How does puffing behavior alter during the smoking of a single cigarette?

We examined changes in puffing behavior during the course of a single cigarette in 76 subjects seen on 6 occasions each (456 cigarettes). The puff volume fell on average by 33% during a cigarette and puff duration by 39%, the interpuff interval rose by 75%, but the pressure drop and the maximum flow and pressure achieved during puffing hardly changed. There were highly significant differences between subjects but not between sessions, or when subjects were grouped according to tar yield of the cigarette or by sex. Individual puff volumes with a single cigarette were highly correlated with puff duration (except in a few individuals with irregular puffing patterns), but not generally with maximum flow rate, suggesting that most smokers reduce volume by taking shorter puffs. This is unlikely to reflect mechanical factors or smoke temperature, and may be a response to changing smoke composition. Variation in puffing patterns between individuals may reflect differences in sensitivity to smoke components and individuals who show little fall in puff volume also show small responses on switching to cigarettes with different tar and nicotine yields. The individual response to smoke might be assessed by an analysis of puffing on a single cigarette.

Long-term effects of switching to cigarettes with lower tar and nicotine yields.

On switching to cigarettes with lower tar and nicotine yields, most individuals smoke more intensively, but it is not clear if this effect persists over a long period. Smoking behaviour was monitored in 10 male and 18 female volunteers at five monthly visits, smoking commercially available cigarettes (tar yield greater than 10 mg), then for six more visits at 6-week intervals after switching (mean reduction of 5.9 mg tar and 0.45 mg nicotine). Puffing behaviour was monitored with a flow sensing holder, and measurements were made before and after smoking of plasma cotinine, carboxyhaemglobin and alveolar carbon monoxide. After switching, cotinine levels only fell 40% of that predicted from the fall in nicotine yields, and there were no systematic trends for the rest of the study. Puff volumes rose (reflecting perhaps the reduced draw resistance of the lower yield cigarettes), and remained higher thereafter. The number of puffs per cigarette appeared to rise on switching, but then decreased again. In conclusion, most effects of switching to lower yield cigarettes appeared to persist for at least 36 weeks, suggesting that the strategy of reducing exposure to cigarette smoke by lowering tar and nicotine yields may be of limited value.

Acute effect of smoking on rebreathing carbon monoxide, breath-hold carbon monoxide and alveolar oxygen.

1. The rise ('boost') in carboxyhaemoglobin (HbCO) on smoking has been studied with alveolar carbon monoxide measurements before and after smoking a cigarette. We re-examined this in 28 subjects with HbCO values compared with rebreathing carbon monoxide [FACO(Rb)] and breath-hold alveolar carbon monoxide and oxygen concentrations, obtained after a 20 s breath-hold [FACO(Bh) and FAO2(Bh), respectively]. Tests were done in the order FACO(Bh) and FAO2(Bh), FACO(Rb), FACO(Bh) and FAO2(Bh) before and after smoking a single cigarette, with HbCO being measured 1 min before and after smoking. 2. The changes were expressed as the relative boost: (Post value-pre value)/(Pre value + post value)/2 X 100 For HbCO the average value was 23.7%, but the FACO(Rb) boost was only 9.8%. The first post-smoking FACO(Bh) boost was 3.9% (5.0 min after smoking), rising to 8.5% 9.4 min later. 3. The FAO2(Bh) values fell from a mean of 15.4% before smoking to 14.3% (5.0 min after smoking) then recovered to 15.4% 9.4 min later, suggesting a transient effect on pulmonary gas exchange. Correction of the first post-smoke FACO(Bh) data for this effect increased the relative boost to 11.5%. Routine FAO2(Bh) measurements may be useful in further smoking studies. 4. We conclude that none of the alveolar sampling techniques gives a reliable measurement of the acute HbCO changes associated with smoking.

Respiratory symptoms in West Sussex firemen.

There are few reports of long term follow up of symptoms in firemen. In a four year study of symptoms in a group of 96 firemen (31 non-smokers, 40 smokers, and 25 ex-smokers) of which 89 remained in the study for its full duration a volunteer control group of 69 male non-smokers from a variety of occupations was also followed up. A history of symptoms and of smoking habits was obtained on entry to the study, then every six months for two years, and annually for a further two years. All those remaining in the study after four years were interviewed and a history of their use of breathing apparatus and of being affected by smoke and fumes was obtained. Symptom frequency was least in control subjects, intermediate in non-smokers and ex-smokers, and most in smokers. Before the study period (history obtained at the first session) smoking increased symptoms 3.9 times and being affected by smoke in the past increased symptoms 2.3 times, compared with non-smokers who had not been affected by smoke. In smokers who had also been affected by smoke symptoms increased by 9.1 times, suggesting a multiplicative effect. During the study period symptom frequency was increased about 4.4 times in smokers and 5.7 times in those who had been affected by smoke at work in the past compared with non-smokers who had not been affected by smoke. In smokers who had also been affected by smoke symptom frequency increased by 7.4 times, the combined effects of the two types of smoker being less than additive. These results suggest that being affected by smoke and fumes at work may be a cause of long term symptoms in firemen. In firemen who are non-smokers and who had not been affected by smoke symptom frequency was similar to that observed in the control subjects. Thus the current routine use of breathing apparatus appears to be effective in preventing long term symptoms.

Lung function in West Sussex firemen: a four year study.

Although firefighting is a hazardous occupation, published evidence of long-term lung damage in firemen is inconsistent. A group of 96 men from the West Sussex Fire Brigade, which covers a simi-rural, semi-urban area, were followed up for between one and four years. They included 31 non-smokers, 40 smokers, and 25 ex-smokers. After four years 12 firemen had been lost to the study. A control group of 69 volunteers, consisting of non-smoking men from various other occupations, were followed up in parallel. Lung function tests, covering a wider range than has been previously used in similar studies, were repeated six monthly for two years and annually for a further two years. The results were expressed in terms of the rate of change with time of the lung function variables. Many of the variables deteriorated in both firemen and controls, but the rate of deterioration was greater in the controls than the firemen for vital capacity, ratio of residual volume to total lung capacity, FEV1, FVC, peak expiratory flow (PEF), flow at 50% and 25% remaining vital capacity (V50 and V25 respectively), and airways resistance (Raw). With respect to PEF, V50, V25, and Raw the control subjects deteriorated more rapidly even than the smokers and ex-smokers among the firemen. Alveolar mixing efficiency (AME), a measure of small airways function, did not change significantly over the study period in any group. Non-smoking firemen had the highest mean value of AME, decreasing through ex-smokers, controls, and smokers. We conclude that these results show no evidence of chronic lung damage in West Sussex firemen; indeed, the firemen as a group show a lower rate of deterioration of lung function with age than do the control subjects. This is attributed to the selection of fit men for the service, continued physical training, and the regular use of breathing apparatus.

Alveolar carbon monoxide: a comparison of methods of measurement and a study of the effect of change in body posture.

1. We have compared rebreathing, breath-hold and mean alveolar methods of measuring alveolar carbon monoxide (CO), at levels similar to those found in smokers, as a preliminary to using them as indirect measures of carboxyhaemoglobin levels. In the present study alveolar CO levels were raised by rebreathing a 2% CO mixture. 2. Breath-hold CO was measured after breath-hold times of 0-35 s in 5 s increments. Using generalized linear models, the maximum value for breath-hold CO was estimated to occur at 23 s. Breath-hold CO after a 20 and 25 s breath-hold were similar to and significantly greater than those of less than 20 s or greater than 25 s. 3. As expired CO increased, the difference between breath-hold and mean alveolar CO became proportionally larger. On average, breath-hold CO was 24% larger than mean alveolar CO. 4. Rebreathing, breath-hold and mean alveolar CO were compared at four different inspired oxygen concentrations. Expired CO increased significantly with increasing oxygen for all three methods. At end-tidal oxygen levels of less than 25%, breath-hold and rebreathing CO were similar, however, the overall mean difference between the three methods was significant. 5. While rebreathing CO was unaffected by changes in ventilation/perfusion of the lung, induced by change in body posture, both breath-hold and mean alveolar CO showed a significant fall with change from the supine to erect posture.(ABSTRACT TRUNCATED AT 250 WORDS)

Is alveolar carbon monoxide an unreliable index of carboxyhaemoglobin changes during smoking in man?

1. We measured alveolar carbon monoxide (CO) after a 20 s breath-holding period and carboxyhaemoglobin both before and after smoking a cigarette on 500 occasions (101 individuals). The two measurements were closely correlated but there was a marked difference in the change or 'boost' after smoking one cigarette. The mean relative boosts ([post value--pre value]/[pre+post]/2) for alveolar CO and carboxyhaemoglobin were 7.7% and 20.3%, while negative boosts (fall rather than the expected rise) were seen in 103 of 500 and three of 500 occasions respectively. In 140 studies a third alveolar CO reading taken 5 min later was slightly larger, but the difference was insignificant. 2. In seven subjects where the carboxyhaemoglobin level was raised by breathing a 2% CO gas mixture, the alveolar CO and carboxyhaemoglobin boosts were similar (71.7% and 75.2% respectively), and they fell sharply subsequently rather than increasing further as occurred after smoking. 3. We conclude that alveolar CO measurements give a useful estimate of carboxyhaemoglobin level if the subject has not smoked for at least half an hour but that measurements of alveolar CO boost are useless since the act of smoking interferes with alveolar sampling. We postulate that cigarette smoking induces a transient change in pulmonary gas exchange.

Psychomotor, pulmonary and exercise responses to sleep medication.

1 Athletes may use benzodiazepines before events to improve sleep, but these drugs may adversely affect performance. 2 Nitrazepam (10 mg) and temazepam (30 mg) were compared with placebo in 27 physical education students, (14 males, 13 females). Treatments were administered at night, using a double-blind, double dummy protocol, for 9 nights. Observations were made in the morning after night 2 and night 9. At least 2 weeks interval was allowed between each treatment. 3 At each examination lung mechanics were measured, a Leeds Sleep Evaluation Questionnaire completed, recognition reaction time, choice reaction time and the critical flicker fusion threshold test were used to assess psychomotor activity and an exercise test was performed. The subject exercised to exhaustion on a bicycle ergometer while ventilation, gas exchange and heart rate were recorded on an FM tape unit for off-line digital analysis. 4 The questionnaire indicated that both drugs were equally effective in promoting and maintaining sleep, but nitrazepam had a marked 'hangover' effect. The psychomotor activity and lung mechanics however seemed unaffected. On day 2, maximum exercise levels attained using either drug were comparable to placebo whilst on day 9 temazepam and placebo were significantly higher than nitrazepam. 5 Heart rate was significantly increased at each exercise level with both drugs. 6 Although there may be some effect of these drugs on athletic performance this is likely to be small especially with temazepam.

Assessment of smoking behaviour and ventilation with cigarettes of differing nicotine yields.

Nine established cigarette smokers were each studied four times, smoking two identical cigarettes on each occasion. After an acclimatization study, they smoked one of three types of cigarettes, either their usual brand or one of two types of special low tar cigarettes. These latter both had tar yields of about 8 mg with nicotine yields of 0.55 (LN) and 0.90 (MN) mg respectively. The test order was randomized between individuals and before using the special cigarettes the subjects were given a pack to accustomize themselves. While smoking each cigarette, magnetic tape recordings were made of puff rate, ventilation measured by respiratory inductive plethysmography (RIP) and nasal airflow measured with a modified oxygen cannula. The data were then processed digitally off-line. Salivary nicotine and alveolar carbon monoxide levels were measured before and after smoking each cigarette, and the cigarette butt was analysed for nicotine. While smoking behaviour varied considerably between the various subjects only small differences were seen between the different cigarette types in puff volume and duration and shape of the puff profile. Some changes in smoking behaviour occurred during the course of smoking a single cigarette. Ventilatory patterns showed consistent inter-subject differences but there were no apparent variations due to the various cigarettes. Most subjects puffed during an expiration with the buccal cavity closed off, and then took a slower, deeper inspiration breathing through the mouth. Others, however, took puffs at any point in the respiratory cycle. The different nicotine yields of the cigarettes produced marked changes in the butt and salivary nicotine measurements, but neither these, nor the changes in alveolar carbon monoxide, were closely related to ventilatory measurements. Possible explanations for these discrepancies are discussed.

The assessment of nocturnal oxygen saturation.

Existing methods of assessing nocturnal episodic hypoxaemia are either insensitive or ignore the majority of the available data. We describe a method of analysis using off-line digital processing. A distribution of oxygen saturation (SaO2) with time is produced from all the available data, and subjected to moment analysis to produce a simple index which describes an entire night's SaO2. Our results suggest that the mean and the coefficient of skew fully described a night's SaO2. However, in subjects with chronic air-flow obstruction, the third moment about 100% oxygen saturation (M3100), a single figure, has the same descriptive power as mean and skew. In 17 subjects with chronic air-flow obstruction a significant correlation was found between both daytime SaO2 and PaCO2 when plotted against either the M3100 or the skew. Measurements made on two occasions in seven subjects showed good reproducibility for the skew and M3100 indices.

Evaluation of the respiratory inductive plethysmograph in man.

We evaluated the respiratory inductive plethysmograph, (RIP), during tidal breathing in eight men and seven women. This device measures movements of the rib cage and abdomen during breathing and adds the signals to produce an indirect record of ventilation. We recorded on magnetic tape, the rib and abdominal signals separately, with a simultaneous ventilation measurement from a pneumotachograph, and analysed them later using a digital computer. One method of calibration, the simultaneous equation technique, was considered in detail. Agreement between the combined RIP signal and a simultaneous ventilation record was normally within 25% except where the calibration was unsatisfactory or the breathing pattern was irregular. The reproducibility of measurements made 5 min apart was good overall, but some subjects showed marked variability. An alternative calibration method which derives indirect isovolume relationships was also examined, but was found to give very erratic results. The most serious error was the alinearity of the rib and abdominal signals, and the problem of describing thoracic movement using only two sensing elements. We conclude that the RIP is a convenient monitor of ventilation during regular tidal breathing, but that it is not quantitative.

Measurement of human nasal ventilation using an oxygen cannula as a pitot tube.

A pressure transducer connected to a nasal oxygen cannula detects fluctuations of about 0.1 kPa (1 cm H2O) during nose breathing because the prongs act as two one-sided pitot tubes in parallel. We describe a digital technique for converting this signal to flow and volume records without encumbering the head except during calibration. The signal could be calibrated or validated using flow measured with a face mask by intubation of the nostrils or using a respiratory inductive plethysmograph. In many subjects, the calibration gave satisfactory results for as long as 30 min, but in some, more frequent checks were needed. Changes in the relative airflow in the two nostrils may upset the results, but this can be corrected by recording and calibrating the pressure from each side separately. The meaurements can be made at high ventilation rates of when oxygen is flowing along the cannula or when gas is being sucked out for analysis.

Can carbon monoxide be absorbed from the upper respiratory tract in man?

To investigate the possible absorption of carbon monoxide into the blood from tobacco smoke confined to the mouth and upper airways, an indirect study was made on 12 normal subjects of the recovery of CO from a bolus administered at various levels during a preceding inspiration. No measurable CO uptake was observed unless the bolus was inhaled early enough in inspiration to reach the alveolar region of the lung. Some movement of a tracer gas, argon, was however seen from the upper airways during breath-holding so that some CO might escape into the lungs this way. No detectable CO uptake occurred in one subject who inspired the bolus into his nasal cavities. We conclude that the elevated carboxyhaemoglobin levels seen in smokers, can only occur when smoke is inhaled into the lung, since no appreciable uptake can occur in the upper airways.

Reproducibility of dynamic compliance and flow-volume curves in normal man.

To evaluate methods proposed for the early detection of small airways obstruction. we have compared the precision of the forced expiratory flow-volume curve and of measurements of the frequency dependence of lung compliance in normal subjects, in 10 of whom these measurements were made on four occasions, and in 5 on two occasions. The maximal expiratory flow rate was highly reproducible, revealing consistent differences between these normal subjects, particularly when measured at 60% of TLC and corrected for differences in body size. The frequency-dependence measurements, expressed as the slope of the regression line relating dynamic compliance to frequency, showed much greater variation between repeated measurements in the same subject. Comparison with earlier published accounts is difficult in view of lack of quantitative data, but the variability between single measurements on different normal subjects appears to be similar to that which we have found when the results are expressed in a comparable manner. Dynamic compliance at a frequency of 1 Hz lay between 48% and 141% of the value obtained by extrapolation to zero frequency.

Cardiorespiratory effects of rapid saline infusion in normal man.

We have studied the cardiorespiratory effects of the rapid infusion (100 ml/min) of 2 liters of saline in four normal seated subjects. Cardiac output and pulmonary arterial pressure increased, while vital capacity (VC) and total lung capacity (TLC) decreased. There was an increase in closing volume (CV) without any detectable change in lung compliance or flow-volume characteristics. There was an increase in Pao2 during infusion period which can be related to better matching of ventilation to perfusion and to improved hemoglobin transport. In the recovery stage as cardiac output, pulmonary arterial pressure, TLC, and VC all returned toward control values CV remained high. In two subjects CV occurred within the normal tidal range of ventilation and in these two subjects Pao2 fell significantly below values obtained in the control period. The results suggest that rapid saline infusion in man can cause interstitial edema and lead to premature airway closure and hypoxemia.