We measure the deposition of cigarette smoke in the human respiratory system, which includes:
These data, when combined with lung physiology and lung clearance data enable tissue dose to be estimated, which may help link exposure to potential disease.
The following page describes in detail these key points:-
All measurements are made using volunteer smokers who have given written informed consent.
Determining deposition relies on making measurements of inhaled and exhaled smoke, puffing behaviour and inhalation behaviour, then modelling the deposition process for both particles and vapours. This allows estimates of smoke deposition in the different regions of the lung (mouth/throat, bronchi, bronchioles, respiratory bronchioles, alveoli).
The main tools we use are:-
Research has shown that different smoke constituents are deposited to different extents - from about 30% to 100% - and that cigarette design features and human inhalation patterns affect the extent to which some smoke constituents are deposited.
One review  suggests that on average 60% to 80% of the mainstream smoke particulate matter is deposited in the lungs after inhalation. This is in contrast to modelled behaviour where only about 20% to 30% of fresh mainstream smoke entering the respiratory tract would be expected to be deposited. The observed deposition of 60% to 80% has been explained by the growth of smoke aerosol particles by water absorption in the humid environment of the lung (hygroscopic growth) and to a lesser extent continuing coagulation and deposition of larger aerosol particles.
Retentions for various constituents have been estimated as:-
Nicotine and semi-volatile smoke constituents are deposited at higher levels than particulate matter because nicotine and other semi-volatile material may evaporate as the smoke is drawn into the lung and diluted. The absorption of the vapour phase material thus provides an additional deposition mechanism. For example - for a typical total deposition of nicotine of 96% - a maximum 78% could be due to deposition of particulate phase nicotine and a minimum 18% could be due to vapour phase deposition . These evaporation processes may also impact on particle diameter and efficiency of deposition.
Most in-house measurements have used solanesol (C45H74O), a high molecular weight species, chosen because its:-
Nicotine has also been used as a retention marker due to the specificity and magnitude of its presence in tobacco and tobacco smoke.
Smoking involves drawing a puff of smoke into the mouth cavity with the soft palate closing the throat. Puff volume may be up to 100ml. The particle size of the smoke aerosol may be influenced by how long the puff is held in the mouth, however, it is principally dependent on its residence time in the cigarette and the time available for coagulation. Therefore, the higher the flow during puffing, the smaller the initial particle size [3,4]. In contrast, the higher the ventilation level of the cigarette filter, the slower the smoke flows through the tobacco rod - resulting in a larger initial particle size. The particle size will also continue to grow through coagulation as it is held in the mouth .
At British American Tobacco we measure smoking behaviour using a Smoking Analyser (SA7), developed in-house. Flows leave the cigarette and are measured inside the holder as they move to the smoker’s mouth.
The SA7 DAT unit uses a pressure transducer to measure pressure differences at 25Hz and converts them to flow and volume values against known flows and pressures. Data on puff number, duration, interval, flow and volume are also analysed.
The human profile can be replicated off-line to measure cigarette delivery to individual consumers.
The screenshot below from the SA7 shows puff flow, puff volume, puff duration, elapsed time, pressure drop and (pre-calibrated) optical tar.
Characterising inhalation behaviour requires measurement of lung volume and the flow rates and durations of inhalation, breath hold and exhalation. The LifeShirt® technology - made by VivoMetrics® - is a miniaturised, ambulatory version of an in-patient system currently used clinically to monitor human respiratory patterns.
The system uses a respiratory monitoring method called inductive plethysmography which monitors breathing patterns at the wearer’s rib cage and abdomen. It is calibrated using inhalation and exhalation of a known, fixed volume.
The screenshot below shows the inhalation and exhalation profile of three cigarette puffs among normal tidal breathing.
Very little is known about how differences in respiratory physiology influence smoke retention, but factors like ventilation asymmetry and disease have been hypothesised as key factors. It has also been observed that smokers who show high or low retention efficiency with one cigarette type, show high or low retention efficiency with most products, even when smoke and inhalation volumes are normalised.
In practice, it will be difficult to clarify this until improved resolution imaging techniques of the human lung have been developed.
Particle diameter significantly influences where - and to what extent - particles are deposited in the human lung [ 7 ]. Smoke particles grow larger in the respiratory tract and an increase in retention efficiency with increasing growth factor has already been demonstrated in vitro.
More recent data suggest these growth factors may be driven by decreased primary particle diameter in freshly generated smoke and that this primary smoke diameter correlates with retention efficiency.
The ability to measure exhaled particle size is an important development and allows us to better understand the cumulative behaviour of the aerosol in the lung and also applies a boundary condition for modelling of aerosol retention behaviour.
Recent measurements using electrical mobility spectrometry suggest exhaled particle diameters range from 215 to 280nm count median diameter (CMD), in a sample set where inhaled concentration ranged from 138 to 180nm CMD [ 6,8 ].
This supports the hypothesis that particle deposition in the lung is driven by sedimentation and Brownian motion processes in the smaller conducting airways.
Improvements in measurement technologies are allowing us to move on from measuring the retention of species such as solanesol and nicotine to those which may be more relevant as smoke toxicants.
These techniques [ 9-14 ] include:
These techniques avoid the fragmentation and ionisation of atmospheric gases allowing a relatively ‘clean’ spectrum to be obtained from a complex matrix. Preliminary real-time measurements have also been carried out for exhaled smoke.
We are extending our range of smoke compounds used in deposition estimates. Compounds in the vapour phase are being studied to help correlate specific compounds in inhaled and exhaled smoke with their respective biomarkers in urine.
It is clear that the retention of toxicants within the smoke is driven by complex and poorly understood mechanisms. But measurement and imaging tools are improving and the hope is that a better understanding of dose may ultimately lead to effective harm reduction tools and measures.