Page 267 - Industrial Ventilation Design Guidebook

228 CHAPTER 5 PHYSIOLOGICAL AND TOXICOLOGICAL CONSIDERATIONS

causes air velocity to decline and the airstrearn to become more diluted. Since
the expiratory wavefront is anticipated to encounter uniform [NH 3] A through-
out the lower conducting airways, increased expiratory flow rates should have
no effect on [NH^ until the wavefront reaches the upper airway. With nasal
expiration, there may be no longitudinal NH 3 concentration gradient except at
the nares, unless NH 3 diffuses from the oral cavity into the oropharynx.
Despite our limited knowledge of [NH 3] A distribution and control, there
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are at least two mathematical models ' that attempt to predict the neutral-
112
ization of inhaled acid aerosols. Cocks and McElroy base their model on acid
particle growth by predicting equilibrium particle size as a function of initial
particle diameter and relative humidity (RH). Molecular diffusion is a major de-
152
terminant of particle growth in the Cocks and McElroy model, particularly
for submicrometric particles, because their size approaches the mean free path
of water vapor. Neutralization of acid particles was determined as a function of
112
time and constant [NH 3] yl at parenchymal conditions. Cocks and McElroy
did not account for higher levels of ammonia in the upper airways, which sug-
gests that the bulk of neutralization will occur in the upper airway, at lower RH
and temperature than in the parenchyma. The effect of a longitudinal intra-air-
way [NH 31^ gradient on neutralization was also not considered.
80
Larson developed a model of acid aerosol neutralization that accounts
for RH and temperature gradients along the airway. The longitudinal gradi-
136
ents used in the model were taken from the model of Martonen and Miller ,
which did not account for airway geometry or ventilation. Two fixed intra-air-
way [NH 3]^ gradients, reflecting oral and nasal breathing, were modeled and
both assumed linear concentration gradients along the airway (with a step
change at the oropharynx during nasal breathing). Dilution due to increased
flow rate was not modeled, nor is it clear whether the [NH^ gradients
80
112
changed during exhalation. Neither Cocks and McElroy nor Larson ac-
counted for gas-phase NH 3 transport (except at the particle surface) or the
possible effect a reduction in oral wall pH, caused by exposure to acid aerosol,
would have on segmental control of [NH 3] yl.
+
Both models predict that two factors would decrease [H ] in the particle: (1)
hygroscopic growth of the particle, which is thought to be capable of reducing
particle [H 2SO 4] from 15.3 M to 0.22 M; and (2) particle neutralization due to
[NH 3] A, which is potentially more significant but likely to be more variable within
an exposed population. Without neutralization, highly acidic submicrometric par-
80
ticles (pH = 0.66) were predicted to be deposited onto distal airway tissues. To
refine our understanding of the potential for acid neutralization to mitigate ad-
verse health effects, the assumptions regarding NH 3 concentration appear to be
critical for any mathematical description of acid aerosol effects. Cocks and
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McElroy demonstrated the importance of NH 3 concentration estimates, with
3
complete neutralization of submicron droplets at 500 |Jig/m NH 3 but less than
3
15% neutralization at 50 jxg/m NH 3. Since measured oral NH 3 concentration
3 78 93
vary over a wide range, 144-1536 jxg/m , ' model predictions would improve
if the factors controlling NH 3 production and [NH 3] A were known.
Mucociliary Escalator
Bacterial and viral inoculants deposited onto airway mucus are normally
inactivated by immunoglobins and macrophages 117 while being physically