The connection between smoking behaviour (number of puffs, puff volume, depth of inhalation, duration of inhalation) and the increase in both nicotine and carboxyhaemoglobin (COHb) in venous blood was investigated with methods developed especially for measurement of the puff volume, the depth of inhalation, and the duration of inhalation in 28 inhaling cigarette smokers. A significant correlation could be demonstrated between the smoking parameters and the nicotine and carboxyhaemoglobin increase. The weighting obtained shows that the number of puffs is the most important parameter affecting the increase in nicotine, whereas the depth of inhalation and the puff volume are of much less relevance. The duration of inhalation does not affect the nicotine level. A significant increase in nicotine cannot be attained in non-inhalative smoking of cigarettes with an acid mainstream smoke (n= 14). The increase in COHb is most affected by the puff volume, and slightly less by the number of puffs and the depth of inhalation. The duration of inhalation does not affect the COHb level.The morbidity and mortality from smoking is dose dependent. There is a correlation with the age of starting smoking and the duration of smoking [10,Abbreviations." C= compliance of the lung; Cst = static compliance of the lung; CO = carbon monoxide; COHb = carboxyhaemoglobin; Dco=diffusion of carbon monoxide in the lung; Hb = haemoglobin; PACO = alveolar partial pressure of carbon monoxide; PcCO = partial pressure of carbon monoxide in the pulmonary capillaries; P(A_olCO = difference in partial pressure between the alveolar cavity and the pulmonary capillaries; VC = vital capacity; lZco = amount of diffusion of carbon monoxide per unit of time 34], the number of cigarettes smoked per day [24,34,59], the tar and nicotine content of the cigarette [35], the number of puffs per cigarette, and the depth of inhalation [10,34,35]. Inhalation and depth of inhalation play a major role in the pathogenesis of most tobacco-related diseases [34,35]. Besides health education, the development of less hazardous cigarettes is called for. Filter-tipped cigarettes have been introduced and the tar/nicotine content of cigarettes has been reduced, but the lowering of nicotine content is of benefit only if the smoker does not satisfy his nicotine requirement by changing his smoking behaviour [8,33]. No precise data are yet available as to how the individual parameters of the smoking technique (number of puffs, puff volume, depth of inhalation, and duration of inhalation) affect the nicotine and COHb level [56].

The effect of the first cigarette in the morning on the airway resistance (R,w) which can be measured by body-plethysmography was investigated in 70 inhaling cigarette smokers. The test population showed a significant (P<0.0005) fall in R,w 8 rain after smoking. A further study (n = 16) showed that the fall in R~w was most likely to be attributable to a decrease in the trapped air. The effect of the first cigarette in the morning on the arterial blood gases and on the alveolar-arterial oxygen difference P(A-a)O2 and carbon dioxide difference P(A-a)CO2 was investigated in 12 inhaling cigarette smokers. Smoking gave rise to a significant (P < 0.0005) fall in the partial pressure of oxygen (PaO2) with compensatory overventilation. At the same time, the P(A-a)O2 and the P(A-a)CO2 increased significantly (P<0.01 and P<0.05, respectively). This effect could be observed for up to 24 min after smoking. In addition, the flow of blood in the pulmonary capillaries was measured in 28 test subjects with the nitrous oxide method ((~N2o) before, and 18-22 min after, smoking the first cigarette in the morning. After smoking, there was a significant (P < 0.0005) fall in the 0N2o by an average of 11.3%. The decrease in the Raw, the fall in the PaO2 with compensatory overventilation, the increase in P(A-a)O2 and P(A-a)CO2 and the decrease in the 0N2o are interpreted as manifestations of pronounced acute ventilation-perfusion mismatching induced by smoking.Abbreviations: Cdyn = dynamic compliance; Cdyn 40 = dynamic compliance at 40 breaths/min; QN~o =pulmonary capillary blood flow measured by the N/O method; P(A-a)= alveolararterial pressure difference; Pa=arterial partial pressure; APAo=alveolar pressure difference measured in the pressureflow curve at zero flow; Raw = airway resistance; sGaw = specific airway conductance; SVI=stroke volume index; TGV= thoracic gas volume; BSA = body surface area

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