Circadian rhythm of peak expiratory flow in children passively exposed and not exposed to cigarette smoke.

Casale, R; Natali, G; Colantonio, D; Pasqualetti, P

doi:10.1136/thx.47.10.801

Cited by 24 publications

(16 citation statements)

References 18 publications

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“…The results are summarised in table 3. One small study of 40 children aged 10–11 years in Italy reported lower average levels but greater variability in PEF in the 20 children exposed to environmental tobacco smoke 36. The sample excluded asthmatics and those with acute respiratory problems, but other details are lacking.…”

Section: Resultsmentioning

confidence: 99%

Health effects of passive smoking bullet 7: Parental smoking, bronchial reactivity and peak flow variability in children

Cook¹,

Strachan²

1998

Thorax

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Background-A systematic quantitative review was conducted of the evidence relating environmental tobacco smoke to bronchial hyperresponsiveness (BHR) during childhood. Methods-Twenty nine relevant studies were identified after consideration of 1593 articles selected by electronic search of the Embase and Medline databases using keywords relevant to passive smoking in children. The search was completed in April 1997. Results-Of 19 studies using challenge tests in children of school age, 10 (5759 children) could be summarised as the odds ratio of being bronchial hyperreactive in children exposed to environmental tobacco smoke compared with those not exposed. The pooled odds ratio for maternal smoking was 1.29 (95% confidence limits 1.10 to 1.50) with no evidence of heterogeneity between studies. However, in five further studies of 3531 children providing some evidence, but not odds ratios, none were statistically significant. A further four studies on 5233 children have collected data but are not published. In contrast, all four studies of circadian variation in peak expiratory flow found increased variation in children exposed to environmental tobacco smoke. Conclusions-A clear eVect of exposure to environmental tobacco smoke on BHR in the general population has not been established. While the meta-analysis suggests a small but real increase in BHR in school aged children, it seems likely that this estimate is biased upwards due to publication bias. In contrast, limited evidence suggests greater variation in peak expiratory flow in children of smoking parents. (Thorax 1998;53:295-301)

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Section: Resultsmentioning

confidence: 99%

Health effects of passive smoking bullet 7: Parental smoking, bronchial reactivity and peak flow variability in children

Cook¹,

Strachan²

1998

Thorax

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“…The adult subjects exposed to passive smoking present an increased, but not significant PEF variability with respect to controls, as is also the case in exposed chil dren [17,18], The increased circadian amplitude in exposed subjects could be related to an increase in bron chial reactivity [13]: tobacco smoke increases bronchial Fig. 3.…”

Section: Discussionmentioning

confidence: 99%

Cosinor Analysis of Circadian Peak Expiratory Flow Variability in Normal Subjects, Passive Smokers, Heavy Smokers, Patients with Chronic Obstructive Pulmonary Disease and Patients with Interstitial Lung Disease

Casale

Pasqualetti²

1997

Respiration

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Peak expiratory flow (PEF) presents a circadian rhythm with a maximum in the afternoon, and a significant variability in its diurnal variations has been reported in normal subjects and in chronic obstructive pulmonary disease (COPD). In order to investigate whether passive smoking, active tobacco smoking, COPD and interstitial lung disease (ILD) are associated with changes in the circadian rhythm of PEF, five groups of adult male subjects, comparable for age, weight and height, were studied: group A: 30 clinically healthy subjects who never smoked, group B: 30 subjects passively exposed to tobacco smoking, group C 30 heavy smokers ( > 20 cigarettes daily for at least 5 years), group D: 30 patients with nonasthmatic COPD (emphysema and/or chronic bronchitis), and group E: 15 patients with ILD (pneumoconiosis). Active tobacco smoking and exposure to passive smoking were assessed by the determination of the urinary cotinine concentration. A portable spirometer was used to measure PEF over a whole day, at 0.00, 6.00, 8.00, 10.00, 12.00, 14.00, 16.00, 18.00, 20.00, 22.00, and 24.00 h, all subjects leading a normal life. The ‘mean cosinor’ method was used for statistical analyses; the PEF variability was evaluated by the amplitude percent mesor (daily mean). All groups showed diurnal fluctuations in PEF values with significant (p < 0.05) circadian rhythms. The peaks of PEF rhythms occurred in the early afternoon, without significant (p > 0.05) differences between the groups. The cosinor mean was significantly (p < 0.05) lower in heavy smokers, in passive smokers, and in COPD patients than in controls. Controls, passive smokers, heavy smokers, COPD and ILD patients presented a PEF amplitude percent mesor (95% confidence limits) of 6.26% (range 4.57-7.95), 7.79% (range 5.07-10.51), 12.60% (range 7.61-17.59), 17.19% (range 10.18-23.50), and 3.98% (range 2.09-5.87), respectively, with significant differences (p < 0.05) between all groups, except between controls and passive smokers. These data suggest that tobacco smoke, both passive and active, does not modify the circadian peak of PEF, but modifies significantly its mesor and amplitude. In this respect, heavy smokers have the same pattern of COPD: lower mesor and greater amplitude; passive smokers present an intermediate situation. An increased diurnal variability in PEF could be considered as an early index of tobacco smoke damage and of developing COPD. When studying diurnal PEF variability, active and passive smoking habits should be considered.

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“…Similar protocols focussing at the effects of ozone, nitrogen oxides or isocyanates for example are widely used to identify the individual risk of healthy and possibly susceptible populations. Casale et al (1992) studied the circadian rhythm of peak expiratory flow in two groups of healthy schoolchildren, one group was passively exposed and the other was not exposed to cigarette smoke. They found an increased peak flow amplitude in the exposed group and speculated that subjects exposed to tobacco smoke may chronologically resemble symptomatic asthmatic patients.…”

Section: Discussionmentioning

confidence: 99%

Effect of 3 hours' passive smoke exposure in the evening on airway tone and responsiveness until next morning

Nowak

Jörres

Schmidt

et al. 1996

International Archives of Occupational and Environmental Health

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To study the effect of environmental tobacco smoke (ETS) exposure in the evening on nocturnal changes in airway tone and responsiveness, 17 subjects with mild asthma (mean +/- SD age, 26 +/- 5 years, FEV1% pred., 89 +/- 14%) were exposed to either ambient air (sham) or ETS (20 ppm CO) for 3 h (7:00 to 10:00 p.m.). Seven subjects had a history of ETS-induced respiratory symptoms. Spirometry was performed 2 h before exposure (5:00 p.m.), every 30 min during exposure, and at 11:00 p.m., 3:00 a.m., and 7:00 a.m. The provocative concentrations of methacholine necessary to decrease FEV1 by 20%, PC20FEV1, were assessed at 5:00 p.m., 11:00 p.m., 3:00 a.m., and 7:00 a.m. Compared with pre-exposure measurements, mean FEV1 values during and after ETS exposure were significantly lower than with sham exposure = 0.013 and 0.026). This effect, however, was due to a significant response in single individuals. The higher bronchial responsiveness after ETS than after sham exceeded one doubling concentration in 4, 5, and 4 patients at 11:00 p.m., 3:00 a.m., and 7:00 a.m., respectively. The opposite effect was observed in 2, 2, and 2 patients, respectively. There was no statistically significant mean effect of ETS on airway responsiveness during night; however, there was significant heterogeneity in individual responses (P = 0.0002). Patients with and without a history of ETS-induced symptoms did not show different responses to experimental ETS exposure. In conclusion, our data suggest that in single adult subjects with mild asthma, acute exposure to ETS in the evening can produce a deterioration of airway tone and responsiveness during the night, with wide interindividual variability in the response.

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Circadian rhythm of peak expiratory flow in children passively exposed and not exposed to cigarette smoke.

Cited by 24 publications

References 18 publications

Health effects of passive smoking bullet 7: Parental smoking, bronchial reactivity and peak flow variability in children

Health effects of passive smoking bullet 7: Parental smoking, bronchial reactivity and peak flow variability in children

Cosinor Analysis of Circadian Peak Expiratory Flow Variability in Normal Subjects, Passive Smokers, Heavy Smokers, Patients with Chronic Obstructive Pulmonary Disease and Patients with Interstitial Lung Disease

Effect of 3 hours' passive smoke exposure in the evening on airway tone and responsiveness until next morning

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