Particle Formation and Growth in Gases from Totally Filtered Mainstream Cigarette Smoke

208

245

Tobacco smoke is an aerosol that contains both gaseous and suspended particulate material (PM). The particles are largely liquid droplets containing a wide variety of condensed organic compounds. Each compound in the smoke will partition between the gas and PM phases and will always seek a state of gas/particle equilibrium. When tobacco smoke is inhaled, a compound such as nicotine can deposit in the respiratory tract (RT) by four different mechanisms: (1) direct gas deposition (DGD) of the portion of the compound that is initially in the gas phase of the inhaled smoke; (2) evaporative gas deposition (EGD) of PM-phase compound by evaporation to the gas phase, then deposition; (3) particle deposition, evaporation from the deposited particle, then deposition from the gas phase (PDE); and (4) particle deposition with diffusion (PDD) into RT tissue. Three of the mechanisms (DGD, EGD, and PDE) involve volatilization from the PM phase. The relative importance of all the mechanisms is therefore greatly affected by the volatility of the compound from the PM phase as it is set by the compound's gas/particle partitioning constant K(p) through the compound's vapor pressure. For a largely nonvolatile compound such as benzo[a]pyrene, only PDD will likely be important. For a semivolatile compound such as nicotine, all four mechanisms can be important. Because tobacco smoke alkaloids such as nicotine can exist in protonated as well as free-base form, the fraction alpha(fb) of the compound that is in the neutral free-base form in the PM phase plays a critical, pH-dependent role in determining the relative importance of the four mechanisms. Equations are developed that can be used to ascertain the importance of the DGD and EGD mechanisms. The value of alpha(fb) for nicotine in a tobacco smoke PM is set by pH(eff), the effective pH of the PM phase. Historically, a primary method for measuring "smoke pH" has involved the direct exposure of a pH electrode to tobacco smoke. This method cannot yield direct insight into pH(eff) or alpha(fb) values because (1) problems exist in using such an electrode to measure smoke PM-phase pH, and (2) by itself, a measurement of the pH of tobacco smoke PM says nothing about the effects of PM-phase activity coefficients of protonated and free-base nicotine on the nicotine species distribution. The "acidic" values that have typically been measured for cigarette "smoke pH" by the direct pH electrode method are therefore neither reliable nor useful in determining the relative distribution of PM-phase nicotine among the protonated and free-base forms. The dependence of the volatility of nicotine from tobacco smoke PM on alpha(fb) means that measuring the gas/particle distribution of nicotine under equilibrium conditions in a tobacco smoke by denuder samplers (or by another method) can yield information about the nicotine K(p) for that smoke. Knowledge of K(p,fb), the partitioning constant for nicotine in the free-base form, then allows calculation of alpha(fb) through the relation K(p) = K(p,fb)/alpha(fb...

Section: “Impact”mentioning

confidence: 99%

A Consideration of the Role of Gas/Particle Partitioning in the Deposition of Nicotine and Other Tobacco Smoke Compounds in the Respiratory Tract

Pankow

2001

208

245

“…As illustrated in Figure 2, MS smoke is a reactive, dynamic aerosol composed of heterogeneous particles suspended in a gasphase (43)(44)(45)(46)(47). Smoke constituents can evaporate from particles; gases can deposit onto particles (48)(49)(50). Once MS smoke aerosol enters the body, four discrete mechanisms can describe the deposition of constituents (51) (see Figure 3 and its caption) (13).…”

Section: Introductionmentioning

confidence: 99%

Possible Role of Ammonia on the Deposition, Retention, and Absorption of Nicotine in Humans while Smoking^†

Seeman¹

2007

This perspective presents an overview of the properties of tobacco smoke aerosol and the possible effect of ammonia on the deposition location, retention and the amount and rate of nicotine absorption during cigarette smoking. Three main mechanisms describe the absorption of smoke constituents: (A) gas-phase constituents deposit directly; (B) particles deposit and the constituents then diffuse through the particle into the biological buffer and then into the tissue; and (C) particulate phase constituents evaporate from the particles and then deposit from the gas phase. Nicotine from smoking deposits and is absorbed predominately in the lungs. When particles deposit on the lung-blood interfaces, nicotine is absorbed rapidly, regardless of the acid-base nature of the particles. This is due to the buffering capacity of the lung-blood interfaces and the small mass of nicotine per puff distributed over a large number of particles depositing onto a huge lung surface. The composition of both tobacco smoke aerosol particles and the gas phase are time dependent. Ammonia in mainstream smoke evaporates faster from particles than nicotine. It is, therefore, unlikely that ammonia can significantly affect the volatility of MS smoke nicotine from particles in the smoke aerosol. It is certain that no single measurement of tobacco or of smoke, especially one made under equilibrium conditions, can adequately characterize the time-dependent properties of mainstream smoke aerosol. Thus, the fraction of nonprotonated freebase nicotine in trapped, aged smoke particulate matter has not been shown to be a useful predictor of the amount or total rate of nicotine uptake in human smokers. Similarly, "smoke pH" and "pHeff" are not useful practical parameters for providing understanding or predictability of tobacco smoke chemistry or nicotine bioavailability.

“…SOAs are potentially more toxic than precursor VOCs and can result in adverse health effects ( − ). Typically, SOAs can be found in the ultrafine (particle diameter ≤ 100 nm) and fine (particle diameter ≤ 1 μm) fractions of atmospheric particulate matter.…”

Section: Introductionmentioning

confidence: 99%

“…Smaller particles can produce greater biologic effects as a result of high ambient concentrations and large surface area. The exposure effects of atmospheric SOA on biological organs have been studied, but the mechanism of resultant biological effects has not yet been established ( − ). One of the major limitations in studies of health effects of SOA is the aerosol exposure techniques.…”

Section: Introductionmentioning

confidence: 99%

Exposure of BEAS-2B Cells to Secondary Organic Aerosol Coated on Magnetic Nanoparticles

Jang

Ghio

Cao

2006

Toxicological investigation suggests that exposures to complex secondary organic aerosol (SOA) products can result in adverse health effects in biological systems. However, the mechanism of adverse health effects is not yet understood. One of the major restrictions in studies of health effects of SOA is a particle exposure technique. In this study, we applied an innovative soft targeting technology using magnetic nanoparticles (MNP) to deliver SOAs onto target biological systems under a magnetic field. The exploratory exposure technology using MNP was demonstrated for the SOAs created from the reaction of ozone with alpha-pinene in an indoor Teflon film chamber. SOA increased the release of the proinflammatory mediator interleukin-8 by respiratory epithelial cells. These results support that MNP can effectively deliver SOAs to epithelial cells in vitro resulting in a significant biological effects.