Smoking foes try to stop parents from lighting up

Anti-smoking activists who are driving cigarettes from public places across the country are now targeting private homes -- especially those with children.

Their efforts so far have contributed to regulations in three states -- Maine, Oklahoma and Vermont -- forbidding foster parents from smoking around children. Parental smoking also has become a critical point in some child-custody cases, including ones in Virginia and Maryland.

In a highly publicized Virginia case, a judge barred Caroline County resident Tamara Silvius from smoking around her children as a condition for child visitation. Mrs. Silvius, a waitress at a truck stop in Doswell, Va., calls herself "highly disappointed" with the court's ruling.

"I'm an adult. Who is anybody to tell me I can't smoke or drink?" she said in an interview yesterday.

An appeals court upheld the ruling, but not before one judge raised questions about the extent to which a court should become involved in parental rights and whether certain behavior is harmful or simply not in a child's best interest. Mrs. Silvius says she complied with the decision by altering her smoking habits.

"My children know not to come around when I'm on the front porch with my morning coffee, tending to my cows or out in my garden, because I'm having a cigarette," she said. Still, she thinks this was not a matter for the courts because it was not proven that she posed a risk to her children's health.

Well, then, since we actually have an open mind, most of us, please do tell us what "scientific" study supports your opinions. Be creative. No one has yet been able to find a non-discredited study that links second hand smoke to anything. Linking SHS to mental disease in opponents doesn't count!

First of all, you either missed or ignored my point. Anecdote is not science. Do you agree?

You want studies? Feel free to critique any of the following studies, which are just a sampling of the many that are freely available in peer reviewed scientific publications.

Environ Health Perspect. 2005 Oct;113(10):1349-53. Related Articles, Links Second-hand smoke-induced cardiac fibrosis is related to the Fas death receptor apoptotic pathway without mitochondria-dependent pathway involvement in rats. Kuo WW, Wu CH, Lee SD, Lin JA, Chu CY, Hwang JM, Ueng KC, Chang MH, Yeh YL, Wang CJ, Liu JY, Huang CY. Department of Biological Science and Technology, China Medical University, Taichung, Taiwan. Exposure to environmental tobacco smoke has been epidemiologically linked to heart disease among nonsmokers. However, the molecular mechanism behind the pathogenesis of cardiac disease is unknown. In this study, we found that Wistar rats, exposed to tobacco cigarette smoke at doses of 5, 10, or 15 cigarettes for 30 min twice a day for 1 month, had a dose-dependently reduced heart weight to body weight ratio and enhanced interstitial fibrosis as identified by histopathologic analysis. The mRNA and activity of matrix metalloprotease-2 (MMP-2), representing the progress of cardiac remodeling, were also elevated in the heart. In addition, we used reverse-transcriptase polymerase chain reaction and Western blotting to demonstrate significantly increased levels of the apoptotic effecter caspase-3 in treated animal hearts. Dose-dependently elevated mRNA and protein levels of Fas, and promoted apoptotic initiator caspase-8 (active form), a molecule of a death-receptor-dependent pathway, coupled with unaltered or decreased levels of cytosolic cytochrome c and the apoptotic initiator caspase-9 (active form), molecules of mitochondria-dependent pathways, may be indicative of cardiac apoptosis, which is Fas death-receptor apoptotic-signaling dependent, but not mitochondria pathway dependent in rats exposed to second-hand smoke (SHS). With regard to the regulation of survival pathway, using dot blotting, we found cardiac insulin-like growth factor-1 (IGF-1) and IGF-1 receptor mRNA levels to be significantly increased, indicating that compensative effects of IGF-1 survival signaling could occur. In conclusion, we found that the effects of SHS on cardiomyocyte are mediated by the Fas death-receptor-dependent apoptotic pathway and might be related to the epidemiologic incidence of cardiac disease of SHS-exposed nonsmokers. PMID: 16203245 [PubMed - in process]

Thorax. 2005 Oct;60(10):794-5. Directly measured second hand smoke exposure and asthma health outcomes. Eisner MD, Klein J, Hammond SK, Koren G, Lactao G, Iribarren C. Division of Occupational and Environmental Medicine, Department of Medicine, University of California, San Francisco, San Francisco, CA 94117, USA. eisner@itsa.ucsf.edu BACKGROUND: Because they have chronic airway inflammation, adults with asthma could have symptomatic exacerbation after exposure to second hand smoke (SHS). Surprisingly, data on the effects of SHS exposure in adults with asthma are quite limited. Most previous epidemiological studies used self-reported SHS exposure which could be biased by inaccurate reporting. In a prospective cohort study of adult non-smokers recently admitted to hospital for asthma, the impact of SHS exposure on asthma health outcomes was examined. METHODS: Recent SHS exposure during the previous 7 days was directly measured using a personal nicotine badge (n = 189) and exposure during the previous 3 months was estimated using hair nicotine and cotinine levels (n = 138). Asthma severity and health status were ascertained during telephone interviews, and subsequent admission to hospital for asthma was determined from computerised utilisation databases. RESULTS: Most of the adults with asthma were exposed to SHS, with estimates ranging from 60% to 83% depending on the time frame and methodology. The highest level of recent SHS exposure, as measured by the personal nicotine badge, was related to greater asthma severity (mean score increment for highest tertile of nicotine level 1.56 points; 95% CI 0.18 to 2.95), controlling for sociodemographic covariates and previous smoking history. Moreover, the second and third tertiles of hair nicotine exposure during the previous month were associated with a greater baseline prospective risk of hospital admission for asthma (HR 3.73; 95% CI 1.04 to 13.30 and HR 3.61; 95% CI 1.0 to 12.9, respectively). CONCLUSIONS: Directly measured SHS exposure appears to be associated with poorer asthma outcomes. In public health terms, these results support efforts to prohibit smoking in public places.

Mutat Res. 2004 Nov;567(2-3):427-45. Related Articles, Links Genotoxicity of environmental tobacco smoke: a review. Husgafvel-Pursiainen K. Department of Industrial Hygiene and Toxicology, Finnish Institute of Occupational Health, Helsinki, Finland. kirsti.husgafvel-pursiainen@ttl.fi Environmental tobacco smoke (ETS), or second-hand smoke, is a widespread contaminant of indoor air in environments where smoking is not prohibited. It is a significant source of exposure to a large number of substances known to be hazardous to human health. Numerous expert panels have concluded that there is sufficient evidence to classify involuntary smoking (or passive smoking) as carcinogenic to humans. According to the recent evaluation by the International Agency for Research on Cancer, involuntary smoking causes lung cancer in never-smokers with an excess risk in the order of 20% for women and 30% for men. The present paper reviews studies on genotoxicity and related endpoints carried out on ETS since the mid-1980s. The evidence from in vitro studies demonstrates induction of DNA strand breaks, formation of DNA adducts, mutagenicity in bacterial assays and cytogenetic effects. In vivo experiments in rodents have shown that exposure to tobacco smoke, whole-body exposure to mainstream smoke (MS), sidestream smoke (SS), or their mixture, causes DNA single strand breaks, aromatic adducts and oxidative damage to DNA, chromosome aberrations and micronuclei. Genotoxicity of transplacental exposure to ETS has also been reported. Review of human biomarker studies conducted among non-smokers with involuntary exposure to tobacco smoke indicates presence of DNA adducts, urinary metabolites of carcinogens, urinary mutagenicity, SCEs and hypoxanthine-guanine phosphoribosyltransferase (HPRT) gene mutations (in newborns exposed through involuntary smoking of the mother). Studies on human lung cancer from smokers and never-smokers involuntarily exposed to tobacco smoke suggest occurrence of similar kinds of genetic alterations in both groups. In conclusion, these overwhelming data are compatible with the current knowledge on the mechanisms of carcinogenesis of tobacco-related cancers, occurring not only in smokers but with a high biological plausibility also in involuntary smokers.

BMC Cell Biol. 2004 Apr 5;5:13. Related Articles, Links Effects of "second-hand" smoke on structure and function of fibroblasts, cells that are critical for tissue repair and remodeling. Wong LS, Green HM, Feugate JE, Yadav M, Nothnagel EA, Martins-Green M. Department of Cell Biology and Neuroscience, University of California, Riverside, California, USA. lwong@citrus.ucr.edu BACKGROUND: It is known that "second-hand" cigarette smoke leads to abnormal tissue repair and remodelling but the cellular mechanisms involved in these adverse effects are not well understood. Fibroblasts play a major role in repair and remodelling. They orchestrate these processes by proliferating, migrating, and secreting proteins such as, cytokines, growth factors and extracellular matrix molecules. Therefore, we focus our studies on the effects of "second-hand" cigarette smoke on the structure and function of these cells. RESULTS: We used sidestream whole (SSW) smoke, a major component of "second-hand" smoke, primary embryonic fibroblasts, cells that behave very much like wound fibroblasts, and a variety of cellular and molecular approaches. We show that doses of smoke similar to those found in tissues cause cytoskeletal changes in the fibroblasts that may lead to a decrease in cell migration. In addition, we also show that these levels of cigarette smoke stimulate an increase in cell survival that is reflected in an increase and/or activation of stress/survival proteins such as cIL-8, grp78, PKB/Akt, p53, and p21. We further show that SSW affects the endomembrane system and that this effect is also accomplished by nicotine alone. CONCLUSIONS: Taken together, our results suggest that: (i) SSW may delay wound repair because of the inability of the fibroblasts to migrate into the wounded area, leading to an accumulation of these cells at the edge of the wound, thus preventing the formation of the healing tissue; (ii) the increase in cell survival coupled to the decrease in cell migration can lead to a build-up of connective tissue, thereby causing fibrosis and excess scarring.

Cancer Epidemiol Biomarkers Prev. 2004 Feb;13(2):320-3. Related Articles, Links Exon 5 polymorphisms in the O6-alkylguanine DNA alkyltransferase gene and lung cancer risk in non-smokers exposed to second-hand smoke. Cohet C, Borel S, Nyberg F, Mukeria A, Bruske-Hohlfeld I, Constantinescu V, Benhamou S, Brennan P, Hall J, Boffetta P. International Agency of Research on Cancer, Lyon, France. PURPOSE: The objective of the study was to examine the association of three exon 5 variants in the O(6)-alkylguanine DNA alkyltransferase (AGT) gene involved in the repair of the mutagenic DNA lesion O(6)-alkylguanine formed by nitrosamines, with lung cancer risk in never-smokers. EXPERIMENTAL DESIGN: Exon 5 of the AGT gene was sequenced in genomic DNA from 136 cases and 133 hospital- or population-based controls for whom questionnaire information on second-hand smoke and diet was available to determine the frequencies of the Gly(160)Arg, Ile(143)Val, and Lys(178)Arg variant alleles. RESULTS: No codon (160)Arg variant alleles were found in the study population. The codon (143)Val and (178)Arg variant alleles, present at allele frequencies of 0.07, showed 100% linkage. The odds ratio (OR) of lung cancer for these variant carriers was 2.05 [95% confidence interval (CI) 1.03-4.07]. The risk varied between the different lung cancer pathologies with an increased risk for adenocarcinoma (OR 2.67, 95% CI 1.21-5.87) or small cell carcinoma (OR 4.83, 95% CI 0.91-25.7) but not for squamous cell carcinoma (OR 1.07, 95% CI 0.27-4.18). Compared with individuals carrying the mutant alleles unexposed to second-hand smoke, the OR for exposed variant carriers was 1.95 (95% CI 0.53-1.15); a similar interaction, although not significative, was observed for low consumption of cruciferous vegetables and for green vegetables and tomatoes. CONCLUSIONS: These results point toward a role of AGT polymorphisms in lung cancer susceptibility among never-smokers, in particular among subjects exposed to environmental carcinogens.

Nicotine Tob Res. 2003 Dec;5(6):943-6. Related Articles, Links Secondhand smoke and earaches in adolescents: the Florida Youth Cohort Study. Lee DJ, Gaynor JJ, Trapido E. University of Miami, Tobacco Research and Evaluation Coordinating Center, Sylvester Comprehensive Cancer Center, Miami, FL 33101, USA. dlee@med.miami.edu The association between second-hand smoke exposure and adolescent middle ear problems has not been examined. A random sample stratified by region was drawn from a list that included approximately 40% of all Florida households with children in grades 4-7. A total of 785 Florida adolescents initially enrolled in the 4th-7th grade participated in three telephone interviews conducted over a 24-month period. At the round 3 interview, 10.3% of participants reported one or more earaches within the previous 30 days. Several second-hand smoke exposure questions asked at each of the three interviews were associated with the number of reported earaches. Stepwise polytomous logistic regression indicated that parental smoking inside the home reported at the round 3 interview was associated with the number of reported earaches (OR=3.11, 95% CI=1.70-5.66). Once this variable was selected, none of the other second-hand smoke exposure variables offered additional predictive value (p>.1). None of the non-second-hand smoke exposure variables, including the participant's own history of tobacco use, had any association with the reporting of earaches (p>.05). Second-hand smoke exposure is associated with self-reported earaches in adolescents. These findings should be replicated in a study in which clinical measures of middle ear function are performed.

Cancer Cell. 2003 Sep;4(3):191-6. Related Articles, Links Comment in: Cancer Cell. 2003 Sep;4(3):159-60. Second hand smoke stimulates tumor angiogenesis and growth. Zhu BQ, Heeschen C, Sievers RE, Karliner JS, Parmley WW, Glantz SA, Cooke JP. Cardiology Research, VA Medical Center, University of California, San Francisco, CA 94143, USA. Exposure to second hand smoke (SHS) is believed to cause lung cancer. Pathological angiogenesis is a requisite for tumor growth. Lewis lung cancer cells were injected subcutaneously into mice, which were then exposed to sidestream smoke (SHS) or clean room air and administered vehicle, cerivastatin, or mecamylamine. SHS significantly increased tumor size, weight, capillary density, VEGF and MCP-1 levels, and circulating endothelial progenitor cells (EPC). Cerivastatin (an inhibitor of HMG-coA reductase) or mecamylamine (an inhibitor of nicotinic acetylcholine receptors) suppressed the effect of SHS to increase tumor size and capillary density. Cerivastatin reduced MCP-1 levels, whereas mecamylamine reduced VEGF levels and EPC. These studies reveal that SHS promotes tumor angiogenesis and growth. These effects of SHS are associated with increases in plasma VEGF and MCP-1 levels, and EPC, mediated in part by isoprenylation and nicotinic acetylcholine receptors.

Tob Control. 2001 Dec;10(4):383-8. Related Articles, Links Comment in: Tob Control. 2004 Sep;13(3):319-20. How many deaths are caused by second hand cigarette smoke? Woodward A, Laugesen M. Department of Public Health, Wellington School of Medicine, PO Box 7343, Wellington South, New Zealand. woodward@wnmeds.ac.nz OBJECTIVES: To estimate the number of deaths attributable to second hand smoke (SHS), to distinguish attributable and potentially avoidable burdens of mortality, and to identify the most important sources of uncertainty in these estimates. METHOD: A case study approach, using exposure and mortality data for New Zealand. RESULTS: In New Zealand, deaths caused by past exposures to second hand smoke currently number about 347 per year. On the basis of present exposures, we estimate there will be about 325 potentially avoidable deaths caused by SHS in New Zealand each year in the future. We have explored the effect of varying certain assumptions on which the calculations are based, and suggest a plausible range (174-490 avoidable deaths per year). CONCLUSION: Attributable risk estimates provide an indication for policy makers and health educators of the magnitude of a health problem; they are not precise predictions. As a cause of death in New Zealand, we estimate that second hand smoke lies between melanoma of the skin (200 deaths per year) and road crashes (about 500 deaths per year).

Rev Saude Publica. 2000 Feb;34(1):39-43. Related Articles, Links [Effects of environmental tobacco smoke on lower respiratory system of children under 5 years of age] [Article in Portuguese] Pereira ED, Torres L, Macedo J, Medeiros MM. Departamento de Medicina Clinica, Faculdade de Medicina da Universidade Federal do Ceara, Fortaleza, CE, Brasil. eanes@portalnet.com.br OBJECTIVE: To determine the effects of second-hand smoke in the respiratory system of children under 5 years old. METHODS: A cross sectional study of a total of 1,104 children under 5 years old. Information about respiratory symptoms and illness, family history of respiratory diseases, smoking habits of household members and housing conditions were assessed by home interviews with the children's parents. RESULTS: We studied 546 boys and 558 girls. Among 611 children exposed to second-hand smoke, 82% had respiratory problems (odds ratio = 1.64; 95% confidence interval: 1.21-2.20). Children whose parents were smokers at the time of the survey were more likely to experience wheezing than children of nonsmoking parents (odds ratio = 1.66; 95% confidence interval: 1.21-2.27), shortness of breath (odds ratio = 1.91; 95% confidence interval: 1. 36-2.67), morning and day time or night coughs (odds ratio = 1.58; 95% confidence interval: 1.09-2.28). The odds ratio for asthma, bronchitis and pneumonia was greater for children exposed to second-hand smoke (odds ratio = 1.60; 95% confidence interval: 1. 11-2.31). CONCLUSIONS: Maternal smoking, paternal smoking, family history of respiratory diseases, and housing conditions are considered risk factors for respiratory diseases in children.

J Am Coll Cardiol. 1997 Dec;30(7):1878-85. Related Articles, Links Effects of second-hand smoke and gender on infarct size of young rats exposed in utero and in the neonatal to adolescent period. Zhu BQ, Sun YP, Sudhir K, Sievers RE, Browne AE, Gao L, Hutchison SJ, Chou TM, Deedwania PC, Chatterjee K, Glantz SA, Parmley WW. Department of Medicine and Cardiovascular Research Institute, University of California San Francisco, 94143-0124, USA. OBJECTIVES: We sought to assess the effects of second-hand smoke (SHS) and gender on infarct size in young rats exposed in utero or in the neonatal to adolescent period, or both. BACKGROUND: We previously demonstrated that exposure to SHS increases infarct size in a rat model of ischemia and reperfusion, with a dose-response relation. These results are consistent with epidemiologic studies demonstrating that SHS increases risk of death from heart disease. METHODS: Thirty-one pregnant female rats were randomly divided into two groups: those exposed to SHS and a control group (non-SHS). After 3 weeks, each rat had given birth to 10 to 12 rats. One hundred one neonatal rats were divided into four groups according to exposure to SHS in utero (SHSu) and randomized to SHS exposure in the neonatal to adolescent period (SHSna). After 12 weeks, all rats were subjected to 17 min of left coronary artery occlusion and 2 h of reperfusion. RESULTS: Birth mortality was higher in the SHSu group than in the non-SHSu group (11.9% vs. 2.8%, p < 0.001). Body weight of neonatal rats at 3 and 4 weeks in the two SHSu groups was lower than that of rats in the two non-SHSu groups (p < 0.001). Exposure to SHSna increased endothelin-1 levels in plasma (p = 0.001). In all 70 young rats who survived the neonatal period, infarct size (Infarct mass/Risk area x 100%) was greater in the SHSna groups than in the non-SHSna groups (p = 0.005) and in the male groups than in the female groups (p < 0.001). CONCLUSIONS: Exposure to SHS in the neonatal to adolescent period and male gender increased myocardial infarct size in a young rat model of ischemia and reperfusion. These results are consistent with epidemiologic studies demonstrating that SHS increases the health risk to neonates and adolescents.

Circulation. 1994 Sep;90(3):1363-7. Related Articles, Links Inhalation of steady-state sidestream smoke from one cigarette promotes arteriosclerotic plaque development. Penn A, Chen LC, Snyder CA. Nelson Institute of Environmental Medicine, New York University Medical Center, Tuxedo 10987. BACKGROUND: A number of epidemiologic studies have suggested that every year environmental tobacco smoke (second-hand smoke) is responsible for tens of thousands of deaths, mostly from heart disease, in the United States. Environmental tobacco smoke is composed mainly (80% to 85%) of aged and diluted sidestream smoke. The remainder is exhaled mainstream smoke. Among the thousands of compounds that have been identified in environmental tobacco smoke are a number of carcinogens, including polynuclear aromatic hydrocarbon carcinogens, such as benzo(a)pyrene. We have demonstrated previously that a number of carcinogens, including benzo(a)pyrene, promote plaque development after injection into cockerels. There have been almost no studies showing a direct stimulatory effect of environmental tobacco smoke on plaque development. Recently we demonstrated that cockerels exposed to sidestream smoke for approximately 0.4% of their projected lifespan exhibited accelerated development of arteriosclerotic plaques. In that study, cockerels in specially designed inhalation chambers were exposed to the steady-state sidestream smoke from 5 cigarettes for 6 h/d for 16 weeks. This level of exposure is high but environmentally plausible. Statistically significant increases in plaque size were demonstrated in the smoke-exposed cockerels. METHODS AND RESULTS: In the present study, exposure levels were decreased by a factor of 5. Thirty cockerels were exposed to the steady-state sidestream smoke from 1 cigarette for 6 hours per day for 16 weeks. The smoke was mixed with filtered air. Ten control cockerels were exposed to filtered air only. Levels of smoke surrogates, including carbon monoxide and total suspended particulates, were measured three times a day. Again, there was a statistically significant increase in plaque size in the smoke-exposed cockerels. To place these studies within a context of environmental relevance, levels of carbon monoxide were measured independently over 1 to 3 hours in four bars where there was heavy smoking. Measured carbon monoxide levels were as high or higher in the bars than they were in the exposure chambers during the 1-cigarette sidestream-smoke study. CONCLUSIONS: Experimental exposure to secondhand smoke at levels equal to or even below those routinely encountered by people in smoke-filled environments is sufficient to promote arteriosclerotic plaque development.

Environ Res. 1994 May;65(2):161-71. Related Articles, Links Passive smoking in obstructive respiratory disease in an industrialized urban population. Dayal HH, Khuder S, Sharrar R, Trieff N. Department of Preventive Medicine and Community Health, University of Texas Medical Branch at Galveston 77555-1009. We examined the risk of obstructive respiratory disease associated with tobacco smoke in indoor air, independent of active smoking, ambient air pollution, and some of the other sources of residential indoor air pollution. Data came from a probability sample survey of nine neighborhoods in Philadelphia conducted in 1985-1986, leading to information on approximately 4200 individuals. While for never-smokers the prevalence of obstructive respiratory conditions was proportional to the level of environmental tobacco smoke, this second-hand smoke was not a factor in the frequency of such problems among current smokers. In a series of analyses restricted to never-smokers, each of the 219 index cases of obstructive respiratory disease was matched by age, gender, and neighborhood to three randomly selected controls where matching by neighborhood effectively controlled for ambient air pollution. Both matched and unmatched two-sample analyses showed a statistically significant difference (P = 0.019 and 0.016, respectively) between cases and controls with respect to the level of tobacco smoke in the indoor environment. A conditional logistic regression-matched analysis revealed that heating and cooking as sources of indoor air pollution were not associated with the case/control status. However, the odds ratio for passive smoking at a level of more than one pack per day in the house environment was 1.86 (95% CI, 1.21-2.86). The results show that passive smoking is a significant risk factor for obstructive respiratory disease for never-smokers in an industrialized urban population.

Chest. 1991 Jul;100(1):39-43. Related Articles, Links Respiratory illness in nonsmokers chronically exposed to tobacco smoke in the work place. White JR, Froeb HF, Kulik JA. Physical Education Department, University of California San Diego, La Jolla 92093-0117. We evaluated CO levels as an index of cigarette smoke in the work place and analyzed diary entries on respiratory symptoms, eye irritation, chest colds and lost days from work due to respiratory illness in 40 passive smokers (nonsmokers chronically exposed to tobacco smoke in the work place) and 40 control subjects (nonsmokers not exposed to tobacco smoke in the work place) matched for age and gender. Passive smokers experienced greater CO levels during the workday. Also they reported significantly more cough, greater phlegm production, more shortness of breath, greater eye irritation, more chest colds and more days lost from work due to chest colds than control subjects. Nonsmoking workers and their employers are likely to incur significant financial loss because of missed workdays due to illnesses resulting from exposure to second-hand tobacco smoke.

Am Rev Respir Dis. 1988 Aug;138(2):296-9. Related Articles, Links Environmental exposure to tobacco smoke and lung function in young adults. Masi MA, Hanley JA, Ernst P, Becklake MR. Department of Epidemiology and Biostatistics, McGill University, Montreal, Quebec, Canada. The relationship between lung function and environmental exposure to tobacco smoke (passive smoking) was studied in 293 nonsmoking young men and women, 15 to 35 yr of age. A self-administered mailed questionnaire was used to assess the lifetime environmental exposure to cigarette smoke at home and at work for each subject. Lung function information used here had been gathered in the course of a previous study of the determinants of lung function in early adulthood. In men, maximal midexpiratory flow rate (FEF25-75) decreased in relation to an index of cumulative lifetime environmental exposure to tobacco smoke at home, after taking into account the effects of cumulative exposure at work as well as age, height, body size, respiratory pressures, and cooking fuels used at home. The components of this exposure index most closely related to the reduction in FEF25-75 were maternal smoking habits and exposure to second-hand smoke during childhood. In women, the diffusing capacity of the lung (DLCO) decreased in relation to cumulative exposure to tobacco smoke at work, after accounting for the effects of cumulative lifetime exposure at home and the other factors mentioned above. These findings contribute to the gathering evidence that environmental exposure to tobacco smoke is harmful to respiratory health, and suggest that the effects are not insignificant. For instance, the FEF25-75 of a young man 20 yr of age who had never smoked and always lived at home would be 800 ml less if both his parents smoked than if they did not.(ABSTRACT TRUNCATED AT 250 WORDS)

J Laryngol Otol. 2005 Dec;119(12):955-7. Related Articles, Links Passive smoking, allergic rhinitis and nasal obstruction in children. De S, Fenton JE, Jones AS, Clarke RW. ENT Department, Alder Hey Children's Hospital, Liverpool, UK. Allergic rhinitis is a common cause of nasal obstruction in childhood. This prospective study looked at the effect of passive smoking on nasal obstruction in children with and without allergic rhinitis. Eighty-one children took part. Each child was asked to score his or her degree of nasal obstruction on a visual analogue scale. Exposure to passive smoking was determined subjectively using a parental questionnaire, and objectively by measuring the urinary cotinine/creatinine ratio. Results were tabulated using Microsoft Excel and analysed with SPSS statistical software. Nasal obstruction was significantly worse in children with a positive history of allergic rhinitis (p < 0.05). There was also a trend towards a higher nasal obstruction score in children without allergic rhinitis exposed to passive smoking compared to those who were not so exposed. As would be expected, nasal obstruction is worse in children with allergic rhinitis than in those without. Passive smoking tends to increase the symptom of nasal obstruction in children without allergic rhinitis.

Pediatr Int. 2005 Dec;47(6):635-9. Related Articles, Links Decreased total antioxidant capacity and increased oxidative stress in passive smoker infants and their mothers. Aycicek A, Erel O, Kocyigit A. Department of Pediatrics, Children's Hospital at Sanliurfa, Sanliurfa, Turkey. Abstract Background: Smoking has many adverse health effects in infants and adults. The purpose of the study was to study the effect of passive cigarette smoking on oxidative and antioxidative status of plasma in passive smoker infants and their mothers and to compare with those of non-smokers. Methods: Subjects were randomly chosen from infants aged 8-26 weeks and their mothers aged 20-34 years. Passive smoker infants (n = 29) and their mothers (n = 29) were defined as having other family members who smoked six or more cigarettes per day continually for at least 8 weeks. Non-smokers were defined as infants (n = 30) and their mothers (n = 24) who had never been exposed to passive smoking. The antioxidative status of plasma were perused by measuring the total antioxidant capacity. Oxidative status was evaluated by predicating total peroxide level, oxidative stress index, protein oxidation and lipid peroxidation. Results: Plasma concentrations of total antioxidant capacity were significantly lower in passive smoker infants and their mothers than non-passive smoker infants and their mothers. However, lipid peroxidation and oxidative stress index were remarkably higher in passive smoker infants and their mothers than those of non-passive smoker infants and their mothers. There were significant correlations between the oxidative and antioxidative parameters of the passive smoker infants and their mothers. Conclusions: Oxidants are increased and antioxidants are decreased in passive smoker infants and their mothers than those of non-smokers. Passive smoker infants and their mothers are exposed to potent oxidative stress.

J Asthma. 2005 Jul-Aug;42(6):463-7. Related Articles, Links Asthma attack associated with oxidative stress by exposure to ETS and PAH. Leem JH, Kim JH, Lee KH, Hong Y, Lee KH, Kang D, Kwon HJ. Department of Occupational and Environmental Medicine, Inha University Hospital, Incheon, Korea. ekeeper@inha.ac.kr Asthma is primarily an airways inflammatory disease, and the bronchial airways have been shown to be particularly susceptible to oxidant-induced tissue damage. OBJECTIVE: The purpose of this study was to investigate whether pulmonary inflammation in asthma is associated with exposure to environmental oxidants such as polycyclic aromatic hydrocarbon (PAH) and environmental tobacco smoke (ETS). METHOD: We assessed the exposure level of PAH and ETS by using urinary 1-hydroxypyrene glucuronide (1-OHPG) and cotinine. We estimated oxidative damage and inflammatory cytokine levels from 16 asthma patients and 16 patients in stable conditions 1 to 2 months later. RESULTS: Our study showed that the levels of oxidative damage, as measured by malondialdehyde (MDA), were significantly increased (p = 0.006) during the asthma attacks. Proinflammatory and anti-inflammatory cytokines were both increased during the asthma attacks compared to the stable conditions at follow-up. Interleukin (IL-6) and IL-10 were especially increased significantly (p = 0.015 and p < 0.001, respectively). Correlations were observed between inflammatory cytokines such as IL-6 and IL-1beta (p = 0.034). CONCLUSION: This study supports the results of in vitro studies that oxidative stress, specifically lipid peroxidation, contributes to the pathophysiology of asthma. Therefore, environmental interventions based on this better understanding are needed to significantly reduce oxidant stress and prevent or minimize the development of asthmatic symptoms.

Life Sci. 2005 Sep 12; [Epub ahead of print] Related Articles, Links Passive cigarette smoking increases isoprostane formation. Ahmadzadehfar H, Oguogho A, Efthimiou Y, Kritz H, Sinzinger H. Wilhelm Auerswald Atherosclerosis Research Group (ASF) Vienna, Austria. Passive smoking has been demonstrated to exert a variety of deleterious effects eventually resulting in vascular damage. Isoprostanes, a reliable marker of in vivo oxidation injury, have been shown to increase in active cigarette smoking. Data for passive smoking are lacking. We were examining the isoprostane 8-epi-PGF(2alpha) in 12 smokers and non-smokers exposed daily to passive cigarette smoke for 12 days. Plasma samples stored at liquid nitrogen from people having been examined earlier were used. Prevalues of 8-epi-PGF(2alpha) are higher in cigarette smokers. Exposure to passive smoking causes a significant increase in 8-epi-PGF(2alpha) in non-smokers, while in smokers there is only a trendwise increase. After repeated passive smoke exposure, 8-epi-PGF(2alpha) in non-smokers approaches the respective values of smokers. There is a significant correlation of 8-epi-PGF(2alpha) to the thromboxane (plasma, serum, conversion from exogenous precursor, 11-dehydro-TXB(2)) parameters (MDA, HHT- conversion) examined in these patients before. The findings document a significant temporary increase in in vivo oxidation injury due to passive smoke favouring development and/or progression of vascular disease.

Epidemiology. 2005 Sep;16(5):672-80. Related Articles, Links Environmental tobacco smoke and risk of adult leukemia. Kasim K, Levallois P, Abdous B, Auger P, Johnson KC; Canadian Cancer Registries Epidemiology Research Group. Departement de medecine sociale et preventive, Faculte de Medecine, Universite Laval, Sainte-Foy, Quebec, Canada. BACKGROUND: The role of environmental tobacco smoke (ETS) in the causation of lung and breast cancer has been repeatedly evaluated over recent years. In contrast, its impact on the risk of adult leukemia has received little attention. METHODS: We used the lifetime residential and occupational ETS exposure histories from a population-based sample of 1068 incident and histologically confirmed adult leukemia cases and 5039 population controls age 20 to 74 years to evaluate the relationship between ETS exposure and adult leukemia risk among nonsmokers in Canada. The duration of exposure and smoker-years index were used as indices of ETS exposure. We restricted our analysis to the 266 case and 1326 control subjects who reported being lifetime nonsmokers and provided residential ETS exposure history for at least 75% of their lifetime. RESULTS: No association was found for most leukemia subtypes, and in particular for acute myeloid leukemia. In contrast, the risk for chronic lymphocytic leukemia was clearly associated with ETS exposure, with an adjusted odds ratio of 2.3 (95% confidence interval = 1.2-4.5) for more than 83 smoker-years of residential exposure and 2.4 (1.3-4.3) for more than 72 smoker-years of occupational exposure. There was a dose-response relationship for chronic lymphocytic leukemia with both indices of exposure. Risk was not higher with recent exposure, using time-window-exposure analyses. CONCLUSIONS: Regular long-term ETS exposure may be a risk factor for chronic lymphocytic leukemia.

Here are the real facts, don't let anyone fool you with the American Lung Cancer info, they are biased.

Fact: In 1993 the EPA issued a report which claimed that Environmental Tobacco Smoke (ETS) caused 3,000 deaths per year.

Fact: ETS is commonly referred to as Second Hand Smoke (SHS). The two terms are interchangeable.

After reading each of the following facts, ask yourself "Does this fact make the study more credible, or less credible?

Fact: The EPA announced the results of the study before it was finished.

Fact: The study was a Meta Analysis, an analysis of existing studies.

Meta Analysis is very difficult to do accurately, and is the easiest kind of study to fake and manipulate. With a disease as rare as lung cancer, leaving out just a few important studies can skew the results considerably.

The term "Meta Study" is often used to describe this type of report, but the word "study" is inaccurate. The EPA has never conducted nor financed a single ETS study. They have only analyzed the studies of others. It is more accurate to refer to it as an analysis, and to its publication as a report.

Fact: The first step in a meta analysis is identifying all of the relevant studies. The EPA located 33 studies that compared ETS exposure to lung cancer rates.

Fact: The EPA selected 31 of the 33 studies. Later they rejected one of their chosen studies, bringing the total to 30.

Fact: On page 3-46 of the report the EPA estimates, based on nicotine measurements in non-smokers blood, "this would translate to the equivalent of about one-fifth of a cigarette per day."

Fact: Studies that measured actual exposure by having non-smokers wear monitors indicate even this low estimate is exaggerated. Actual exposure (for people who live and/or work in smoky environments) is about six cigarettes per year. (See also the study by Oak Ridge National Laboratories.)

Fact: In 1995 The Congressional Research Service (CRS) released a review of the EPA report.

The CRS was highly critical of both the EPA's methods and conclusions.

Fact: According to the CRS "The studies relied primarily on questionnaires to the case and control members, or their surrogates, the determine EST exposure and other information pertinent to the studies.

Questionnaires can be notoriously inaccurate, as discussed in Epidemiology 102, but in this case some of them were not even filled out by the people being studied, but by "surrogates." In other words, some of the information was unverified hearsay.

Fact: The CRS pointed out that "from a group of 30 studies. . six found a statistically significant (but small) effect, 24 found no statistically significant effect and six of the 24 found a passive smoking effect opposite to the expected relationship."

Fact: Three other large US studies were in progress during the EPA's study. The EPA used data from one uncompleted study, the Fontham study, and ignored the other two, Brownson and Kabat.

Fact: The Fontham study showed a small increase in risk. The CRS report referred to it as "a positive risk that was barely statistically significant." (p. 25)

Fact: The CRS report said the Brownson study, which the EPA ignored, showed "no risk at all." (p.25)

Fact: The "scientists" who conducted the Fontham study refused to release their raw data for years. Philip Morris recently won a lawsuit to gain access to it.

Most researchers routinely make their raw data available after studies have been published. Does Fontham's refusal to make the data available make them more credible, or less credible?

Fact: The EPA based their numbers on a meta analysis of just 11 studies. The analysis showed no increase in risk at the 95% confidence level.

Fact: Even after excluding most of the studies, the EPA couldn't come up with 3,000 deaths, but they had already announced the results. So they doubled their margin of error. Let me repeat that, because it may seem hard to believe: After failing to achieve their pre-announced results by ignoring half of the data, they doubled their margin of error!

Would any legitimate epidemiologist keep their job if they were caught doubling their margin of error to support a pre-announced conclusion?

Fact: After juggling the numbers, The EPA came up with an RR (Relative Risk) of ETS causing lung cancer 1.19. In layman's terms that means:

• Exposure to the ETS from a spouse increases the risk of getting lung cancer by 19%. • Where you'd usually see 100 cases of cancer you'd see 119.

Fact: A RR of less than 2.0 is usually written off as and insignificant result, most likely to be due to error or bias. An RR of 3.0 or higher is considered desirable. (See Epidemiology 101 for more details.)

This rule is routinely ignored when the subject is second hand smoke.

Facts: In review: The EPA ignored nearly two-thirds of the data. The EPA then doubled their margin of error to come up with their desired results. Even with all this manipulation, the numbers are still far too low to be considered statistically significant.

Fact: Although the EPA declared ETS was a Class A carcinogen with an RR of 1.19, in analysis of other agents they found relative risks of 2.6 and 3.0 insufficient to justify a Group A classification.

Fact: In 1998 Judge William Osteen vacated the study - declaring it null and void after extensively commentating on the shoddy way it was conducted. His decision was 92 pages long.

Fact: Osteen used the term "cherry-picking" to describe he way the EPA selected their data. "First, there is evidence in the record supporting the accusation that EPA "cherry picked" its data. Without criteria for pooling studies into a meta- analysis, the court cannot determine whether the exclusion of studies likely to disprove EPA's a priori hypothesis was coincidence or intentional. Second, EPA's excluding nearly half of the available studies directly conflicts with EPA's purported purpose for analyzing the epidemiological studies and conflicts with EPA's Risk Assessment Guidelines."

Fact: Osteen found other deep flaws in the the EPA's methodology. In his judgment he stated: "The record and EPA's explanations to the court make it clear that using standard methodology, EPA could not produce statistically significant results with its selected studies. Analysis conducted with a .05 significance level and 95% confidence level included relative risks of 1. Accordingly, these results did not confirm EPA's controversial a priori hypothesis. In order to confirm its hypothesis, EPA maintained its standard significance level but lowered the confidence interval to 90%. This allowed EPA to confirm its hypothesis by finding a relative risk of 1.19, albeit a very weak association. EPA's conduct raises several concerns besides whether a relative risk of 1.19 is credible evidence supporting a Group A classification. First, with such a weak showing, if even a fraction of Plaintiffs' allegations regarding study selection or methodology is true, EPA cannot show a statistically significant association between ETS and lung cancer."

Fact: The following is another direct quote from Judge Osteen's decision: "In this case, EPA publicly committed to a conclusion before research had begun; excluded industry by violating the Act's procedural requirements; adjusted established procedure and scientific norms to validate the Agency's public conclusion, and aggressively utilized the Act's authority to disseminate findings to establish a de facto regulatory scheme intended to restrict Plaintiffs, products and to influence public opinion. In conducting the ETS Risk Assessment, disregarded information and made findings on selective information; did not disseminate significant epidemiologic information; deviated from its Risk Assessment Guidelines; failed to disclose important findings and reasoning; and left significant questions without answers. EPA's conduct left substantial holes in the administrative record. While so doing, produced limited evidence, then claimed the weight of the Agency's research evidence demonstrated ETS causes cancer. Gathering all relevant information, researching, and disseminating findings were subordinate to EPA's demonstrating ETS a Group A carcinogen."

Most of the media ignored the judge's decision.

When confronted with this decision, many anti-tobacco activists and organizations harp on the fact that Judge Osteen lives in South Carolina. The obvious implication is that he's influenced by the tobacco industry in his state. It may also be an appeal to the "stupid southerner" stereotype.

Fact: Judge Osteen has a history of siding with the government on tobacco cases.

Fact: In 1997 Judge Osteen ruled the FDA had the authority to regulate tobacco.

So much for his alleged bias.

Fact: Although this study has been thoroughly debunked by science and legally vacated by a federal judge, it is still regularly quoted by government agencies, charity organizations and the anti-smoking movement as if it were legitimate.

Fact: Anyone referring to EPA classifying ETS as a Class A carcinogen is referring to this study.

Opinion: You should seriously question the credibility of anyone who refers to this study, or any of the conclusions that it reached, as if they were facts. That includes everyone who refers to the EPA's ruling that ETS is a Class A Carcinogen. Once they do, every subsequent statement they make should be considered highly suspicious until it is thoroughly verified.

Fact: Most of the information on this page was gleaned from Judge Osteen's 92 page decision, the CRS report, and the EPAs study.

You are strongly encouraged to read these documents yourself. You can find the judge's entire decision here. The CRS report is available here. The EPA report over six hundred pages long, and we recommend you order a hard copy. It is available to US citizens at no charge. Call (800) 438-4318 and ask for document EPA/600/6-90/006F. The title of the report is "Respiratory Health Effects of Passive Smoking: Lung Cancer and Other Disorders." It is also available as on line as a pdf file. It is nearly four megabytes, so it may take a while to download.

Fact: Carol Browner, the former head of the EPA, still insists that this study is valid!

The Facts About Secondhand Smoke

The WHO Study

Smoking Out Bad Science

Disclaimer: Opinions posted on Free Republic are those of the individual posters and do not necessarily represent the opinion of Free Republic or its management. All materials posted herein are protected by copyright law and the exemption for fair use of copyrighted works.