A rough estimation of the amounts of tobacco smoke components taken up by active and passive smoking suggests that, in the case of passive smoking, gas phase constituents in ETS are of greater relevance than particle-bound substances. Since this aspect is of importance for the risk evaluation of passive smoking, it was decided that it should be investigated further in a series of exposure studies with human volunteers. The ETS exposure conditions were characterized by measuring tobacco smoke components such as carbon monoxide (CO), nitrogen oxides (NOx), nicotine, formaldehyde, tobacco-specific nitrosamines (N-nitrosonornicotine (NNN), 4-methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), benzo(a)pyrene (BaP) and particulate matter in the air of the exposure room. The biomonitoring covered carboxyhemoglobin (COHb), thioethers and mutagenic activity in urine. These parameters were compared to those observed after controlled active smoking. It was found that urinary thioether excretion increased in non-smokers after extremely high ETS exposure. This effect could be attributed to gas phase ETS components. Urinary mutagenicity was not measurably increased in non-smokers under these conditions. This indicates that in passive smoking, as opposed to smoking, the gas phase might be more important in terms of possible effects than the particulate matter. It would, therefore, be misleading to make extrapolations based on the burden of smoking to establish the burden of passive smoking.
[Show abstract][Hide abstract] ABSTRACT: To determine whether British lung cancer (LC) trends are adequately explained by cigarette smoking trends, and whether modelling using aggregated smoking prevalence estimates can validly replace modelling using individual smoking histories.
Observed LC trends for 1955-1985 for both sexes and three age groups were compared with multistage model predictions using smoking history data from two surveys (HALS, AHIP). The modelling used the individual smoking data directly or aggregated prevalence estimates. It allowed for variation in age of starting and stopping smoking, amount smoked, tar levels, and environmental tobacco smoke (ETS) exposure.
Observed male LC rates fell faster than predicted by a model (with the first and penultimate stages assumed affected by smoking) that allowed for variation in amount smoked and in tar level (with some provision for "compensation"), and was based on aggregated smoking data from HALS. The discrepancy equated to an annual change unexplained by smoking of -2.4%, -2.8%, and -1.9% for ages 35-44, 45-54, and 55-64. The annual unexplained changes were less in women, and reversed at age 55-64; -1.7%, -0.8%, and +0.8% for the three ages. They were similar using individual smoking histories (-2.6%, -1.8%, and -1.6%; women, -0.9%, -0.5%, and +0.2%). The discrepancies were unexplained by plausible alternative multistage parameters, full allowance for tar reduction, alternative estimates of amount smoked, or ETS.
British LC trends cannot be fully explained by cigarette consumption trends, implying factors other than cigarette smoking contribute importantly to overall risk. Predictions using aggregated prevalence estimates provide useful information.
Journal of Epidemiology & Community Health 03/1998; 52(2):82-92. DOI:10.1136/jech.52.2.82 · 3.50 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Passive smoking impairs the elasticity of the aorta in patients with coronary heart disease. We therefore studied the effect of passive smoking on wave reflection in the aorta, a marker of arterial stiffness, in healthy subjects.
We examined the effects of acute exposure to passive smoking on blood pressure and the aortic pressure waveform in healthy young men (n = 10) and women (n = 11), aged 26 +/- 5 years (mean +/- SEM) compared with 12 healthy controls, aged 24 +/- 2 years (six female) who were exposed to room air. The aortic pressure waveform was derived with radial applanation tonometry (SphygmoCor, AtCor Medical, version 6.2) and the augmentation index, a measure of arterial wave reflection in the aorta, calculated. Blood pressure (Omron Model HEM-705 CP, Omron Corporation, Tokyo, Japan) and augmentation index were measured at baseline, 15, 30 and 60 min after exposure to environmental tobacco smoke (carbon monoxide 25-30 p.p.m. for 60 min) or room air.
Passive smoking was associated with an increase in brachial (124 +/- 4-137 +/- 3 mmHg, P < 0.01) and aortic systolic blood pressure (110 +/- 3-123 +/- 4 mmHg, P < 0.01) at 60 min in the male subjects only. The augmentation index increased from -1.7 +/- 5 to 14 +/- 5 at 60 min (P < 0.001) only in the male subjects. The transit time of the pulse did not change significantly. The change in augmentation index was independent of the increase in blood pressure. Brachial and aortic diastolic blood pressure and heart rate did not change significantly in either male or female subjects. No haemodynamic changes were observed in the control group.
Acute exposure to passive smoking has a deleterious effect on the arterial pressure waveform in healthy young males but not in females, suggesting a possible protection of female gender from functional changes in arteries.
British Journal of Clinical Pharmacology 01/2004; 57(1):37-43. DOI:10.1046/j.1365-2125.2003.01958.x · 3.88 Impact Factor
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