Test type influences the expression of lithium chloride-induced hyperalgesia

Male and female strain A/J mice were exposed to environmental tobacco smoke that was generated by burning Kentucky 1R4F reference cigarettes. Exposures lasted 6 hours per day, 5 days per week for a total of 5 months, followed by a 4-month recovery period in air. Chamber concentrations of total suspended particulate matter (TSP) ranged from 50 to 90 mg/m3. Under these conditions, the average lung tumor multiplicity was 1.2 to 1.4 tumors per lung, significantly higher (p < 0.05) than in concomitant controls. ETS exposure led to a comparatively modest increase in cell proliferation in the alveolar zone during the first 2 weeks and in the terminal airways during the first 6 weeks. In the nasal passages cell proliferation was increased throughout, but reverted down to normal when the animals were placed in air. Smoke exposure increased immunostaining for cytochrome P4501A1 in airways and parenchyma. Exposure to the smoke gas phase only produced a similar increase in lung tumor multiplicity as did exposure to full smoke, but failed to induce P4501A1. This suggested that gas-phase constituents play an important role in tobacco smoke carcinogenesis. The strain A/J lung tumor model is thus suitable to study questions associated with tobacco smoke toxicity and carcinogenicity.     

Quantification of alterations in structure and function of elastin in the arterial media

The effect of environmental tobacco smoke (ETS) exposure on adults with asthma has not been well characterized. In a prospective cohort study of 451 nonsmoking adults with asthma, we evaluated the impact of ETS exposure on asthma severity, health status, and health care utilization over 18 mo. There were 129 subjects (29%; 95% CI, 25-33%) who reported regular ETS exposure, falling into three categories: exposure at baseline but none at follow-up (n = 43, 10%), no baseline exposure and new exposure at follow-up (n = 56, 12%), and exposure at both baseline and follow-up (n = 30, 7%). In cross-sectional analyses, subjects with baseline ETS exposure had greater severity-of-asthma scores (score difference, 1.7; 95% CI, 0. 2-3.1), worse asthma-specific quality of life scores (score difference, 3.5; 95% CI, 0.03-7.0), and worse scores on the Medical Outcomes Study SF-36 physical component summary (score difference, 3. 0; 95% CI, 0-6.0) than unexposed subjects. They also had greater odds of emergency department visits (odds ratio [OR] = 2.1; 95% CI, 1.2-3.5), urgent physician visits (OR = 1.9; 95% CI, 1.1-3.3), and hospitalizations (OR = 1.9; 95% CI, 1.02-3.6). In longitudinal follow-up, subjects reporting ETS cessation showed improvement in severity-of-asthma scores (score reduction, -3.2; 95% CI, -4.4 to -2. 0) and physical component summary scores (score increase, 5.3; 95% CI, 2.6-8.1). Environmental tobacco smoke cessation decreased the odds of emergency department visits (OR = 0.4; 95% CI, 0.2-0.97) and hospitalizations (OR = 0.2; 95% CI, 0.04-0.97) after adjustment for covariates. Environmental tobacco smoke initiation was associated with greater asthma severity only in subjects with high-level (>= 3 h/wk) exposure (score increase, 1.4; 95% CI, 0.03-2.7). In conclusion, self-reported ETS exposure is associated with greater asthma severity, worse health status, and increased health care utilization in adults with asthma.     

Evaluation of acoustic rhinometry and posterior rhinomanometry as tools for inhalation challenge studies

Objective measures of upper respiratory function are needed to understand the effects of inhaled toxicants on the nasal passages. Acoustic rhinometry (AR) is a simple new technique that determines nasal volume by measuring the cross-sectional area of the upper airway as a function of the distance along the nasal passage. This study compares acoustic rhinometry with the more traditional posterior rhinomanometry (NAR) and correlates these objective measures with the symptom of nasal congestion. Healthy young adults (n = 29) were studied on 4 days, each separated by at least 1 wk, in a climate-controlled environmental chamber for 6 h, with exposure to clean air or sidestream tobacco smoke (SS) (2 h, 1, 5, and 15 ppm CO). The coefficient of variation for single measurements was 8-15% (AR) and 4% (NAR); for across-day measurements it was 15-25% (AR) and 13-15% (NAR); and for between days it was 19-27% AR and 17-21% (NAR). These coefficients were similar in subjects with a history of environmental tobacco smoke sensitivity (ETS-S) and those with no history of ETS sensitivity (ETS-NS). At baseline, the perception of unilateral nasal congestion was significantly correlated with unilateral nasal dimensions or nasal resistance; the symptom of baseline bilateral nasal congestion (estimated for both nasal passages simultaneously) correlated less well with objective measures of nasal patency. Under challenge conditions (SS at 1-15 ppm CO), there were typically significant correlations between changes in unilateral congestion and both unilateral rhinomanometry and acoustic rhinometry, but correlations of bilateral congestion and measurable dimensions were much lower. ETS-S and ETS-NS subjects differed in correlations between bilateral subjective and objective measures: ETS-S subjects showed significant correlation between baseline congestion and NAR; in contrast, ETS-NS subjects showed significant correlation between baseline congestion and acoustic rhinometry. These results indicate that NAR and AR are complementary tests for use in inhalation challenge studies and have different correlations with nasal congestion under baseline and challenge conditions.     

Effects of acute passive smoking on exercise-induced bronchoconstriction in asthmatic children

This study was designed to investigate the acute effects of environmental tobacco smoke (ETS) in children with mild asthma during rest and exercise. We studied 13 children [8 males, 5 females; mean age 10 (range 8-13) yr; mean forced expired volume in 1 s (FEV1) 93% (range 82-108%) of predicted] with exercise-induced bronchoconstriction [46 +/- 4% (SE) fall in FEV1 after exercise during cold air breathing]. Children were exposed to ETS (20 ppm carbon monoxide) or ambient air (AA) for 1 h. During the first 54 min of exposure, children were at rest, and during the last 6 min they exercised on a bicycle ergometer (2 W/kg body wt). Spirometry was performed before and during exposure and after exercise. Respiratory symptoms were recorded before and after exposures. In seven children the experiments with AA and ETS were done in duplicate. FEV1 between 5 and 54 min of exposure at rest decreased by 3.2 +/- 0.8% (SE) during AA and by 7.2 +/- 2.3% during ETS exposure compared with preexposure values; the difference between AA and ETS was statistically significant (P = 0.04). The drop in FEV1 was achieved within 5 min and did not change with ongoing exposure. Analysis of individual data revealed that the mean changes during ETS were mainly effected by three children with a significant fall and one child with a significant improvement in FEV1 (P < 0.05). Maximum postexercise fall of FEV1 was 25 +/- 4% after AA and 24 +/- 3% after ETS, which did not differ significantly. Upper and lower respiratory tract symptoms were not significantly different between exposures.(ABSTRACT TRUNCATED AT 250 WORDS)     

Evaluation of the effect of environmental exposure to tobacco smoke on variability of peak expiratory flow rate in children

A panel study was conducted in autumn (116 children) and repeated in spring (66 children) to test the hypothesis that the individual variability of peak expiratory flow rate (PEFR) depends on the environmental exposure to tobacco smoke (ETS). PEFR was measured twice a day (morning: PEFR-M; evening: PEFR-E), using individual meters at homes, in children exposed (ETS+) and not exposed (ETS-) to tobacco smoke at home. In examined groups the individual variability of PEFR-M was--on average--8.0% (ETS+; autumn), 8.1% (ETS+; spring), 10.5% (ETS-; autumn) and 7.7% (ETS-; spring). The individual variability of PEFR-E was 8.0% (ETS+; autumn), 7.9% (ETS+; spring), 9.5% (ETS-; autumn) and 7.4% (ETS-; spring). The results of multivariate analysis of within- and between-subject variability showed the presence of statistically significant within-subject variability only in ETS+ group (PEFR-M in autumn; PEFR-M and PEFR-E in spring). With all the limitations of a panel study design the findings suggest that environmental exposure to tobacco smoke in children affects the degree of within-subject variability of PEFR in children.     

The carcinogenic potential of the gas phase of environmental tobacco smoke

Female strain A/J mice were exposed to unfiltered or HEPA-filtered environmental tobacco smoke (ETS). Total suspended particulates (TSP) in the full smoke exposure chamber was 78.5 mg/m3 and in the filtered smoke chamber 0.1 mg/m3; nicotine concentrations in the full and filtered smoke chamber were 13.4 and 3.1 mg/m3, respectively. Animals exposed to filtered ETS (6 h a day, 5 days a week) and killed after 5 months had a higher lung tumor incidence and multiplicity than controls maintained in filtered air, although the differences were not statistically significant. Animals exposed to filtered and full ETS and allowed to recover in air for 4 months had an average of 1.2 +/- 0.3 tumors per lung and 1.3 +/- 0.3 tumors per lung, respectively. Air exposed control animals had an average tumor multiplicity 0.5 +/- 0.1 tumors per lung. Increased immunostaining for CYP 1A1 was not evident in the lung of animals exposed to filtered smoke. Based on the chamber concentrations of selected nitrosamines and polycyclic aromatic hydrocarbons, the possible maximum uptakes by the mice of NNK, NNN and benzo[a]pyrene during the 5 months exposure period were three to six orders of magnitude below doses reported in the literature to produce 1 lung tumor in strain A/J mice. It was concluded that the gas phase of ETS is as carcinogenic as is full ETS. The carcinogenicity of the gas phase may be due to some as yet unidentified, yet highly potent carcinogens or by placing a substantial, possibly free radical-mediated oxidative stress on the lung.     

Analysis of nicotine and cotinine in the hair of hospitality workers exposed to environmental tobacco smoke

The purpose of this study was to determine if hair nicotine and cotinine levels reflect relative exposure to environmental tobacco smoke (ETS) in subjects who worked in the hospitality industry, where public smoking was permitted. Hair samples from 26 subjects were analyzed by gas chromatograph/mass spectrometry techniques for nicotine and cotinine. An exposure gradient was shown for nicotine but not cotinine. Among nonsmokers, those working in bars where there are no public smoking restrictions had the highest hair nicotine levels, which were close to levels found in smokers. Nicotine measured in hair is useful as a biological marker for exposure to ETS from multiple sources. Bar workers in particular are exposed to high levels of ETS, which may adversely affect the health of nonsmokers.     

Passive smoking and evolution of lung function in young adults. An 8-year longitudinal study

The objective of the study was to examine the relation between exposure to environmental tobacco smoke (ETS) and the rate of change in ventilatory lung function in young adults during a study period of 8 years, with an additional aim to recognize susceptible subgroups. The study population consisted of 117 never smokers, who were 15-40 years of age at the time of an initial examination when they underwent spirometry and a standardized interviewer-administered questionnaire on respiratory health, and were re-examined 8 years later. Lifetime exposure to ETS at home and at work before the start of the study was ascertained at an early stage of the study, and exposure during the study period was recorded at the 8-year examination. The relations between home and work ETS exposure before and during the study period and the rate of change in forced expiratory volume in one second (delta FEV1 in ml/yr) and in mean forced expiratory flow during the middle half of the forced vital capacity (delta FEF25-75 in 1/sec/yr) were studied in linear regression models including potential confounders and other determinants of the outcome. There was no statistically significant relation between ETS exposure during or before the study period and evolution of FEV1 or FEF25-75. The 95% confidence intervals of the estimates indicated that ETS exposure was unlikely to have a physiologically relevant effect. A statistically significant but physiologically unimportant relation was observed between cumulative home ETS exposure before the study and delta FEV1 in the subgroup of subjects 25 years of age or younger. There was no evidence of modification by atopy, wheezing or gender. The results suggest that exposure to environmental tobacco smoke in young adulthood at home and in office work environment does not lead to a clinically important ventilatory impairment in such exposure levels as experienced in Canadian housing conditions. This does not refute the possibility that higher exposure due to more frequent smoking in smaller indoor spaces with lower rates of ventilation may be harmful.     

Smoking at home: The impact of smoking cessation on nonsmokers' exposure to environmental tobacco smoke.

Nonsmokers who live with smokers are at increased risk for chronic disease. This study evaluated the impact of eliminating smoking in the home on nonsmokers' environmental tobacco smoke (ETS) exposure. Nonsmokers participated in measurements of their ETS exposure before and after the smoker in their home quit smoking. A matched comparison group of nonsmokers from nonsmoking homes was also included. ETS exposure was assessed using passive nicotine monitors, an exposure diary, and a questionnaire. Nonsmokers from smoking homes had significantly higher exposure to ETS than those from nonsmoking homes. There was a 60% reduction in nicotine levels following smoking cessation by the household smoker. However, there were still detectable levels of nicotine measured at posttest. These results have important implications for individual risk reduction and public health policy. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

The carcinogenicity of environmental tobacco smoke

Male strain A/J mice were exposed for 6 h a day, 5 days a week to environmental tobacco smoke (ETS) generated from Kentucky 1R4F reference cigarettes. Chamber concentrations were 87 mg/m3 of total suspended particulate matter (TSP), 246 p.p.m. of CO and 16 mg/m3 of nicotine. After 5 months, 33% of the ETS exposed and 11% of the control animals had one or several lung tumors; the difference was statistically not significant. A second group of animals exposed for 5 months to ETS was allowed to recover for another 4 months in filtered air. When they were killed, 85% of the ETS animals had lung tumors (average number per lung: 1.4 +/- 0.2), whereas in the control group 38% had lung tumors (average number of lung tumors in all animals 0.5 +/- 0.2). The differences in tumor incidence and multiplicity were statistically significant. More than 80% of all tumors were adenomas, the rest adenocarcinomas. When animals were pretreated with a carcinogen, lung tumor multiplicity was lower in the ETS exposed animals after 5 months compared with controls injected with a carcinogen and kept in air. However, after an additional 4 month recovery period in air, lung tumor multiplicities were the same in ETS plus carcinogen exposed mice as in carcinogen-treated air-exposed controls. Histopathologic and morphometric analysis of the lung tissue failed to reveal any differences between ETS exposed and control animals. However, immediately after ETS exposure, immunohistochemistry revealed increased staining for CYP1A1 in airway epithelia and lung parenchyma; following recovery in air, the staining disappeared again. Analysis of cell kinetics showed an initial burst of increased DNA synthesis in the epithelial cells of the airways and a smaller early positive response in the parenchyma. Feeding of butylated hydroxytoluene during ETS exposure did not modulate lung tumor development. It was concluded that ETS is a pulmonary carcinogen in strain A/J mice.     

Do the nonsmoking daughters of smokers tend to marry smokers? Implications for epidemiological research on environmental tobacco smoke: the IARC collaborative study

The IARC collaborative study on exposure to environmental tobacco smoke (ETS) involved collecting interview data and biochemical indicators of exposure from 1369 nonsmoking women in 13 centers in 10 countries. Information on childhood and adulthood exposure to other people's smoke and duration of this exposure from both parents and spouse was gathered at the interview. Of the 900 women whose husbands smoked (current or exsmokers), 71.3% had one or both parents who smoked (predominantly the father), whereas among the 277 women married to never-smokers, only 60.3% had at least one parent who smoked. The odds ratio for the daughter of a smoker to marry a smoker was, therefore, 1.64 (95% confidence interval = 1.24-2.17; P > 0.001), and there was an exposure-response relation between the number of years of childhood exposure to ETS from the parents and the likelihood of being married to a smoker. These results show that nonsmoking women married to smokers are more likely to have been exposed to tobacco pollution during their whole life. Because the duration of exposure is known to be important in the genesis of lung cancer, some of the excess risk of lung cancer in nonsmoking women married to smokers may be due exposure to ETS from parents during childhood.     

Effect of environmental tobacco smoke on LDL accumulation in the artery wall

BACKGROUND: Previous research has shown that exposure to environmental tobacco smoke (ETS) increases the risk of atherosclerosis. To test the hypothesis that exposure to ETS increases LDL accumulation in the artery wall, we developed a model to measure the rate of LDL accumulation in individually perfused rat carotid arteries after the artery had been perfused with plasma taken from rats exposed to ETS (ETS-plasma). METHODS AND RESULTS: Rats were exposed to ETS in a chamber in which steady-state sidestream smoke was continuously circulating. After exposure, blood from the animals was collected. Carotid arteries from unexposed rats were perfused first with normal plasma containing fluorescently labeled LDL. Then the same arteries (10 arteries from five rats) were perfused with ETS-plasma plus fluorescently labeled LDL. Photometric measurements were made during perfusion of the arteries with fluorescently labeled LDL, and rate of LDL accumulation (mV/min) and lumen volume (mV) (volume of fluorescently labeled LDL solution) were determined. Perfusion with ETS-plasma increased the rate of LDL accumulation (mean +/- SEM, 6.9 +/- 1.8 mV/min) compared with control (1.6 +/- 0.40 mV/min, P < or = .02). LDL accumulation was primarily dependent on LDL interaction with ETS-plasma rather than the interaction of ETS-plasma with the artery wall. Also, ETS-plasma significantly increased lumen volume (43.3 +/- 5.1 mV) compared with control (35.1 +/- 4.4 mV, P < or = .005). CONCLUSIONS: Exposure to ETS acutely increased LDL accumulation in perfused arteries. Repeated exposure to ETS may represent important early events in atherogenesis.     

The usefulness of three biallelic restriction fragment length polymorphisms versus a polymorphic dinucleotide tandem repeat polymorphism at the low-density-lipoprotein receptor gene locus for diagnosis of familial hypercholesterolemia

The DNA adduct 8-hydroxy-2'-deoxyguanosine (8-OHdG) has been widely used as a biomarker for oxidative stress. Bulky DNA adducts, which are detectable by the 32P-postlabelling method, provide evidence for exposure to and metabolic activation of large, mainly apolar compounds, e.g. polycyclic aromatic hydrocarbons. We determined both types of adducts in placental tissues of 30 term pregnancies and related the adduct levels to the exposure to tobacco smoke and the plasma antioxidant status. Urine and plasma continine concentrations were used to select 10 nonsmokers, 9 nonsmokers exposed to environmental tobacco smoke (ETS) and 11 smoking women. Placental levels of 8-OHdG were 0.84 +/- 0.11, 0.90 +/- 0.21 and 0.83 +/- 0.20/10(5) deoxyguanosine bases (dG) for nonsmokers, nonsmokers exposed to ETS and smokers, respectively. The differences between the groups were not significant. Smoking women had significantly lower plasma vitamin C and beta-carotene concentrations than nonsmoking women or nonsmoking women exposed to environmental tobacco smoke. The 8-OHdG adduct level in placental DNA was inversely correlated with the plasma vitamin E concentration (r = -0.47, P < 0.05). There was no association between placental 8-OHdG adducts and vitamin A, C and beta-carotene in plasma. In total, 15 different adducts could be identified in the 30 placenta samples by the 32P-postlabelling method. There was a strong inter-individual variation in both the number of adducts and adduct intensities. No smoking-related or vitamin-related effects on adduct patterns or intensities were found. Our findings suggests that, within the limits of the methods used, tobacco smoke exposure during pregnancy does not lead to a measurable increase in placental DNA adduct levels and that vitamin E appears to have a protective effect on placental 8-OHdG formation.     

Uptake and metabolism of nicotine by the isolated perfused rabbit lung

In order to investigate the possibility of pulmonary first-pass metabolism of nicotine inhaled in tobacco smoke, the absorption and disposition of 14C-nicotine were studied in an isolated perfused rabbit lung preparation after nicotine administration directly into the perfusing blood and tobacco smoke administration via in the inspired tracheal air. After administration into the perfusing medium, the rate of nicotine metabolism was first-order and dose-independent at the two doses studies (0.1 and 1.0 mg) but lung metabolic clearance was quite low (3 ml/min) relative to whole body clearance (140 ml/min) measured by administering 14C-nicotine to intact rabbits. Accumulation of nicotine by lung was not extensive (13-23% of the dose administered). After administration of tobacco smoke from 14C-nicotine-spiked cigarettes, absorption of nicotine was rapid but the rate of metabolism was markedly reduced compared to the studies in which drug was administered in the perfusing medium. This reduction in the rate of metabolism was apparently caused by some component of tobacco smoke but was shown to be unrelated to the level of carbon monoxide in the perfusate. The slow clearance of nicotine by rabbit lung (which is further reduced after smoke administration) compared to a high pulmonary blood flow rate makes unlikely the possibility of significant first-pass lung metabolism in smokers.     

Respiratory health effects of exposure to environmental tobacco smoke

During the last 25 years, several hundred papers have been published on the respiratory health effects of environmental tobacco smoke (ETS). Various independent assessments have concluded that ETS causes lung cancer in adult nonsmokers and increases the risk of various noncancer effects, principally in children. The effects on children include pneumonia, bronchitis and bronchiolitis in young children; chronic middle ear effusion; increased frequency and severity of attacks among asthmatics; possible induction of asthma in previously asymptomatic individuals; small reductions in lung function; and symptoms of upper respiratory tract irritation. In nonsmoking adults, ETS exposure is associated with irritation of the eyes, nose, and throat, and with wheezing, symptoms of bronchitis, shortness of breath, and decreased lung function. The results of recent studies not only confirm and strengthen the above findings but also provide strong suggestive evidence that ETS causes sinonasal cancer and is a risk factor for sudden infant death syndrome. To mitigate such a preventable environmental health impact, public health measures to reduce involuntary ETS exposure are warranted.     

Differential exposure misclassification in case-control studies of environmental tobacco smoke and lung cancer

We review some of the literature on the effects of exposure misclassification on the statistical analysis of case-control studies. In particular, we focus on evidence for exposure misclassification which may be different for cases and controls in studies of environmental tobacco smoke (ETS). For example, such misclassification could induce relative risk estimates below unity for low exposure which appears to be the case in U.S. lung cancer and ETS studies. We describe procedures for systematically examining the sensitivity of dose-response statistics on exposure misclassification. The procedures demonstrate how p-values for the null hypothesis of no dose-response trend could be adjusted to account for exposure misclassification. The adjustment procedures were applied to an example based on a recently published large study of ETS and lung cancer in which a p-value for trend was reported as 0.03. In this example it is seen that modest differential exposure misclassification can induce substantial increases in the actual p-value, changing what appears to be statistically significant to decidedly nonsignificant.     

Exposure to toxic air contaminants in environmental tobacco smoke: an assessment for California based on personal monitoring data

The contribution of environmental tobacco smoke (ETS) to the exposure of adult nonsmoking Californians was determined for selected toxic air contaminants (TACs). The assessment was based on published measurements of ETS emission factors and personal exposures to volatile organic compounds. The human exposure studies were conducted in three California areas--Los Angeles, Pittsburgh/Antioch, and Woodland--between 1984 and 1990. We derived unexposed and passive population exposure distributions by randomly sampling the monitoring results for individuals classified according to exposure status (active smoker, passively exposed or unexposed to ETS during monitoring). The differences between the unexposed and passive distributions were used to estimate the ETS-only contribution for exposure to benzene, styrene, o-xylene, and m,p-xylene. Emission factors were then employed to infer the ETS-caused exposure to thirteen other compounds. The estimated arithmetic mean increments of 24-hour exposure attributable to ETS for the nonsmoking Californian population (age > or = 7) exposed to ETS are as follows (results in units of microgram m-3 exposure concentration; results using two different emission factors presented as a range): acetaldehyde 11-15; acetonitrile 7.0; acrylonitrile 0.49; benzene 1.02; 1,3-butadiene 0.75-2.3; 2-butanone 1.4; o-cresol 0.17; m,p-cresol 0.41; ethyl acrylate < 0.015; ethylbenzene 0.49-0.64; formaldehyde 6.5-8.2; n-nitrosodimethylamine 0.0028; phenol 1.4; styrene 0.36; toluene 3.1-3.2; o-xylene 0.77; m,p-xylene 0.99. The 90% confidence limits on these estimates due to the limited sample size in the studies are roughly x/ divided by 6. For four widely studied compounds, ETS is estimated to contribute the following percentages to the total inhalation exposure of all nonsmoking Californians: o-xylene 5%; m,p-xylene 3%; benzene 5%; and styrene 8%.     

Personal sampling of particles in adults: relation among personal, indoor, and outdoor air concentrations

To investigate the validity of outdoor particulate matter with a 50% cutoff diameter of 10-microm (PM10) concentrations as a measure of exposure in time series studies, the association between personal and outdoor concentrations, within subjects, over time was investigated. Repeated measurements of personal, indoor, and outdoor PM10 were conducted among 37 nonsmoking, 50- to 70-year-old adults, living in Amsterdam, Netherlands, 1994. Regression analyses were conducted for each subject separately, and the distribution of the individual regression and correlation coefficients was investigated. Furthermore, the extent to which differences among personal, indoor, and outdoor concentrations could be explained was studied. The median Pearson's R between personal and outdoor concentrations was 0.50. Excluding days with exposure to environmental tobacco smoke (ETS) improved the correlation to a median R of 0.71. The estimated cross-sectional correlations were lower, 0.34 and 0.50, respectively. Outdoor concentrations (mean, 42 microg/m3) exceeded indoor concentrations (mean, 35 microg/m3) but underestimated personal exposures (mean, 62 microg/m3). The major part of the difference between personal and outdoor concentrations could be attributed to exposure to ETS, living along a busy road, and time spent in a vehicle. The results show a reasonably high correlation between personal and outdoor PM10 within individuals, providing support for the use of ambient PM10 concentrations as a measure of exposure in epidemiologic studies linking the day-to-day variation in particulate matter air pollution to the day-to-day variation in health endpoints such as mortality, hospital admissions, respiratory symptoms, and lung function.     

Intervention within days for some orbital floor fractures: the white-eyed blowout

OBJECTIVE: Exposures to respirable suspended particles (RSP) and environmental tobacco smoke (ETS) were assessed in Prague, Czech Republic, to determine the range and degree of personal exposure by means of personal monitoring over a 24-h period. DESIGN: Self-reported nonsmokers were randomly selected from a representative sample of the population of Prague. Housewives were recruited into one group, primarily for assessment exposures in the home, and office workers were recruited into a second group for assessment of the contribution from the workplace. METHODS: A total of 238 randomly selected nonsmoking subjects collected air samples near their breathing zone by wearing personal monitors for 24 h. Samples collected were analyzed for RSP, nicotine, 3-ethenylpyridine, and ETS particles (using ultraviolet absorbance, fluorescence, and solanesol measurements). Saliva cotinine analyses were also undertaken to confirm the nonsmoking status of the subjects. RESULTS: The most highly exposed subjects in this study were office workers both living and working with smokers. Median time-weighted average exposure concentrations of 60 microg m(-3)RSP, 16 microg m(-3)ETS particles, and 1.6 microg m(-3) nicotine were determined for these subjects, who also had the highest median saliva cotinine level of 2.4 ng ml(-1). Housewives living in nonsmoking households were the least exposed subjects in this study, showing levels of 32 microg m(-3) RSP, 0.17 microg m(-3) ETS particles, and 0.15 microg m(-3) nicotine. As based upon median levels of ETS particles and nicotine, no group would potentially inhale or be exposed to more than 10 cigarette equivalents per year (CE/y) and the least exposed would inhale less than 1 CE/y. The most highly exposed (90th percentile levels) nonsmokers in this study, who both worked and lived with smokers, would potentially inhale up to 29 CE/y. Overall, the workplace was estimated to contribute between 45% and 49% of the annual exposure to nicotine and ETS particles, respectively. On the basis of determined saliva cotinine concentrations, a misclassification rate of between 1.7% and 2.5% was calculated. CONCLUSION: Highest exposures were apparent for office workers both working and living in smoking environments. and our findings suggest a significant contribution to overall ETS particle and nicotine levels from the workplace where smoking takes place. Overall, the rates at which subjects were determined to have misclassified their smoking status in this study were the lowest observed in any of the European cities investigated to date. Clearly, a more sensitive method of analysis for cotinine in body fluids is needed for more accurate determination of the levels expected for nonsmokers.     

Lifetime exposure to environmental tobacco smoke among urban women: differences by socioeconomic class

This study sought to determine cumulative lifetime exposure to environmental tobacco smoke (ETS) among urban women in relation to sociodemographic factors. In a population survey carried out in Geneva, Switzerland, during 1993-1995, a representative sample of 1,883 women aged 35-74 years answered interview questions on lifetime ETS exposure. Exposed women were defined as those who had spent at least 1 hour daily in a smoky environment during 1 or more years. The prevalence of current ETS exposure was 31.0% among 1,458 never or former smokers. Lifetime prevalence was 58.3% among 1,061 never smokers. The home (42.1%) and the workplace (39.6% of employed women) were the most frequent sources of ETS exposure, leisure time activity being a secondary source. Throughout a lifetime, work accounted for the greatest average intensity of exposure (on average, 19 hours of exposure per week), while the longest duration of exposure (on average, 18 years) was in the home. Cumulative lifetime exposure (intensity (in hours/week) x duration) from all sources combined was 308 hours/week-years, which can correspond to 30.8 hours/week over a period of 10 years or 20.5 hours/week over a period of 15 years. Women from low socioeconomic classes had more intense and longer exposures than women from higher socioeconomic classes, mainly because of work exposure. Both the intensity and the duration of lifetime ETS exposure were greater than previously suspected. Reduction of ETS exposure in the workplace should be a public health priority.