Environmental tobacco smoke and the risk of cardiovascular disease

Disease risk due to smoking is not limited to smokers only. Passive smoking, exposure to environmental tobacco smoke, is associated with adverse health effects, and it increases the risk of several diseases. This paper summarizes the cardiovascular effects of tobacco smoke and the current data on the effects of environmental tobacco smoke on the development of cardiovascular disease. According to the results of epidemiologic and experimental studies, environmental tobacco smoke has marked harmful effects on the cardiovascular system. It is estimated that it increases the risk of an acute event of coronary heart disease by 25-35%. Even though the number of studies conducted in the work environment is small, there is no reason to assume that the cardiovascular effects of environmental tobacco smoke differ markedly between the home and the workplace. Firm and timely actions are needed to protect people from exposure to environmental tobacco smoke, both in occupational and other environments.     

Environmental tobacco smoke and pregnancy outcome

BACKGROUND: Recent reviews conclude that environmental tobacco smoke (ETS) leads to diminished birth weight. However, the threshold and magnitude of that effect is uncertain. We aimed to determine the magnitude and shape of the relations between ETS and various adverse pregnancy outcomes using a highly sensitive biochemical assay. METHODS: Maternal serum specimens were collected from more than 3000 women enrolled in California's prenatal screening program in 1992 and analyzed for cotinine. Information on pregnancy outcomes was obtained from live birth/fetal death records and hospital questionnaires. We conducted analyses on 2777 woman-live birth pairs and 19 woman-fetal death pairs in which the mother was presumed to be a nonsmoker (midtrimester cotinine levels < or =10 ng/mL). RESULTS: In multiple logistic regression analyses, the odds ratios of fetal death, preterm delivery, and term-low birth weight were 3.4, 1.8, and 1.8, respectively, in the highest cotinine quintile (0.236-10 ng/mL), compared with the lowest quintile (<0.026 ng/mL). In adjusted linear models, there was a linear dose-dependent effect of log cotinine on mean birth weight (-109 g) and mean infant length (-0.84 cm) over the range of cotinine values. Linear relations were not found with respect to infant head circumference or the ratio of brain weight to body weight. Infant's body mass index declined with exposures above approximately 0.5 ng/mL cotinine. We estimated that ETS levels at or above 0.05 ng/mL (experienced by 62% of the study population) accounted for 12% of all adverse outcomes. CONCLUSIONS: ETS exposure in pregnant women adversely affects pregnancy by increasing fetal mortality and preterm delivery at higher exposure levels and slowing fetal growth across all levels of ETS exposure.     

Risk factors for exposure to environmental tobacco smoke among ethnically diverse women in the United States

The likelihood of exposure to environmental tobacco smoke (ETS) has been shown to vary across sociodemographic characteristics, health behaviors, and the type of smoking restrictions at work. Women may be particularly at risk. The purpose of our study was to assess differences in the likelihood of exposure to ETS at home and at work among an ethnically diverse sample of women age 40 and older in the United States. We used data from the U.S. Women's Determinants Study and restricted the sample to include only nonsmoking women (n = 2326). Unadjusted and adjusted odds ratios (aOR) for exposure to ETS by sociodemographic characteristics, health risk behaviors, and the type of workplace smoking policy were calculated using logistic regression. Exposure to ETS at home was associated with being American Indian/Alaska Native (aOR 1.5, 95% CI 1.0, 2.6), age 40-44 (aOR 1.6, 95% CI 1.0, 2.6) and 45-54 (aOR 1.8, 95% CI 1.2, 2.6), having eighth grade (aOR 2.1, 95% CI 1.3, 3.6) or high school education (aOR 2.2, 95% CI 1.4, 3.3), inadequate fruit and vegetable consumption (aOR 1.5, 95% CI 1.0, 2.1), and not getting screened for breast cancer (aOR 1.5, 95% CI 1.1, 2.0). Women who did not have regular breast (aOR 1.3, 95% CI 1.9, 1.9) and cervical (aOR 2.0, 95% CI 1.5, 5.3) cancer screening were more likely to be exposed to ETS at work. Exposure to ETS at work was higher among women with some high school education (aOR 2.8, 95% CI 1.5, 5.3) and high school graduates (aOR 3.1, 95% CI 1.9, 5.1) and substantially higher for women who worked where smoking was allowed in some (aOR 15.1, 95% CI 10.2, 22.4) or all (aOR 44.8, 95% CI 19.6, 102.4) work areas. Larger effect sizes were observed for the relationship between selected risk factors and ETS exposure at work than for ETS exposure at home. Among individual risk factors, lower education level was most strongly related to ETS exposure at work. The likelihood of being exposed to ETS at work was highest for women whose workplace smoking policies allowed smoking in some or all work areas.     

Environmental tobacco smoke and carotid arterial stiffness

BACKGROUND: Although active smoking acutely increases arterial stiffness, the association between arterial stiffness and chronic exposure to environmental tobacco smoke (ETS) has not been evaluated. We used baseline data from the Vitamin E Atherosclerosis Prevention Study to evaluate the association between ETS exposure and arterial stiffness among 227 healthy adult nonsmokers. METHODS: B-mode ultrasonograms of the common carotid artery were used to compute the carotid arterial wall stiffness index beta. Beta was compared by the number of sources and daily hours of ETS exposure. RESULTS: The carotid stiffness index beta was positively associated with age, body mass index (BMI), fasting glucose, and common carotid artery intima-media thickness (IMT). In the total sample, beta was not related to the number of ETS exposure sources. The carotid stiffness index beta increased with number of sources and daily hours of ETS in subjects with BMI > or =27.1 kg/m2 and IMT > or =0.707 mm. The association was not apparent in subjects with lower BMI or IMT (for number of ETS sources, interaction P values=0.006 and 0.01, respectively). For number of ETS sources, but not hours of exposure, positive associations were apparent among females (but not males) and among subjects > or =55 years old (but not younger subjects). CONCLUSIONS: These data indicate that arterial stiffness is adversely associated with ETS in a dose-dependent manner among individuals with higher BMI and greater carotid artery IMT.     

Environmental tobacco smoke and breast cancer incidence

To evaluate whether environmental tobacco smoke (ETS) influences breast cancer incidence, data from a population-based case-control study were analyzed. Respondents with available ETS information assessed by in-person questionnaires included 1356 newly diagnosed cases and 1383 controls. Relative to nonsmokers who reported no residential ETS exposure throughout the life course, the odds ratios (OR) for breast cancer were not substantially elevated in relation to ETS exposure, active smoking, or a joint measure of active and passive smoking (OR, 1.15, 95% CI, 0.90, 1.48). An increased OR, however, was noted among nonsmokers who lived with a smoking spouse for over 27 years (2.10, 95% CI, 1.47, 3.02), although no dose-response was evident. Also, among women with hormone-receptor-positive tumors only, the OR for both active and passive smoking was increased (1.42 for ER+ PR+, 95% CI, 1.00, 2.00). Our data suggest that if there is an effect for ETS on breast cancer, that effect is restricted to selected subgroups of women, such as those with long-term exposure from a smoking spouse.     

Double exposure. Environmental tobacco smoke

One study after another is finding strong associations between a variety of human illness and exposure to environmental tobacco smoke (ETS). A 1986 report by the U.S. Surgeon General concluded that ETS is a cause of disease, including lung cancer, in healthy nonsmokers. Other reports have documented causal associations between ETS and lower respiratory tract infections, middle ear disease and exacerbation of asthma in children, heart disease, retardation of fetal growth, sudden infant death syndrome, and nasal sinus cancer. However, the findings from many of these studies remain controversial. A number of scientists remain skeptical about the association between ETS and serious illness in nonsmokers, charging that scientific journals either fail to publish pro-tobacco findings and meta-analyses or disregard those that are published. They also claim that many epidemiological studies declare causal associations based on marginal odds ratios.     

Environmental tobacco smoke in hospitality venues in Greece

Background  

Exposure to environmental tobacco smoke is a major threat to public health. Greece, having the highest smoking prevalence in the European Union is seriously affected by passive smoking. The purpose of this study was to measure environmental tobacco smoke (ETS) exposure in the non smoking areas of hospitality venues and offices in Greece and to compare the levels of exposure to levels in the US, UK and Ireland before and after the implementation of a smoking ban.     

Environmental tobacco smoke and canine urinary cotinine level

Epidemiologic studies of companion animals such as dogs have been established as models for the relationship between exposure to environmental tobacco smoke (ETS) and cancer risk in humans. While results from these studies are provocative, pet owner report of a dog's ETS exposure has not yet been validated. We have evaluated the relationship between dog owner's report of household smoking by questionnaire and dog's urinary cotinine level. Between January and October 2005, dog owners presenting their pet for non-emergency veterinary care at the Foster Hospital for Small Animals at Cummings School of Veterinary Medicine, Tufts University, were asked to complete a 10-page questionnaire measuring exposure to household ETS in the previous 24 h and other factors. A free-catch urine sample was also collected from dogs. Urinary cotinine level was assayed for 63 dogs, including 30 whose owners reported household smoking and 33 unexposed dogs matched on age and month of enrollment. Urinary cotinine level was significantly higher in dogs exposed to household smoking in the 24 h before urine collection compared to unexposed dogs (14.6 ng/ml vs. 7.4 ng/ml; P=0.02). After adjustment for other factors, cotinine level increased linearly with number of cigarettes smoked by all household members (P=0.004). Other canine characteristics including age, body composition and nose length were also associated with cotinine level. Findings from our study suggest that household smoking levels as assessed by questionnaire are significantly associated with canine cotinine levels.     

Environmental tobacco smoke exposure and small-for-gestational-age birth.

The aim of this analysis was to examine the effect of environmental tobacco smoke exposure on the risk of small-for-gestational-age (SGA) birth. The study population included 2,283 nonsmokers from a nested cohort study undertaken in southern Connecticut from 1988 to 1992. The duration and intensity of exposures incurred at multiple locations during the third trimester of pregnancy were measured by postpartum interview. The effect of exposure on birth weight and on incidence of SGA birth was assessed by multivariate logistic and linear regression. An estimated 26.5% of the women had been exposed to environmental tobacco smoke for at least 1 hour per week during the third trimester. The median duration of exposure among the exposed over all locations was 5 hours per week. The adjusted odds ratio for SGA birth in exposed mothers compared with unexposed mothers, using a dichotomous exposure variable, was 0.82 (95% confidence interval: 0.51, 1.33). The adjusted birth weight difference associated with exposure was -1.2 g (95% confidence interval: -43.3, 41.0). No effect of environmental tobacco smoke exposure on fetal growth was seen in this relatively homogeneous upper middle class group of women exposed at low levels. This is reassuring for women exposed at low levels, but it does not exclude the possibility of an effect in women exposed to higher levels of environmental tobacco smoke.     

Environmental tobacco smoke and risk of spontaneous abortion

BACKGROUND: Studies of exposure to environmental tobacco smoke (ETS) and risk of spontaneous abortion are limited to a few studies of self-reported exposure, and the results have been inconsistent. The aim of this study was to investigate risk of early spontaneous abortion related to ETS and active smoking as defined by plasma cotinine levels. METHODS: We conducted a population-based case-control study in Uppsala County, Sweden, between January 1996 and December 1998. Cases were 463 women with spontaneous abortion at 6 to 12 completed weeks of gestation, and controls were 864 pregnant women matched to cases according to the week of gestation. Exposure status was defined by plasma cotinine concentrations: nonexposed, <0.1 ng/mL; ETS-exposed, 0.1-15 ng/mL; and exposed to active smoking, >15 ng/mL. Multivariable analysis was used to estimate the relative risk of spontaneous abortion associated with exposure to ETS and active smoking. RESULTS: Nineteen percent of controls and 24% of cases were classified as having been exposed to ETS. Compared with nonexposed women, risk of spontaneous abortion was increased among both ETS-exposed women (adjusted odds ratio = 1.67; 95% confidence interval = 1.17-2.38) and active smokers (2.11; 1.36-3.27). We could not show a differential effect of exposure to ETS or active smoking between normal and abnormal fetal karyotype abortions. CONCLUSIONS: Nonsmoking pregnant women exposed to ETS may be at increased risk of spontaneous abortion. Given the high prevalence of ETS exposure, the public health consequences of passive smoking regarding early fetal loss may be substantial.     

Environmental tobacco smoke and risk of adult leukemia

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.     

The smoke free movies initiative in the United States

Movies influence fashion, lifestyles, and represent smoking as an acceptable behaviour. In fact the greatest tobacco companies built relationships with Hollywood's actors and producers, in order to show smoking and cigarette brands in films. All over the world laws have been developed, in order to restrict smoking and tobacco advertising. Films showing tobacco do not violate these laws, even in those states where tobacco advertising is restricted. Moreover, films are better than any other commercial advertisements because the audience is total unconscious of the sponsor's involvement. Stanton Glantz, Medicine Professor at San Francisco University, is the voice of the movement for smoke-free movies. A lot of studies show that cigarette smoking is more frequently in '90s movies than in 60's and 70's movies. The smoking actors seem to be attractive, strong, healthy and successful. Films showing smoking influence tomorrow's customers: adolescents. Teenagers watching "smoking films" are the most exposed to start smoking. Hence the need to educate Hollywood industry, in order to have smoke-free movies.     

Environmental tobacco smoke exposure during infancy.

We collected information about household smoking habits from 518 mothers when they made their first well child visit with a 6 to 8-week old infant. A urine sample was also collected from the infant, the cotinine concentration measured, and the measurement correlated with data provided by the mother. Eight percent of the infant urine cotinine values fell at or above 10 micrograms/L in the 305 households where no smoking was reported. Corresponding rates were 44 percent in the 96 households where a member other than the mother smoked, 91 percent in the 43 households where only the mother smoked, and 96 percent in the 74 households where both the mother and another household member smoked. In households where the mother smoked, infant urine cotinine levels were lower in the summer, and higher when the infant was breast-fed. A screening question about family smoking habits in conjunction with well child care could effectively define a group of infants exposed to environmental tobacco smoke and thus be at greater risk for respiratory diseases.     

Environmental tobacco smoke leakage from smoking rooms

Twenty-seven laboratory experiments were conducted in a simulated smoking room to quantify rates of environmental tobacco smoke (ETS) leakage to a nonsmoking area as a function of the physical and operational characteristics of the smoking room. Data are presented for the various types of leakage flows, the effect of these leaks on smoking room performance and nonsmoker exposure, and the relative importance of each leakage mechanism. The results indicate that the first priority for an effective smoking room is to maintain it depressurized with respect to adjoining nonsmoking areas. The amount of ETS pumped out by the smoking room door when it is opened and closed can be reduced significantly by substituting a sliding door for the standard swing-type door. An "open doorway" configuration used twice the ventilation flow of those with smoking room doors, but yielded less reduction in nonsmoker exposure. Measured results correlated well with results modeled with mass-balance equations (R(2) = 0.82-0.99). Most of these results are based on sulfur hexafluoride (SF(6)) tracer gas leakage. Because five measured ETS tracers showed good correlation with SF(6), these conclusions should apply to ETS leakage as well. Field tests of a designated smoking room in an office building qualitatively agreed with model predictions.