Effects of Environmental Tobacco Smoke on Respiratory Symptoms and Pulmonary Function

The aim of this study was to examine the effects of environmental tobacco smoke (ETS) on pulmonary function and respiratory symptoms. During periodic medical examination, 392 French nonsmokers responded to an interviewer-administered questionnaire. Then spirometry was performed to assess pulmonary function. All of the subjects were carefully examined by two occupational physicians. ETS exposure at the workplace was more common than this exposure at home (20% vs. 5%). ETS exposure was significantly associated with forced vital capacity (FVC; ?3.16%; 95% CI: ?5.67 to ?0.64) and forced expiratory volume in 1s (FEV1; ?2.90%; 95% CI: ?5.59 to ?0.23). Abnormal FVC results were significantly increased in exposed subgroup [odds ratio = 2.71 (95% CI: 1.09 to 6.75)]. We did not find any significant dose-response relationship between ETS exposure and lung function results. The effects of ETS exposure on respiratory symptoms and diseases (asthma, wheezing, chronic bronchitis, and dyspnea) were not significant. Thus, this study showed that there was a significant inverse association between exposure to ETS and pulmonary function. Even pulmonary function results inferior to the lower limit of normal may be possible. A stricter legislation against ETS is proposed.     

Tobacco Smoke Upper Respiratory Response Relationships in Healthy Nonsmokers

This study determined exposure-response relationships to sidestreamtobacco smoke (2 hrs; 0, 1, 5, and 15 ppm CO) in 29 healthynonsmoking young adults. Sixteen subjects had no history ofenvironmental tobacco smoke rhinitis (ETS-NS) while 13 subjectshad a history of FTS rhinitis (ETS-S). Eye irritation and odorperception showed a statistically significant exposure responsein both groups headache was significant in ETS-S and nose irritationwas significant in ETS-NS subjects. Significant postexposure(P1) symptoms were first reported at 1 ppm CO among both groups,but in 3/9 symptoms were significantly greater at this exposurelevel in ETS-S subjects. Nasal congestion, rhinorrhea, and coughincreased significantly at 15 ppm CO only. In EFS-S subjects,nasal volume decreased and nasal resistance increased in anexposure-response fashion. ETS-NS subjects had a qualitativelydifferent shape to the exposure-response curve; significantdimensional reductions in mid- and posterior nasal volume occurredwith exposure at 1 ppm CO but not at 5 ppm CO and reductionsin posterior nasal volume occurred at 15 ppm CO exposure. Thesestudies indicate subjective and objective response relationshipswith exposure to sidestream tobacco smoke at concentrationsfrom 1 to 15 ppm CO. Some differences are noted among the twosubject groups in the magnitude of some symptoms at the lowestexposure level and in the qualitative shape of the acousticrhinometry and nasal resistance exposure-response curves.     

Environmental Tobacco Smoke Exposure and Risk of Breast Cancer in Nonsmoking Women: A Review with Meta-Analyses

Recent authoritative reviews consider smoking has no effect on breast cancer risk, but some studies report an increase from environmental tobacco smoke (ETS). We reviewed the overall evidence on ETS and breast cancer in nonsmoking women. We extracted details of available studies, derived relative risk (RR) estimates with confidence intervals (CIs) for various ETS exposure indices and conducted meta-analyses. Using an index for each study most closely equivalent to “spouse ever smoked,” a weak, but significant, association was seen (random-effects RR = 1.12, 95% CI = 1.02–1.24, n = 22). However, the estimates were heterogeneous: close to 1.0 for prospective, North American and larger studies, and those adjusting for many potential confounders, but significantly (p < .05) elevated in case-control, European, and smaller studies, and those accounting for fewer potential confounders. Risk was increased in premenopausal women (RR = 1.54, 95% CI = 1.16–2.05, n = 10), but not postmenopausal women. Dose-response findings were similarly heterogeneous. No significant increase was seen for ETS in childhood or the workplace or from the spouse specifically, but an increase was seen for total exposure (RR = 1.54, 95% CI = 1.17–2.04, n = 6). Increases mainly derive from case-control studies asking detailed ETS histories, where RRs depend heavily on who is classified in the totally unexposed reference group, and may be prone to recall bias. Results from prospective studies using similar histories are needed. Study weaknesses and possible publication bias also limit interpretation. Because of the inherent implausibility that ETS exposure might cause breast cancer, given the similar risks of smokers and nonsmokers, one cannot confidently conclude ETS exposure increases risk in nonsmokers.     

A Critical Examination of OSHA's Assessment of Risk Associated with Workplace Exposure to Environmental Tobacco Smoke

In response to a request for information on indoor air quality problems, the U.S. Occupational Health and Safety Administration (OSHA) has proposed a rule addressing indoor air quality in general, and especially environmental tobacco smoke (ETS), in indoor work environments. As justification for the proposed rule, OSHA relies on a quantitative risk assessment used to provide estimates of lifetime risk of lung cancer and heart disease associated with workplace exposure to ETS. However, there are a number of concerns regarding the OSHA risk assessment. (i) The form of the underlying mathematical model used in the risk assessment is inappropriate. (ii) OSHA was highly selective in choosing what data values to use in their risk assessment. (iii) Many data values required as input to the OSHA risk assessment model are simply not known at this time. When such values are required, known, but possibly inappropriate, values were substituted. The conclusions arrived at by OSHA on the basis of this risk assessment seem unwarranted.     

Environmental Tobacco Smoke: Experimental Facts and Societal Issues

Involuntary exposure to environmental tobacco smoke (ETS) inpublic or in working places is considered to be a serious riskto human health. This symposium addressed several issues oftoxicological interest that are associated with exposure toETS. Epidemiologic evidence obtained in human studies suggeststhat "passive smoking" increases the risk of developing lungcancer in nonsmokers and favors the development of respiratorytract infections in children. Comparatively few data are availablefrom animal studies that provide experimental support of theobservations. Exposure of pregnant or neonate rats to cigarettesidestream smoke (SS) affects developmental patterns of drugmetabolizing enzymes that may persist up to 90 days. In youngroosters, SS accelerates the development of arterioscle-roticplaques. On the other hand, exposure of adult rats for up to90 days induces only transient signs of damage in the nasalpassages, but not in the deep lung, and this only at extremelyhigh concentrations of ETS. So far, experimental toxicologyhas provided comparatively few data on the correlation betweenexposure to ETS and adverse health effects. Yet, such data areneeded, particularly since many conclusions drawn from the epidemiologicalstudies remain open to criticism and questions.     

Exposure of Adult Mice to Environmental Tobacco Smoke Fails to Enhance the Immune Response to Inhaled Antigen

Epidemiologic evidence supports a role for environmental tobacco smoke (ETS) in the occurrence and severity of allergies/asthma. However, neither the precise combination of ETS and allergen exposure nor the mechanism (or mechanisms) by which these factors interact and contribute to asthma induction is known. Animal model studies have failed to establish a convincing relationship between ETS exposure and asthma induction, perhaps because of methodological inadequacies. Here, we tested the hypothesis that ETS inhalation would provoke an asthmatic response by overcoming normal airway tolerance to inhaled antigens. Our protocol combined daily ETS exposure with nose-only sensitization to ovalbumin. Three strains of mice were tested, each with a different level of susceptibility to airway hypersensitivity. Immunological responses were assessed by immunoglobulin production. Airway inflammation was assessed by bronchoalveolar lavage differentials and lung histopathology. Airway hyperresponsiveness was determined by methacholine challenge. The mice produced ovalbumin-specific antibodies following ovalbumin exposure in a strain-dependent manner. Only the A/J mice produced detectable levels of ovalbumin-specific immunoglobulin (Ig) E. Both A/J and BALB/c mice produced ovalbumin-specific IgG1 antibodies. The C57Bl/6 mice did not produce detectable levels of antibodies. The A/J mice also exhibited airway inflammation following ovalbumin exposure. Neither the C57Bl/6 nor the BALB/c mice exhibited signs of airway inflammation. Exposure to ETS failed to enhance ovalbumin-specific antibody production, airway inflammation, or hyperresponsiveness. Together these results indicate that ETS exposure accompanied by nose-only allergen sensitization fails to overcome aerosol tolerance in adult mice.     

The Retention of Tobacco Smoke Constituents in the Human Respiratory Tract

Measurements on the retention of cigarette smoke constituents in the human respiratory tract have been undertake for more than 100 years. The first studies on nicotine retention were begun by Lehmann in Germany in 1903 and published in 1908. The first studies on the retention of smoke particulate matter were published by Baumbereger in the United States in 1923. Since those early publications, many studies have been undertaken, more or less continuously. This article is a review of the work that has been done over the last 100 years, including a large number of unpublished studies undertaken by British American Tobacco in Southampton, UK. The techniques used have evolved over the years and there is a certain amount of variation in the data. However, the general trends in the results are reassuringly consistent. The bulk of the studies indicate that, on average, 60 to 80% of the mainstream smoke particulate matter is retained in the lungs after inhalation. For nicotine, carbon monoxide, nitric oxide, and aldehydes the total retentions are of the order of 90–100, 55–65, 100, and approximately 90%, respectively, during cigarette smoke inhalation. For most smoke constituents the retentions in the mouth only are considerably smaller than in the whole respiratory tract. The lung retention values for smoke particulate matter are dependent on the depth of inhalation, hold time in the lungs, exhalation volume, and other factors. However, the degree of nicotine retention following inhalation is not markedly influenced by changes in respiratory parameters. Furthermore, the percentage retentions for smoke particulate matter and nicotine are smaller for nonsmoking subjects exposed to environmental tobacco smoke than with active smoking. The smoke retentions are related to properties of the smoke aerosol particles and gases and their behavior as they travel through the respiratory tract. This includes particle growth in the respiratory tract and evaporation of gases out of the particles, and relevant aspects of these processes are also reviewed.     

Interindividual Differences in Hair Uptake of Air Nicotine and Significance of Cigarette Counting for Estimation of Environmental Tobacco Smoke Exposure

Abstract: Hair from 80 male subjects, smokers and non-smokers, was exposed continously in a dynamic exposure chamber to constant nicotine vapour concentrations of 20, 200 or 2000 μg/m³ for 72 hr. Subgroups of high and low nicotine adsorbing hair were also exposed intermittantly to environmental tobacco smoke for 8 months. Air and hair concentrations of nicotine were determined by gas chromatography/mass spectrometry. The chamber experiments demonstrated a hair nicotine uptake which followed a second order relation to the applied concentrations of nicotine, y=–0.00018x²+0.715x+1.13, r²=0.99999. The function and the experimental points showed linearity up to an air nicotine vapour concentration of about 200 μg/m³ covering the most relevant range of environmental exposure. An approximately 7- and 2-fold interindividual variation was observed in the hair uptake rate constant of nicotine vapour for the investigated material within the 10 to 90 and 25 to 75% percentiles, respectively. The factors causing this variation were not identified. It was shown that subject age, hair diameter and hair content of eumelanin were without correlation to the rate constants of hair nicotine uptake. The exposure of subgroups of hair to environmental tobacco smoke showed similar uptake profiles of nicotine as that experienced with exposure to pure nicotine vapour, supporting the relevance of controlled chamber nicotine vapour exposures as a relevant tool for the evaluation of hair nicotine uptake from a more complex environmental situation. Standardized measurements of air nicotine vapour and particulate concentrations in a modern office during 8 hr periodical smoking periods, showed that the number of cigarettes smoked was a poor indicator for the estimation of individual exposure to environmental tobacco smoke constituents. Hair nicotine measurements so far seem to be superior to other suggested methodologies for estimation of environmental tobacco smoke exposure, but further studies should be initiated to identify factors determining the rate constant of hair nicotine uptake.     

Health Effects of Subchronic Exposure to Environmental Levels of Hardwood Smoke

Hardwood smoke is a contributor to both ambient and indoor air pollution. As part of a general health assessment of multiple anthropogenic source emissions conducted by the National Environmental Respiratory Center, a series of health assays was conducted on rodents exposed to environmentally relevant levels of hardwood smoke. This article summarizes the study design and exposures, and reports findings on general indicators of toxicity, bacterial clearance, cardiac function, and carcinogenic potential. Hardwood smoke was generated from an uncertified wood stove, burning wood of mixed oak species. Animals were exposed to clean air (control) or dilutions of whole emissions based on particulate (30, 100, 300, and 1000 μm g/m³). F344 rats, SHR rats, strain A/J mice, and C57BL/6 mice were exposed by whole-body inhalation 6 h/day, 7 days/wk, for either 1 wk or 6 mo. Effects of exposure on general indicators of toxicity, bacterial clearance, cardiac function, and carcinogenic potential were mild. Exposure-related effects included increases in platelets and decreases in blood urea nitrogen and serum alanine aminotransferase. Several other responses met screening criteria for significant exposure effects but were not consistent between genders or exposure times and were not corroborated by related parameters. Pulmonary histopathology revealed very little accumulation of hardwood smoke particulate matter. Parallel studies demonstrated mild exposure effects on bronchoalveolar lavage parameters and in a mouse model of asthma. In summary, the results reported here show few and only modest health hazards from short-term to subchronic exposures to realistic concentrations of hardwood smoke.     

Histological Alterations in Male A/J Mice Following Nose-Only Exposure to Tobacco Smoke

The incidence and multiplicity of grossly observed and microscopic lesions of the respiratory tract of A/J mice exposed nose-only to mainstream smoke (50, 200, or 400 mg total particulate matter/m³ from 2R4F cigarettes) was compared to those of filtered air controls. Animals were necropsied at the end of exposure (5 mo) or following 4 or 7 mo of recovery. Lungs were visually inspected for tumors at all necropsies and examined histopathologically at 9 and 12 mo. At 5 mo no tumors were recorded. No significant elevations in tumor incidence or multiplicity were recorded although at 9 mo multiplicity was elevated in the mid-exposure group (0.90 versus 0.55 tumors per animal for controls). At 12 mo, multiplicity was increased over the 9-mo necropsy at all exposures except 200 mg/m³; however, there were no dose-related trends in multiplicity or incidence. Histopathological alterations included hyperplasia, metaplasia, and inflammation of the nose and larynx and proliferative lesions of the lungs. At 9 mo, the multiplicity of focal lung lesions was 1.4 per animal in controls but averaged 1.0 among smoke-exposed groups. There was an inverse relation (p < .059) between smoke concentration and the percentage of hyperplastic lesions at 9 mo. At 12 mo the high-exposure group had slightly increased multiplicity of 2.3 lesions compared with 1.6 among controls, while the percentage of hyperplasic lesions was similar between groups. Nose-only inhalation of mainstream tobacco smoke resulted in chronic inflammatory changes of the respiratory tract yet failed to produce statistically significant changes in tumor incidence or multiplicity.     

Inconsistency between Workplace and Spousal Studies of Environmental Tobacco Smoke and Lung Cancer

In a risk assessment released at the end of 1992, the U.S. Environmental Protection Agency (EPA) concluded that environmental tobacco smoke (ETS) is a known human lung carcinogen. The Agency reached that conclusion primarily on the basis of epidemiologic studies of self-reported never-smoking women, in which the exposure index was marriage to a smoker. However, the use of the spousal smoking exposure surrogate introduces many potential confounding factors. Such confounding and bias due to denial of active smoking are likely explanations for weak and inconsistent reported ETS-lung cancer associations. This contention is supported by the results of 14 worldwide studies of lung cancer and ETS exposure in the workplace, which in combination indicated no risk elevation. Workplace ETS-lung cancer studies are not subject to the bias and confounding introduced by the spousal smoking exposure surrogate. The EPA ignored the workplace studies in its risk assessment and extrapolated the results of spousal smoking studies to workplace and other sources of ETS exposure. In its estimate of ETS-attributable lung cancer deaths in the United States, the EPA ascribed over 70% of the deaths to nonspousal ETS exposure, primarily workplace exposure. Considered in their entirety, the ETS-lung cancer epidemiologic data do not support a causal inference or provide a scientific basis for government regulation of smoking in the workplace.     

Prenatal Tobacco Exposure and Brain Morphology: A Prospective Study in Young Children

It is well known that smoking during pregnancy can affect offspring health. Prenatal tobacco exposure has been associated with negative behavioral and cognitive outcomes in childhood, adolescence, and young adulthood. These associations between prenatal tobacco exposure and psychopathology in offspring could possibly be explained by the influence of prenatal tobacco exposure on brain development. In this prospective study, we investigated the association between prenatal tobacco exposure, behavioral and emotional functioning and brain morphology in young children. On the basis of age and gender, we matched 113 children prenatally exposed to tobacco with 113 unexposed controls. These children were part of a population-based study in the Netherlands, the Generation R Study, and were followed from pregnancy onward. Behavioral and emotional functioning was assessed at age 6 with the Child Behavior Checklist. We assessed brain morphology using magnetic resonance imaging techniques in children aged 6–8 years. Children exposed to tobacco throughout pregnancy have smaller total brain volumes and smaller cortical gray matter volumes. Continued prenatal tobacco exposure was associated with cortical thinning, primarily in the superior frontal, superior parietal, and precentral cortices. These children also demonstrated increased scores of affective problems. In addition, thickness of the precentral and superior frontal cortices was associated with affective problems. Importantly, brain development in offspring of mothers who quit smoking during pregnancy resembled that of nonexposed controls (no smaller brain volumes and no thinning of the cortex). Our findings suggest an association between continued prenatal tobacco exposure and brain structure and function in school-aged children.     

Environmental Tobacco Smoke in the Nonsmoking Section of a Restaurant: A Case Study

This study tested the concentrations of environmental tobacco smoke (ETS) components in a small restaurant/pub with smoking and nonsmoking areas-a facility outfitted with a heat-recovery ventilation system and directional airflow. The ETS levels in the nonsmoking area were compared with those in other similar restaurants/pubs where indoor smoking is altogether prohibited. The results indicate that ETS component concentrations in the nonsmoking section of the facility in question were not statistically different (P < 0.05) from those measured in similar facilities where smoking is prohibited. The regulatory implications of these findings are that ventilation techniques for restaurants/pubs with separate smoking and nonsmoking areas are capable of achieving nonsmoking area ETS concentrations that are comparable to those of similar facilities that prohibit smoking outright.     

Experimental Wood Smoke Exposure in Humans

Experimental studies are used to evaluate effects of human exposure to diesel exhaust and concentrated ambient particles. This article describes a system for studying exposure of humans to wood smoke. Wood smoke was generated using a wood stove placed outside an exposure chamber that can hold at least 10 subjects. A partial flow of the generated wood smoke from the stove was mixed with filtered indoor air. Personal and stationary measurements were performed of PM_2.5 and PM₁ mass concentrations and various volatile organic compounds (VOCs): 1,3-butadiene, benzene, and aldehydes. In addition, particulate matter (PM) mass, number concentrations, and size distributions of particles (0.007–6.7 μm), as well as nitrous oxides, CO₂, and CO, were measured online. Filters were analyzed for trace elements and black smoke. Polycyclic aromatic compounds, toluene, and xylenes were determined in stationary samples. Results of the first experiment showed no differences between personal and stationary measurements for particles or VOCs. Consequently, stationary measurements can be used to predict personal exposure. All PM mass (about 250 μg/m³) was in the PM₁ fraction. Subjective symptoms were generally weak, while clear objective signs were found, for example, in biomarkers of inflammation. With careful control of the combustion process, relatively constant mass and number concentrations were obtained over each exposure session. By varying the combustion and dilution of the wood smoke, different exposure scenarios can be achieved and thus, knowledge about which of the properties of particles and gaseous compounds are crucial for the effects.     

Mechanisms Involved in A/J Mouse Lung Tumorigenesis Induced by Inhalation of an Environmental Tobacco Smoke Surrogate

Abstract

Lung tumors have been reproducibly induced in A/J mice exposed to a surrogate for experimental environmental tobacco smoke (ETSS) in a 5-mo inhalation period followed by 4 mo without further exposure. In order to increase our mechanistic understanding of this model, male mice were whole-body exposed for 6 h/d, 5 d/wk to ETSS with a particulate matter concentration of 100 mg/m³. Food restriction regimens were included to model or exceed the ETSS-related impairment of body weight development. Half of the mice were pretreated with a single ip injection of urethane to study the effect of the above treatments on lung tumor development induced by this substance. At 5 mo, the tumor response was statistically the same for all groups of non-pretreated mice; however, the expected urethane-induced lung tumorigenesis was significantly inhibited by approximately 25% by ETSS and food restriction. This inhibition was accompanied by a threefold increase in blood corticosterone as a common stress marker for both ETSS and food restriction. At 9 mo, in mice not pretreated, the lung tumor incidence and multiplicity were significantly increased by twofold in the ETSS group; in the urethane-treated groups, the same high tumor multiplicity was reached regardless of previous treatment. The predominant tumor type in all groups was bronchiolo-alveolar adenoma. There was no induction of a specific K-ras mutation pattern by ETSS exposure. These data suggest a stress-induced inhibition of lung tumorigenesis in this model, explaining the need for the posttreatment period.     

Accomodation to Restricted Tobacco Smoke Intake in Cigarette Smokers

Smoking behavior was studied for four weeks in 18 volunteers given cigarettes cut to half their normal length for one week, and marked with a red line at the half-way point for another week. Although there was a small tendency (NS) to light up more of the half-cigarettes than normal cigarettes, none of the subjects compensated for decreased nicotine intake by doubling the number of cigarettes they smoked. It was concluded from these short-term findings that the use of half-cigarettes is a simple, low cost method which may induce smokers to decrease their tobacco use.     

Stress and Hypothermia in Mice in A Nose-Only Cigarette Smoke Exposure System

In nose-only exposure systems, animals need to be restrained inside a tube, which leads to stress. Stress is known to cause hyperthermia in rodents. Chronically repeated episodes of hyperthermia could be detrimental to animal health and influence results of nose-only exposure studies. Therefore we investigated whether hyperthermia occurred in male C57BL/6J mice that were restrained for increasing lengths of time, using nosepieces held at room temperature, preheated at 37°C, or thermostat controlled at different temperatures, with and without exposure to different concentrations of cigarette smoke. Body temperature, body weight, plasma corticosterone levels, and adrenal weights were recorded. Restraint using nosepieces at room temperature caused a time-dependent decrease in body temperature, which could be reversed by preheating the nosepieces to 37°C. Cigarette smoke dose-dependently caused an additional decrease, which was counteracted by controlling nosepiece temperature at 38°C. During 3 mo of exposure using heated nosepieces, Δ body temperature remained constant. Body weight gain did not differ between smoke-exposed and room air-breathing animals exposed using either heated or room-temperature nosepieces, but both groups gained significantly less weight, while adrenal weights were significantly and similarly increased, when compared to unrestrained littermates. Plasma corticosterone levels did not differ between the three groups. In conclusion, during restraint in nose-only exposure tubes with room temperature metal nosepieces, mice suffer a pronounced hypothermia. Preventing this by heating the nosepieces does not reduce the stress experienced by the animals.     

Media Exposure and Tobacco,Illicit Drugs,and Alcohol Use Among Children and Adolescents: A Systematic Review

ABSTRACT

The authors systematically reviewed 42 quantitative studies on the relationship between media exposure and tobacco, illicit drug, and alcohol use among children and adolescents. Overall, 83% of studies reported that media was associated with increased risk of smoking initiation, use of illicit drugs, and alcohol consumption. Of 30 studies examining media content, 95% found a statistically significant association between increased media exposure and negative outcomes. Similarly, of the 12 studies evaluating the quantity of media exposure, 67% reported an association with a negative outcome. Overall, all 17 of the identified longitudinal studies supported a causal association between media exposure and negative outcomes over time. The evidence was strongest for links between media exposure and tobacco use; it was moderate for illicit drug use and alcohol use. Substantial variability in methodological rigor across studies and expanding definitions of media exposure contribute to persistent gaps in the knowledge base.