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BRIEF REPORT |
Laboratory of Applied Physiology (G.S.M., A.D.F., A.Z.J., A.E.C., Y.K.), Department of Exercise and Sport Sciences, University of Thessaly, Trikala GR42100, Greece; School of Health Sciences (D.K.), Department of Biochemistry and Biotechnology, University of Thessaly, 41110 Larissa, Greece; Department of Immunology and Histocompatibility (A.E.G.), School of Medicine, University of Thessaly, and Department of Respiratory Medicine (K.G., T.K.), University Hospital of Larissa, 411 10 Larissa, Greece; and Centre of Toxicology Science and Research (M.N.T., A.M.T.), School of Medicine, University of Crete, TK 71003 Crete, Greece
Address all correspondence and requests for reprints to: Giorgos S. Metsios, Department of Sports and Exercise Science, University of Thessaly, Karies, Trikala GR42100, Greece. E-mail: gm{at}wlv.ac.uk.
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Abstract |
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Objective: The objective was to assess experimentally the effects of 1 h of moderate passive smoking in a controlled simulated bar/restaurant environment on the metabolism and thyroid hormone levels in healthy nonsmokers.
Participants: Eighteen (nine females, nine males) healthy individuals (mean ± SD: age, 25.3 ± 3.1 yr; height, 174.0 ± 10.1 cm; weight, 65.2 ± 13.7 kg) participated in the study.
Design: In repeated-measures randomized blocks, participants visited the laboratory on 2 consecutive days. In the experimental condition, they were exposed to 1 h of moderate passive smoking at a carbon monoxide concentration of 23 ± 1 ppm in an environmental chamber, whereas in the control condition participants remained in the same chamber for 1 h breathing normal atmospheric air.
Main Outcome Measures: In both conditions, cotinine serum and urine levels, resting energy expenditure (REE), as well as concentration of T3, free T4, and TSH were assessed before participants entered the chamber and immediately after their exit. Heart rate and blood pressure were tested in 10-min intervals during all REE assessments.
Results: The mean ± SD difference of serum and urine cotinine levels (–0.27 ± 3.94 vs. 14.01 ± 6.54 and 0.05 ± 2.07 vs. 7.23 ± 3.75, respectively), REE (6.73 ± 98.06 vs. 80.58 ± 120.91) as well as T3 and free T4 (0.05 ± 0.11 vs. 0.13 ± 0.12 and 0.02 ± 0.15 vs. 0.22 ± 0.20) were increased in the experimental compared with the control condition at baseline and follow-up (P < 0.05). No statistically significant variation was observed in the mean difference of the remaining parameters (P > 0.05). Serum and urine cotinine values were linearly associated with REE (P < 0.05).
Conclusion: One hour of passive smoking at bar/restaurant levels is accompanied by significant increases in metabolism and thyroid hormone levels.
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Introduction |
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In questioning the effects of passive smoking on metabolism and thyroid function, the existing perplexity is further exacerbated by the scarcity of published data (8, 9). Given the lack of relevant investigations, the objective of the present investigation was to assess experimentally the effects of 1 h of passive smoking in a controlled simulated bar/restaurant environment on the metabolism and thyroid hormone levels of healthy nonsmokers.
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Subjects and Methods |
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The experimental protocol conformed to the standards set by the Declaration of Helsinki and was approved by the University of Thessaly ethical review board. Eighteen (nine females, nine males) healthy adults (mean ± SD: age, 25.3 ± 3.1 yr; height, 174.0 ± 10.1 cm; weight, 65.2 ± 13.7 kg) volunteered and signed informed consents. Exclusion criteria included: smoking, evidence of cardiac or pulmonary disease, previous/current thyroid disorders, pregnancy, current disease/medications known to affect the thyroid, pituitary function, or metabolic status. We ensured that participants were euthyroid by excluding those who revealed concentrations of thyroid hormones above/below normal levels [normal ranges: T3, 0.8–1.8 ng·ml–1; fT4, 0.8–1.9 ng·dl–1; TSH, 0.5–5 µIU·ml–1 (10)] in the baseline measurement (see Experimental design).
Experimental design
Participants visited the laboratory on 2 consecutive days (to minimize day-to-day variation in the examined parameters) after a 12-h overnight fast where they randomly underwent two different conditions. In the experimental condition, participants were exposed to 1 h of passive smoking inside an environmental chamber. In the control condition they remained in the same chamber for 1 h while breathing normal sea-level air. In both conditions, participants were assessed for REE, cotinine levels, and thyroid hormone levels before they entered the chamber (baseline) and immediately after (follow-up). Heart rate [obtained via telemetry (Polar, Kempele, Finland)] and arterial blood pressure [assessed using a sphygmomanometer (Spirit AS007, Medscope, Maidstone, UK)] were also monitored every 10 min during all REE assessments. Both conditions began at 0730 h and were conducted by the same well-trained investigators using identical precalibrated equipment.
Exposure conditions
During both conditions (i.e. experimental and control), participants were seated at rest for 1 h inside a 6 x 5 x 4-m environmental chamber (air temperature, 24 C; air velocity, 0.05 m·sec–1; humidity, 45%). In the experimental condition, participants were exposed to passive smoke adjusted at a CO concentration of 23 ± 1 ppm to meet concentrations previously reported for bar/restaurant environments (11). We checked for gradients of gas concentrations and particle density by continuously measuring different areas inside the chamber using a Horiba (MEXA-311GE; Horiba Instruments, Sunnyvale, CA) CO-CO2 analyzer. The desired CO concentration of the gas mixture was achieved by combustion of cigarettes from various popular brands. In the control condition, the air inside the chamber was identical to normal environmental conditions (O2, 20.93%; CO2, 0.04%; N, 78.1%) for the entire period of the exposure.
Data collection
Serum and urine cotinine.
Serum and urine cotinine, a preferable biomarker to carboxyhemoglobin (12), was used to assess passive smoking exposure at baseline and follow-up in both conditions. Both serum and urine samples were obtained to ensure validity because, although urine is the specimen of choice for passive smoking (cotinine concentration is 
10x higher than in circulation), such samples may be subject to contamination. For serum cotinine analyses, 5 ml of whole blood was used from the total 10 ml collected from an antecubital vein. For urine cotinine analyses, first morning urine void (80 ml) was collected in polyethylene specimen jars (Fisher Scientific, Pittsburgh, PA) at baseline in both conditions. While inside the chamber, participants were advised to hydrate ad libitum with water. Another specimen of equal quantity was collected at follow-up. All samples were immediately frozen at –20 C until analyzed.
The serum sample preparation of cotinine biochemical analysis included mixture of an aliquot (1 ml) of each sample with 1 ml of buffer solution (pH 6.88). The urine sample preparation included mixture of an aliquot (5 ml) of each sample with 2.5 ml of buffer solution (pH 6.88). Analyses were conducted via electron ionization mass spectrometric confirmatory analysis performed using a Finnigan Mat GCQ system equipped with an HP-5MSI (30 m x 0.25 mm internal diameter x 0.25 µm) capillary column (J&W Scientific, Folsam, CA). The mass spectrometer was operated at the selected ion-monitoring mode and was programmed for the detection of m/z = 84 for cotinine. Under the analysis conditions, cotinine eluted at 6.16 min.
REE. In both conditions, participants were tested for REE at baseline and follow-up. Measurements began at 0730 h with participants being awake less than 30 min after a 12-h overnight fast and having refrained from strenuous physical activity for 72 h before testing but also during the 2 assessment days. REE measurements were conducted with participants in a supine position on a comfortable medical bed inside a semidarkened, temperature-controlled room (22 ± 1 C) with external distractions minimized. Participants were asked to refrain from sleeping and hyperventilating during the procedure. Breath-by-breath data were collected and averaged every 20 sec for 40 min via the open-circuit method using a metabolic cart (Vmax29, Sensormedics Corp., Yorba Linda, CA), which was calibrated before each test using standard gases of known concentration. REE was calculated via the Weir equation (13) using values from 30 min (excluding the first and last 5 min) and was expressed per 24 h.
Thyroid hormones. Blood collection and immediate sample processing for the determination of T3, fT4, and TSH levels was identical to that previously described for serum cotinine. In the current analysis, the remaining 5 ml of whole blood was used (from the total of 10 ml collected). Total T3, fT4, and TSH levels were determined using an electrochemiluminescent immunoassay analyzer (Hitachi E170, Roche Diagnostics Gmbh, Mannheim, Germany). Controls from Bio-Rad were used for T3, fT4, and TSH protocols (Bio-Rad Laboratories, Irvine, CA). Intraassay coefficients of variation were 4.8, 4.9, and 3.7% for T3, fT4, and TSH, respectively.
Statistical analyses
To address the decreased variability expected among repeated measurements within a single individual, we compared the mean difference in each measurement (i.e. follow-up and baseline) between the two conditions (i.e. experimental minus control). Pearson’s correlation coefficient or Spearman’s rank correlation coefficient (see Results) was used to detect possible linear relationships between cotinine concentration (serum and/or urine) and REE, T3, fT4, and TSH in the two conditions for the same measurement (i.e. baseline or follow-up). To ensure that the comparatively long half-life of specific indices (e.g. cotinine and fT4) did not influence our results, ANOVA was used to detect differences between the group of participants (n = 9) performing the experimental condition first in sequence (group 1) and those (n = 9) performing the experimental condition second in sequence (group 2). The level of significance was set at P < 0.05.
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Results |
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) were statistically significantly increased in the experimental condition compared with the control (P < 0.05). No statistically significant differences were observed in the mean ± SD difference of the remaining parameters (P > 0.05). The only statistically significant linear relationships detected were between serum (r = 0.74; P < 0.001) and urine (r = 0.68; P < 0.001) cotinine values with REE in the data from the experimental follow-up measurement. ANOVA detected no statistically significant differences (P > 0.05) between the groups of participants performing the experimental condition first or second in sequence in any of the variables (Table 2).
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Discussion |
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We found that the exposure to passive smoke was accompanied by a statistically significant increase in T3 and fT4 levels. TSH showed a nonsignificant decrease in both conditions representing normal diurnal variation (17). These findings are in line with previous results (3, 4) and provide support to the notion that the increases in T3 and fT4 seen in our study were not attributed to an anterior pituitary response (i.e. TSH secretion), but to the probably short-term effects of a different mechanism that cannot be identified with the current data.
Although the increase in T3 and fT4 discussed above would suggest an increase in heart rate and blood pressure through a sympathetic activation, our data showed only a marginal increase in these parameters. Such controversial findings have been reported several times in the literature thus far for both passive and active smoking, suggesting that low or moderate inhalation of tobacco smoke levels is unlikely to cause an increase in heart rate or blood pressure (18).
The observed alterations in metabolism and thyroid hormone levels in response to passive smoking pertain to acute changes and did not arise from an extreme and/or prolonged exposure. The cotinine levels in serum and urine suggest a moderate and brief passive smoking exposure (19), confirming a successful simulation of a bar/restaurant smoking environment. Moreover, the adopted design did not influence our results because no statistically significant differences were detected between the groups of participants performing the experimental condition first or second in sequence. Based on our results and data from chronic active smoking, it could be cautiously suggested that chronic passive smoking (lifestyle incorporating frequent exposures to passive smoke) may have clinical implications such as thyroid (9) and metabolic (20) abnormalities. Limitations of this study include the inherent inability to "blind" the participants and eliminate the psychological effects of passive smoking, the lack of additional biochemical analyses (catecholamines and iodine status), as well as blood testing after the experimental condition to encapsulate peak hormonal changes. It is concluded that a 1-h passive smoking exposure to levels similar to those of bars/restaurants is accompanied by a statistically significant increase in metabolism and thyroid hormone levels of healthy nonsmokers.
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Footnotes |
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First Published Online October 31, 2006
Abbreviations: fT4, Free T4; REE, resting energy expenditure.
Received April 6, 2006.
Accepted October 17, 2006.
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References |
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