Effects Of Secondhand Smoke Research Articles

Cancer risks and Native Americans: The ‘Healthy Living In Two Worlds’ study

Objective: This project collected data on cancer risk factors among urban Native American youth in the northeast to inform development of a prevention initiative. Design: Face to face interviews were conducted. Setting: Interviews were conducted in homes, at a social service agency, and in a private space at a Native American cultural event in Buffalo and Niagara Falls, New York. Methods: Forty-one youth (ages 9–13) and 17 caregivers were interviewed about their health behaviours. Results: Poor dietary choices and a sedentary lifestyle places these youth at risk for developing cancer later in life. Many of these youth’s family members and some of their peers smoke, thus exposing them to the temptation to initiate smoking and the effects of second hand smoke. Conclusion: This data informed development of a curriculum designed to reduce the cancer risk factors of poor diet, recreational tobacco use, and limited physical activity.

Effects of second hand smoke on airway secretion and mucociliary clearance

The airway acts as the first defense against inhaled pathogens and particulate matter from the environment. One major way for the airway to clear inhaled foreign objects is through mucociliary clearance (MCC), an important component of the respiratory innate immune defense against lung disease. MCC is characterized by the upward movement of mucus by ciliary motion that requires a balance between the volume and composition of the mucus, adequate periciliary liquid (PCL) volume, and normal ciliary beat frequency (CBF). Airway surface fluid (ASL) is a thin layer liquid that consists of the highly viscous mucus upper “gel” layer, and the watery lubricating lower “sol” layer. Mucus production, secretion and clearance are considered to play a critical role in maintenance of airway health because it maintains hydration in the airway and traps particulates, bacteria, and viruses. Different types of epithelial cells, including secretory cells, and ciliated cells, contribute to the MCC function. Cigarette smoke (CS) contains chemicals and particulates that significantly affect airway secretion. Active and passive CS-induced chronic obstructive pulmonary disease (COPD) is frequently associated with hyperplasia of goblet cells and submucosal glands (SMGs), thus increasing the secretory capacity of the airways that impairs MCC.

Fatherhood, Smoking, and Secondhand Smoke in North America

In the context of concerns about the effects of secondhand smoke on fetal health and the health of children, North American health promotion interventions have focused on reducing tobacco consumption among women to a greater extent than men. This is problematic when the health effects of men's secondhand smoke in family environments are considered. This article examines this gendered phenomenon in terms of a history of cigarette consumption that positions smoking as masculine. Furthermore, it demonstrates the value of addressing men's smoking using a gendered methodology, with an emphasis on fatherhood as an expression of masculine identity. Garnering health promotion programs to promote a culture of masculinity that is less individualistic, and defined in terms of responsibility and care for others, in addition to the self, has the potential to render men's smoking problematic and challenge the historic linkages between smoking and masculinity.

Sidestream tobacco smoke is a male germ cell mutagen.

Active cigarette smoking increases oxidative damage, DNA adducts, DNA strand breaks, chromosomal aberrations, and heritable mutations in sperm. However, little is known regarding the effects of second-hand smoke on the male germ line. We show here that short-term exposure to mainstream tobacco smoke or sidestream tobacco smoke (STS), the main component of second-hand smoke, induces mutations at an expanded simple tandem repeat locus (Ms6-hm) in mouse sperm. We further show that the response to STS is not linear and that, for both mainstream tobacco smoke and STS, doses that induced significant increases in expanded simple tandem repeat mutations in sperm did not increase the frequencies of micronucleated reticulocytes and erythrocytes in the bone marrow and blood of exposed mice. These data show that passive exposure to cigarette smoke can cause tandem repeat mutations in sperm under conditions that may not induce genetic damage in somatic cells. Although the relationship between noncoding tandem repeat instability and mutations in functional regions of the genome is unclear, our data suggest that paternal exposure to second-hand smoke may have reproductive consequences that go beyond the passive smoker.

Effects of Secondhand Smoke

Effects of Secondhand Smoke

Effect of Secondhand Smoke on Occupancy of Nicotinic Acetylcholine Receptors in Brain

Despite progress in tobacco control, secondhand smoke (SHS) exposure remains prevalent worldwide and is implicated in the initiation and maintenance of cigarette smoking. To determine whether moderate SHS exposure results in brain α(4)β(2)* nicotinic acetylcholine receptor (nAChR) occupancy. Positron emission tomography scanning and the radiotracer 2-[18F]fluoro-3-(2(S)azetidinylmethoxy) pyridine (also known as 2-[(18)F]fluoro-A-85380, or 2-FA) were used to determine α(4)β(2)* nAChR occupancy from SHS exposure in 24 young adult participants (11 moderately dependent cigarette smokers and 13 nonsmokers). Participants underwent two bolus-plus-continuous-infusion 2-FA positron emission tomography scanning sessions during which they sat in the passenger's seat of a car for 1 hour and either were exposed to moderate SHS or had no SHS exposure. The study took place at an academic positron emission tomography center. Main Outcome Measure Changes induced by SHS in 2-FA specific binding volume of distribution as a measure of α(4)β(2)* nAChR occupancy. An overall multivariate analysis of variance using specific binding volume of distribution values revealed a significant main effect of condition (SHS vs control) (F(1,22)=42.5, P<.001) but no between-group (smoker vs nonsmoker) effect. Exposure to SHS led to a mean 19% occupancy of brain α(4)β(2)* nAChRs (1-sample t test, 2-tailed, P<.001). Smokers had both a mean 23% increase in craving with SHS exposure and a correlation between thalamic α(4)β(2)* nAChR occupancy and craving alleviation with subsequent cigarette smoking (Spearman ρ=-0.74, P=.01). Nicotine from SHS exposure results in substantial brain α(4)β(2)* nAChR occupancy in smokers and nonsmokers. Study findings suggest that such exposure delivers a priming dose of nicotine to the brain that contributes to continued cigarette use in smokers. This study has implications for both biological research into the link between SHS exposure and cigarette use and public policy regarding the need to limit SHS exposure in cars and other enclosed spaces.

The Association Between Second Hand Smoke and Low Birth Weight and Preterm Delivery

To determine the association between maternal exposure to SHS and low birth weight and preterm delivery. This cross-sectional study was carried out in the four main governmental hospitals dealing with deliveries in the north of Jordan. A consecutive 8,490 women who delivered in these hospitals between April 2007 and September 2007 were included in the study after excluding those who reported active smoking during the current pregnancy. Pre-structured questionnaire and review of hospital records were used to collect data about maternal background, obstetric history, medical history, and data related to second hand smoke exposure. Overall, 13.8% of women gave birth to a preterm baby and 10.0% gave birth to a low birth weight baby. About 12.6% of women who were exposed to SHS delivered low birth weight babies compared to 7.7% for non exposed women. The rate of preterm delivery among the exposed group was significantly higher than that among the non-exposed group (17.2 vs. 10.6%). In the multivariate analysis, exposure to SHS during pregnancy was significantly associated with increased odds of low birth weight (OR = 1.56 (95% CI 1.31, 1.89)) and preterm delivery (OR = 1.61 (95% CI: 1.30, 1.99)). Exposure of women to SHS during pregnancy is associated with increased odds of low birth weight and preterm delivery. Health care professionals should carry out educational programs to increase awareness and understanding of pregnant women and their husbands about the harmful effects of second hand smoke on birth outcomes.

Exploring the Effects of Secondhand Smoke

Exploring the Effects of Secondhand Smoke

Secondhand Smoke, Vascular Disease, and Dementia Incidence: Findings From the Cardiovascular Health Cognition Study

Recent studies have found that smoking is associated with an increased risk of dementia, but the effects of secondhand smoke (SHS) on dementia risk are not known to have previously been studied. The authors used Cox proportional hazards marginal structural models to examine the association between self-reported lifetime household SHS exposure and risk of incident dementia over 6 years among 970 US participants in the Cardiovascular Health Cognition Study (performed from 1991 to 1999) who were never smokers and were free of clinical cardiovascular disease (CVD), dementia, and mild cognitive impairment at baseline. In addition, because prior studies have found that SHS is associated with increased risk of CVD and that CVD is associated with increased risk of dementia, the authors tested for interactions between SHS and measures of clinical and subclinical CVD on dementia risk. Moderate (16-25 years) and high (>25 years) SHS exposure levels were not independently associated with dementia risk; however, subjects with >25 years of SHS exposure and >25% carotid artery stenosis had a 3-fold increase (hazard ratio = 3.00, 95% confidence interval: 1.03, 9.72) in dementia risk compared with subjects with no/low (0-15 years) SHS exposure and < or =25% carotid artery stenosis. High lifetime SHS exposure may increase the risk of dementia in elderly with undiagnosed CVD.

Effects of Secondhand Smoke on Thyroid Function

Growing evidence suggests that the effects of second hand smoke (SHS) exposure contribute to disruptions in thyroid function. Toxic elements contained in cigarette smoke, such as thiocyanate, may be partially responsible for impaired thyroid hormonogenesis. SHS-induced inflammatory stress, namely interleukin 1beta (IL-1beta), impairs thyroid hormonogenesis and iodine uptake; initiates interleukin 6 (IL-6) production from thyroid epithelial cells and stimulates the expression of molecules that exacerbate thyroid autoimmunity. The link between SHS exposure and thyroid autoimmune disease is not well documented and thus, remains to be fully understood. Elevated inflammatory stress and thyroid hormone secretion in response to SHS exposure initiates catabolic processes that alter body composition via lean body mass breakdown; translating to an elevation in resting energy expenditure of approximately 10%. The combination of certain biological factors, such as sex and/or existing thyroid disease may stimulate differential SHS-induced effects on thyroid function. Nevertheless, exposure to SHS disturbs vital human processes via thyroid disruption.

Smoking Restrictions and Treatment for Smoking: Policies and Procedures in Psychiatric Inpatient Units in Australia

Tobacco smoking is the leading preventable cause of death and disease in Australia. Even though smoking prevalence in the general population has been reduced (20% smoke), prevalence rates remain high among psychiatric inpatients (70%-90%). This study aimed to identify smoking policies and procedures in public psychiatric inpatient units in New South Wales, Australia; the provision of "smoking care" in such units (for example, quit-smoking advice or nicotine replacement therapy); and policies and procedures associated with the assessment of smoking status and provision of smoking care. A cross-sectional survey was mailed to all public psychiatric inpatient units in New South Wales for completion by nurse unit managers. Of the 131 units, 123 units completed and returned surveys (94%). Over one-third (36%) of respondents reported instances in which inpatients began smoking during their admission. A similar proportion (39%) reported that staff provided cigarettes to patients who smoked when patients' supply was expended. Fifty percent of respondents reported that all patients were assessed for smoking status; however, 70% reported that nicotine dependence was not assessed. Units on which staff adhered to smoking restrictions were three times as likely to assess patients' smoking status as units where staff never adhered to restrictions (odds ratio=3.05, p=.01). Inadequate establishment of nonsmoking environments and of smoking restriction enforcement as well as inconsistencies in the provision of smoking care were evident. The findings suggest that failure of psychiatric services to provide smoking care is systemic and not related to particular types of services (for example acute versus nonacute or regional versus metropolitan).

Education on the Dangers of Passive Smoking

Passive smoking causes approximately 50 000 deaths annually in the United States, with the vast majority of these deaths due to heart disease.1 The effects of secondhand smoke on many pathophysiological mediators of coronary artery disease are nearly as large as those of active smoking, including impaired platelet function,2 damage to vascular endothelium and its associated repair mechanisms,3 a rise in inflammatory molecules, and dysfunctional lipid metabolism (Figure).2 The large literature on passive smoking is not limited to cardiovascular disease. Passive smoking causes lung cancer, head and neck cancers, respiratory infections, and obstructive lung disease (chronic obstructive pulmonary disease, asthma) and has been linked with breast cancer in younger women.1,4 Although as of 2008, more than half of the United States was covered by legislation that limits tobacco use in public places and workplaces, the Centers for Disease Control and Prevention found that nearly one half of US nonsmokers continue to be exposed to secondhand smoke.5 Figure. Effects of passive smoking on biological mediators of vascular disease.2,3 NO indicates nitric oxide. Article p 1535 In this issue of Circulation , He et al6 document yet another example of the dangers associated with secondhand smoke exposure: peripheral arterial occlusive disease (PAOD). This is the first study to identify an association between exposure to secondhand smoke and the development of PAOD in any population, particularly among the nonsmoking Chinese women they studied. PAOD is a surrogate marker for coronary artery disease, resulting from similar pathophysiological mechanisms: development of atherosclerosis that leads to vascular stenosis and ischemia, which is manifested as claudication in the extremities. Given the similar underlying mechanisms, the results of the study by He et al6 are not surprising, but …

Barriers associated with implementing a campus‐wide smoke‐free policy

PurposeThe purpose of this study is to review the barriers associated with implementing a campus‐wide smoke‐free policy as perceived by the American Cancer Society's Colleges against Cancer (CAC) Program chapter representatives.Design/methodology/approachFour focus group sessions were conducted at the annual CAC National Leadership Summit in October 2006. A total of 109 participants, or 41.4 percent of the total population of CAC member institutions, attended the focus groups.FindingsAll participants identified encountering barriers at some stage of the implementation process. Three major themes emerged when participants were asked to identify what they perceived to be the most significant barriers to successfully implementing a campus‐wide smoke‐free policy: lack of administrative and staff support, student involvement, and resources.Practical implicationsWith the rising rate of smoking among college students and the release of the 2006 Surgeon General's report citing the harmful effects of secondhand smoke, the need for colleges and universities to take measures not only to curtail the number of smokers, but to limit the exposure to secondhand smoke is intensifying.Originality/valueA study examining the challenges faced by colleges and universities when trying to implement a campus‐wide smoke‐free policy is absent from the literature. The paper helps in identifying the most significant barriers that may encourage efforts among colleges and universities to lessen or eliminate these barriers.

TNF-308 Modifies the Effect of Second-hand Smoke on Respiratory Illness-Related School Absences

Wenten, M, Berhane K, Rappaport EB, et al. Am J Respir Crit Care Med. 2005;172:1563–1568 PURPOSE OF THE STUDY. To investigate the role of tumor necrosis factor (TNF) G→308A, a variant in the promoter region of TNF, that has been associated with inflammatory diseases including asthma in the susceptibility of secondhand-smoke–exposed children to respiratory illness. STUDY POPULATION. A prospective cohort of fourth-grade students (N = 1935) from 27 elementary schools in southern California from whom school-absence data were collected from January to June of 1996. Approximately 70% of the children (n = 1351) provided a buccal cell sample. METHODS. Schools provided daily absence summary information for the study subjects, and each absence was recorded as illness or nonillness. Telephone interviews regarding each illness-related absence were conducted with parents. School absences were classified as lower respiratory illnesses if wet cough, wheeze, or asthma was present. Secondhand-smoke exposure was determined by parent/guardian written responses on self-administered questionnaires and categorized as none, 1 to 29, or ≥30 cigarettes smoked per day inside the home. Asthma status was determined by parental response to the question, “Has a doctor ever diagnosed this child as having asthma?” Buccal cell samples were collected, and the genomic DNA was analyzed for the G-to-A transition polymorphism at position 308 in TNF by polymerase chain reaction and allelic discrimination assays. RESULTS. There was a 51% greater risk of lower respiratory illness–related school absences among children with secondhand-smoke exposure compared with those who were unexposed. Children with the TNF GG genotype exhibited similar absence rates regardless of whether they were exposed or unexposed to secondhand smoke. Unexposed children with at least 1 copy of the TNF G→308A allele had similar absence rates for lower respiratory illnesses compared with children with the TNF G→308GG genotype. However, absence rates in children with the variant A allele and secondhand-smoke exposure were markedly increased. Children with the variant A allele and secondhand-smoke exposure had a 75% increase in risk for illness-related absences compared with unexposed children with the GG genotype. In children with the variant A allele, illness-related absence risk increased as the number of smokers in the home increased. In addition, children with 1 variant A allele who were exposed to ≥30 cigarettes per day had a relative risk of 2.75 for respiratory illness–related school absence compared with unexposed children with the GG genotype. Restricting analysis to children without asthma did not substantially alter the findings. CONCLUSIONS. Secondhand-smoke–exposed children who carried a TNF G→308A variant allele were at highest risk for respiratory illness–related school absences. A strong dose-response relationship in this group of patients was found for respiratory illness–related absence risk in relation to the number of household smokers and number of cigarettes smoked. The genetic susceptibility associated with the TNF G→308A allele is likely mediated by variation in inflammatory responses to secondhand smoke. REVIEWER COMMENTS. Secondhand-smoke exposure is common among children and causes substantial morbidity. However, there is variation in susceptibility to the effects of secondhand smoke. This study demonstrated that differences in genotype of mediators of inflammation may explain variation in susceptibility to secondhand smoke. Additional studies are needed to elucidate differences in genotypes of other inflammatory mediators, which may produce a similar effect. This may provide one more weapon in our arsenal to convince parents to quit smoking or devise protective agents for the exposed.

Perceptions of the Effects of Second-Hand Smoking on the Health of Bar Workers in Ibadan

Perceptions of the Effects of Second-Hand Smoking on the Health of Bar Workers in Ibadan

Out from the haze

Smoking was banned in Californian bars a decade ago, and this week England follows suit. But Kris Novak finds that epidemiologists are still arguing about the effects of second-hand smoke.

Evaluating Community-based Programs for Eliminating Secondhand Smoke Using Evidence-based Research for Best Practices

Extensive research has been conducted on the hazardous effects of tobacco use, and more recently attention has focused on the harmful effects of secondhand smoke (SHS). A growing body of evidence-based research supports best practices for eliminating SHS. This article describes the evaluation and outcomes of a community-based coalition in the midwest that used best practices to educate and change public attitudes on SHS, and thereby promote social policy change for tobacco-free environments. The evaluation model incorporated evidence-based indicators as measures for coalition goal achievement and found the best practices program to be effective for eliminating SHS exposure.

The effects of second-hand smoke on biological processes important in atherogenesis

BackgroundAtherosclerosis is the leading cause of death in western societies and cigarette smoke is among the factors that strongly contribute to the development of this disease. The early events in atherogenesis are stimulated on the one hand by cytokines that chemoattract leukocytes and on the other hand by decrease in circulating molecules that protect endothelial cells (ECs) from injury. Here we focus our studies on the effects of "second-hand" smoke on atherogenesis.MethodsTo perform these studies, a smoking system that closely simulates exposure of humans to second-hand smoke was developed and a mouse model system transgenic for human apoB100 was used. These mice have moderate lipid levels that closely mimic human conditions that lead to atherosclerotic plaque formation.Results"Second-hand" cigarette smoke decreases plasma high density lipoprotein levels in the blood and also decreases the ratios between high density lipoprotein and low density lipoprotein, high density lipoprotein and triglyceride, and high density lipoprotein and total cholesterol. This change in lipid profiles causes not only more lipid accumulation in the aorta but also lipid deposition in many of the smaller vessels of the heart and in hepatocytes. In addition, mice exposed to smoke have increased levels of Monocyte Chemoattractant Protein–1 in circulation and in the heart/aorta tissue, have increased macrophages in the arterial walls, and have decreased levels of adiponectin, an EC-protective protein. Also, cytokine arrays revealed that mice exposed to smoke do not undergo the switch from the pro-inflammatory cytokine profile (that develops when the mice are initially exposed to second-hand smoke) to the adaptive response. Furthermore, triglyceride levels increase significantly in the liver of smoke-exposed mice.ConclusionLong-term exposure to "second-hand" smoke creates a state of permanent inflammation and an imbalance in the lipid profile that leads to lipid accumulation in the liver and in the blood vessels of the heart and aorta. The former potentially can lead to non-alcoholic fatty liver disease and the latter to heart attacks.

SHORT-TERM CIGARETTE SMOKE EXPOSURE POTENTIATES ENDOTOXIN-INDUCED PULMONARY INFLAMMATION

Long-term cigarette smoke exposure is associated with chronic obstructive pulmonary disease. However, the effects of short-term smoke inhalation are less clear, because it may adversely affect the lung only if underlying disease is present. To test this hypothesis, Syrian hamsters were passively exposed to cigarette smoke for 2 hours per day over a period of 3 days either before or after intratracheal instillation of low-dose (20 μg) Escherichia coli endotoxin. The results indicate that short-term smoke exposure can potentiate endotoxin-induced lung inflammation. They also suggest that nonsmokers with underlying lung disease may be particularly vulnerable to the adverse effects of second-hand smoke.

The medical and economic costs of the effects of second-hand smoke on nonsmokers in the US neared $US6 billion in 2004,

The medical and economic costs of the effects of second-hand smoke on nonsmokers in the US neared $US6 billion in 2004,