respiratory outcomes such as runny or stuffed nose, cough with or without cold, difficult (puffed) breathing, wheezing or whistling in the chest irrespective of respiratory infection were considered. In addition, medical visits related to the occurrence of respiratory symptoms were recorded for each child over a six-month study period. In the multivariate Poisson regression analysis, a set of potential confounders has been taken into account such as gender of child, season of birth, gestational age, maternal education, maternal atopy, presence of moulds in households and prenatal level of personal exposure to fine particles. The adjusted rate ratio (RR) estimated for the occurrence of episodes of running nose was significantly higher in infants exposed to prenatal ETS (1.40; 95% confidence interval [CI]: 1.11-1.68) and the corresponding RR estimates for cough, difficult breathing and wheezing were 1.49 (95% CI: 1.15-1.93), 1.96 (95% CI: 1.22-3.16) and 5.12 (95% CI: 2.86-9.16). The rate ratios of doctor consultations attributable to prenatal ETS because of cough was 1.94 (95% CI: 1.49-2.54). The risk estimate for consultations due to difficult breathing was 2.77 (95% CI: 1.76-4.36), and that for wheezing was 5.86 (95% CI: 3.56-9.64). The data strongly support the view about the impact of the in-utero effect of passive smoking on children's respiratory health. Higher utilization rates of doctor consultations in infants attributable to prenatal ETS exposure demand the revision of public health policy, which should be focused also on cessation of smoking practices by all household members during and after the pregnancy period.     

Cigarette smoking and risk of epithelial ovarian cancer (Australia)

Objectives: We studied the association between cigarette smoking and ovarian cancer in a population-based case–control study. Methods: A total of 794 women with histologically confirmed epithelial ovarian cancer who were aged 18–79 years and resident in one of three Australian states were interviewed, together with 855 controls aged 18–79 years selected at random from the electoral roll from the same states. Information was obtained about cigarette smoking and other factors including age, parity, oral contraceptive use, and reproductive factors. We estimated the relative risk of ovarian cancer associated with cigarette smoking, accounting for histologic type, using multivariable logistic regression to adjust for confounding factors. Results: Women who had ever smoked cigarettes were more likely to develop ovarian cancer than women who had never smoked (adjusted odds ratio (OR) = 1.5; 95% confidence interval (CI) = 1.2–1.9). Risk was greater for ovarian cancers of borderline malignancy (OR = 2.4; 95% CI = 1.4–4.1) than for invasive tumors (OR = 1.7; 95% CI = 1.2–2.4) and the histologic subtype most strongly associated overall was the mucinous subtype among both current smokers (OR = 3.2; 95% CI = 1.8–5.7) and past smokers (OR = 2.3; 95% CI = 1.3–3.9). Conclusions: These data extend recent findings and suggest that cigarette smoking is a risk factor for ovarian cancer, especially mucinous and borderline mucinous types. From a public health viewpoint, this is one of the few reports of a potentially avoidable risk factor for ovarian cancer.