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vIT
HEALTH EE.Fk~TS OF INDOOR POLLUTION
I NTRODUCTION
The Committee, charged with characterizing the quality of the
indoor environment and determining the potential adverse health effects
o f pollutants in that environment, selected the following pollutants
for detailed discussion: radon and radon progeny, formaldehyde and
other organic substances, fibrous building materials, combustion
products {resulting from combustion of fuels in space-heating,
water-heating, cooking, hobbies and crafts, etc. I, involuntary smoking,
airborne agents of contagion, and airborne allergen. . These are
obviously only examples of hazardous pollutants. They were chosen
because there was a large volume of Published material available on the
sources of their presence Indoors that could be used to document the
adverse ef feats of human exposure to them. The sources of these and
other pollutants are described in Chapter TV; the biologic responses to
the selected pollutants are discussed here.
~ t is beyond the scope of this report to list all the pollutants
found indoors that are hazardous to human health.
- ~ Some pollutant
sources have been known for a long time but only recently recognized as
important. Cigarette-~moking is an example; although the smoke
components that cause adverse health effects need more study,
considerable progress has been made, as repor~ced in This chapter. The
examples given in this chapter make it plain that humans are exposed to
a variety of potentially hazardous indoor pollutants from diverse
sources. It is hoped that this report will encourage researchers to
broaden the list of hazardous indoor pollutants and to characterize the
hazards, so that the general public and those responsible for pollution
control and abatement can be informed.
Throughout this report, pollutants are mentioned without discussion
of their health effect..
part of the Committee, but rather reflects a decision that the
discussion here be adequate to show that there are indoor pollutants
that cause adverse health effects in humans. The reader's attention is
directed to Chapter lIT, which offers some recommendations for further
health research with respect to there pollutants, for further exposure
This does not constitute an oversight on tne
302
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303
studies, and for public education about effective ways of reducing
exposure to many contaminants encountered indoors.
Pollutants are inhaled, ingested, and absorbed. They may have
effects at their first point of contact with the body, or they may
affect internal organs. They nay be changed physically or chemically
(metabolically) in the process of exerting their effects, or they may
undergo intermediate physical or metabolic changes before exerting an
effect. They may be stored in tissue for a time and be released later;
many of them are eventually excreted. Their own behavior helps to
shape the mechanisms of their effects. Pollutants may act
independently, antagonistically, or synerg istically.
Inhalation is generally the most important route by which toxic
substances enter the body. Inhaled substances may exert their effects
in the lungs, or they may pass from the lungs to other organ systems in
blood, lymph, etc. Ingestion is far less common than inhalation as a
route of exposure, but is important for some toxic substances, such as
lead, arsenic, and mercury. In addition to the direct physical or
chemical effect of ingested substances in the gastrointestinal tract,
they may pass through the tract into the blocPd and be distributed to
other organs. Liquid and vapor-phase pollutants may be absorbed
through the skin and affect the skin, pass through the skin and then
conjugate with tissue protein, or enter the bloodstream and be
distributed further. 2} 24 2S
Environmental agents may exert their effects either by physical or
by chemical-phy~iologic (enzymatic) mean.. The full toxic potential of
most substances is usually not expressed in normal healthy people,
because of the body's defense mechanisms and mechanisms of elimination
or because the substances are sequestered in inactive forms at various
tissue sites (bone, skin, hair, and nails). However, impairment of the
body~s defensive processes may lead to increased toxicity, owing to the
higher concentrations of the substances that build up when the usual
means of elimination or reduction are blocked. Effects can occur
metabolically at the cell or organ level. Various trace substances
(e.g., halogenated hydrocarbons and trace metals) can have their
effects at both levels. 13 21 24 25
Some physical signs give evidence of primary toxicity, such as
contact with substances that produce irritation, inflammation, or
contraction. Some gases, such as carbon monoxide and nitrogen dioxide,
when inhaled can affect the body's capacity to absorb oxygen.
Secondary mechanisms of toxicity include metabolic alteration of
the substance and accumulation of the byproducts from the initial
action of the pollutant. Some substances are detoxified by metabolic
processes (oxidation, reduction, and synthesis}, and the detoxification
mechanisms may themselves cause damage, as in the oxidation of alcohol
to formaldehyde and the reduction of arsenic or manganese, which may
produce more toxic forms.
Respiratory effects can be directly attributed to only a few
pollutants encountered at high concentrations indoors: nitrogen
dioxide, carbon monoxide, formaldehyde, and probably particles are
important in this regard.
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304
Physical factors (such as temperature, humidity, noise, nonionizing
radiation, and light} and their effects are discussed in Chapters Iv
and VITI; knowledge of their effects in the indoor environment is
sketchy and difficult to assess. Information on the health effects of
pollution due to consumer products in general has the same limitations
and is treated in the same way.
A variety of trace metals may be present indoors as a result of
filtration of outdoor sir and as ~ result of indoor sources of
pollutants. These trace metals are also found in the domestic water
and in the diet. Some of them, especially lead and mercury, have
adverse health effects.5 ~ 15 Exposure to mercury indoors may result
from spills of liquid mercury and deterioration of paint. Mercury
vapor is quickly and efficiently absorbed by the lung and may be
absorbed through the skin.22 Although much of the body burden of
lead may come from the diet, the combined effects of air, soil, house
dust, and water as sources o' indoor lead are appreciable. ~ i' 26
The effects of lead and mercury on the brain are well
known ~ ~ ~ ~ ° ~ ~ - 2 ~ ~ 2 2 ~ 2 ~ - 2 ~ Behavioral dysfunctions caused by
lead may occur through modification of the enzymatic response to a wide
variety of toxic agents and through interference with neuromuscular and
ganglionic transmission.' i .
Gastrointestinal symptoms may be produced by inhalation of toxic
substances, such a. lead and mercury, that reach the gastrointestinal
tract through the bile duct.. 22 Organic mercury is also hepatotoxic
and may cause kidney damage by destroying cells in the tubular
system. 27 Lead and arsenic deposited in the kidney at low
concentrations may produce sensitization to damage by endotoxins or
exotoxins, such as analgesics and bacteria, although this is still
debatable. Mercuric chloride may produce acute renal failure.22
Mercury has toxic effects on the thyroid and therefore may have further
systemic effects. I' Cadmium interacts with other nutrients and may
be stored in the kidney and damage capillaries there. 7 t' 27 28 It
also accumulates in the liver at concentrations that depend on age and
smoking habits., Lead can inhibit heme synthesis,~3 especially in
school-age children. Lead, zinc, and delta-aminolevulinic acid (ALA-D}
interact, and porphyrins (free erythrocyte porphyrins and zinc
protoporphyrins) are active in the blood; that activity determines the
influence of lead on heme synthesis.27tPP 2l] 2 2) Lead may
increase the inhibition of ALA-D in erythrocytes, shorten erythrocyte
life span, and produce reticulocytosis or anemia.. ~ ~t It may also
increase hypertension and vascular disease.~i
Lead is stored in the body and has effects related to its storage
or its release. 12 Deposition occurs in soft tissue and bone
tissue--predominantly in the flatter. Effects may occur in those
tissues, but often occur systemically on release of deposited lead or
when the body burden becomes too great.- Release may be caused
by acidosis or fractures. The lead in the soft tissues causes enzyme
inhibition, 12 which in turn can lead to interactions of toxins..
Mercury is a general sensory irritant. It may produce skin
burns, 2 rash, 22 excessive perspiration, easy blushing, partial loss
of scalp hair, 22 or a decrease in hearing. It can affect taste,
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305
ana it produces irritation in the mouth. 22 Mercury poisoning may
affect the sense of touch, owing to the swelling of all extremities,
including ears and nosegay Except for spills of inorganic mercury
and excessive use of mercury-based paint, it is debatable whether
indoor concentrations of mercury are ever high enough to produce those
effecters
This chapter deals with the biologic responses to specific
pollutants and biologic agents. The pollutants discussed are
sidestream cigarette smoke, radon progeny, mineral and vitreous fibers,
formaldehyde, and products of indoor combustion (predominantly carbon
monoxide and nitrogen oxides). Gases not usually found indoors in
moderate or high concentrations--suab as sulfur oxides and ozone--are
not discussed at length. Nor are sources like cooking, which may
produce some particles or hydrocarbons, but about which little is
known. For information on substances that are known to have adverse
effects in the occupational environment or on solvents, dusts, etc.,
which have been reviewed thoroughly, the reader is referred to the
published literature (e.g., reports issued by FDA and CPSC).
Environmental factors that are not known to have adverse biologic
Impact are not discussed here; rather, there are appropriate references
to other chapters.
CES
7.
1. Angle, C. R., and M. S. McIntire. Environmental lead and children:
The Omaha study. J. TDxicol. Environ. Health 5:855-870, 1979.
2. Berkout, P. G., N. J. Paterson, A. C. Ladd, and L. J. Goldwater.
Treatment of skin burns due to alkyl mercury compounds. Arch.
Environ. Bealth 3:592-593, 1961.
Bull, R. J. Effects of trace metals and their derivatives on the
control of brain energy metabolism, pp. 425-440. In S. D. Lee, Ed.
Biochemical Effects of Environmental Pollutants. Ann Arbor, Mich:
Ann Arbor Science Publishers, Inc., 1977.
Dahlgren, O. Aboominal pain in lead workers. Arch. Environ. Health
33:156-159, 1978.
5. Daines, B. H., D. W. Smith, A. Feliciano, and J. R. Trout. Air
levels of lead inside and outside of homes. Ind. Med. Surg.
41~107:26-28, 1972.
6. DuBoi=, K. P. Interactions of chemicals as a result of enzyme
inhibition, pp. 95-107. In D. H. R. Lee, and P. Kotin, Eds.
Multiple Factors in the Causation of Environmentally Induced
Disease. New York: Academic Press, Inc., 1972.
Elinder, C.-G., T. Kjellstrom, L. Friberg, B. Lind, and L. Lineman.
Cadmium in kidney cortex, liver, and pancreas from Swedish
autopsies. Arch. Environ. Health 31:292-302, 1976.
8. Finelli, V. N . Lead, zinc, and 6-aminolevulinate dehydratase,
pp. 351-363. In S. D. Lee, Ed. Biochemical Effects of Environmental
Pollutants. Ann Arbor, Mich.: Ann Arbor Science Publishers, Tnc.,-
1977.
9. Foote, R. S. Mercury vapor concentrations inside buildings. Science
177:513-514, 1972.
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306
10 . Goldberg, A. M. Neurotranamitter mechani - s in inorganic lead
poisoning, pp. 413-423. In S. D. Lee, Ed. Biochemical Effects of
Environmental Pollutants. Ann Arbor, Hich.: Ann Arbor Science
Publishers, Inc., 1977.
11. Goldsmith, J. R., and L. T. Friberg. Effects of air pollution on
human health, pp. 457-610. In A. C. Stern, Ed. Air Pollution. 3rd
ed. Vol. II. The Effects of Air Pollution. New York: Academic
Press, Inc., 1977.
12. Hayes, W. J., Jr., R. A. Neal, and H. H. Sandstead. Role of body
stores in environmentally induced disease - DOT and lead,
pp. 136-164. In D. lI. R. Ice and P. Kotin, Eds. Multiple Factors in
the Causation of Environmentally Induced Disease. New York:
Academic Press, Inc ., 1972.
1 3. He rnberg , S . Lead , pp. 715-?69 . In C. Zenz , 3 :d ., In Occupational
Medicine. Principles and Practical Applications. Chicago: Year Book
Medical Publishers, Inc., 19770
14. Hirschman, S. Z., M. Feingold, and G. Boylen. Mercury in house
paint as a cause of acrodynia. Effect of therapy with N-acetyl-D,L-
penicillamine. N. Engl. J. Hed. 269: 889-893, 1963.
15. Joselow, M. M. Indoor air pollution by Mercury. Ann. Intern. Hed.
78:449-450, 1973.
Kass, E. B. Multiple factors in the causation of renal disease, pp.
83-91. In D. B. K. I`ee and P. Kotin, Eds . Multiple Factors in the
Causation of Environmentally Induced Disease. New York: Academic
Press Inc., 1972.
17. Morse, D. L., W. N. Watson, J. Bousworth, L. E. Witherell, and
P. J. Landrigan. Exposure of children to lead in drinking water.
Am. J. Public Health 69: 711-712, 1979.
18 . Needleman , ~ . L., C . Gunnoe , A. Leviton , R. Reed , ~ . Peres3.e . C .
16.
.
Maher, and P. Barrett. Deficits in psychologic and classroom
performance of children with elevated destine lead levels. N. Engl.
J. Med. 300: 689 - 695, 1979.
19. Petering , H. G., L. Murthy, and F. L. Cerklewski. Role of nutrition
in heavy metal toxicity, pp. 365-376. In S. D. Lee, Ed. Biochemical
Effects of Environmental Pollutants. Ann Arbor, Mich.: Ann Arbor
Science Publishers, Inc., 1977.
2 0 . Reels, B., J. -P. Buchet, R. "uwerys, G. Bubermont , P. Brusux ,
F. Claeys-Thoresu, A. "fontaine, and J. Van Overechelde. Impact of
air pollution by lead on the heme biosynthetic pathway in
school-age children. Arch. Environ. Bealth 31:310-316, 1976.
21. Schanker, L. S. Flow of environmental agents in reaching their site
of action, pp. 6-14 . In D. B. X. Lee, and D. Hinard, Eds.
Physiology, Environment, and Man. New York: Academic Press Inc.,
1970.
22. Sexton, D. J., K. E. Powell, J. Liddle, A. Smrek , J . C . Smith, and
T. W. Clarkson. A nonoccupational outbreak of inorganic mercury
vapor poisoning. Arch. Environ. Bealth 33 :186-191, 1978.
23 . Shy, C., J. Goldsmith, J. Hackney, M. D. Lebowitz , and D. Henzel .
Statement on the Health Effects of Air Pollution: ATS News 4:22-62,
Spring, 1978.
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307
24 . Stokinger, B. E. Means of contact and entry of toxic agents, pp.
7-11. In W. M. Gafafer, Ed. Occupational Disease-: A Guide to Their
Recognition. U.S. Department of Health, Education, and Welfare,
Public Health Service Publication No. 1097. Washington, D.C.: U.S.
Government Printing Off ice, 1964 .
2 5. Stok inger, H . E: . Mode of action of toxic substances, pp. 13-26 . In
W. M. Gafafer, Ed. Occupational Diseases: A Guide to Their
Recognition. U.S. Department of Health, Education, and Welfare,
Public Health Service Publication No. 1097 . Washington, D.C.: U. S .
Government Printing Of f ice, 1964 .
26. Ter Haar, G. An investigation of elevated blood lead levels in
Detroit children. Arch. Environ. Health 34:145-150, 1979.
27 . Waldbott, G. L. Health Effects of Environmental Pollutants . Saint
Louis: The C. V. Mosby Company, 1973. 316 pp.
28. World Health Organization. Health Hazards of the Human Environment.
Geneva: World Health Organization, 1972 . 387 pp.
RADON AND RADON PROGENY
The physical, chemical, and radiologic properties of radon-222
(referred to as radon), radon-220 (thoron), and their progeny and the
principles of dosimetry are summarized in Chapter nl.
The unit of exposure of man is the working level (WL), def ined as
the quantity of short-lived progeny that will result in 1.3 x 105 Rev
of potential alpha energy per liter of air. This is equivalent to a
concentration of short-lived radon progeny in complete equilibrium with
radon-222 at 100 pCi/L in air. The working-level month (WLM) in a term
defined originally for occupational exposure, and 1 WLM is exposure at
1 Wl' for 170 h. Thus, the working-level month is a measure of
cumulative exposure.
The working level is a measure of exposure rate; it has been widely
assumed that, over a 70-yr lifetime, typical total-lifetime background
exposures are in the range of 5-20 WLM. However, the average and
distribution in the United States are not well studied. Some
restrictions on the use of the working level must be noted. First, it
i. not useful for thoron progeny, because the~dose delivered to the
bronchial epithelium for the same amount of potential alpha energy
(1.3 x 105 MeV) per liter of air can be much higher than that of
radon progeny. Second, characterization of the dose to lung airways
based solely on the working level involves a degree of uncertainty:
the distribution of the lung dose depends on the unattached fraction,
the particle size distribution of the aerosol to which the radon
progeny are attached, lung morphometry, breathing rate, etc. Even with
a general knowledge of the physical factors, other uncertainties in
calculating dose are sufficiently great that characterization of ache
exposure atmosphere in terms of any measure more precise than working
level is inappropriate for dose approximation: . The difficulties in
characterizing dose and relating it to effects have been reviewed
recently by Cross et al. ~. It should be noted that deviations in the
exposure environment f rom reference conditions may result in actual
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308
lung doses that differ fro. those expect" on the basis of the
reference condition e assumed.
REVI" OF DOSE AND EXPOSURE cAL`:uLATIoals
The inhalation of radon progeny leads to a very inh~geneous alp"
dose to the human lung. For a variety of reasoner-including
preferential deposition, mucociliary clearance of aerosols deposited on
conductive airways. and the observed tumor sites and types it is
believed (but by no means certain) that the radiation from the
alpha-particle irradiation of the basal cells of the upper bronchial
epithelium is the exposure characteristic cost closely relatable to
carcinogenic risk. However, it is difficult to determine the
alpba-particle close, because of the intractable difficulty of measuring
it _ vitro. Bence, dose calculations bate been based on physical and
biologic models. Dosimetric models have been developed for adults and
Eve been satirized in several recent report. 3~ ·5 ·~ Ad'' --
~e''~.y ~ in'
ase~dePendent model was developed by ~fasnn et al. ~ ' Moreover. the
reference at-~spbere is important for dose calculations, which are
influenced by the fraction of unattached progeny and the particle size
distribution of the progeny. Breathing rate, au~octliery clearance,
lung aorpho~etry, age, and sex aust also be considered.
Depending on assumptione about the equilibrium, unattached fraction
of progeny, carrier aerosol distribution, and the locus of target cells
chosen for the estiastes, calculated dose estimates per working-level
aontb can vary by up to a factor of 100. A comprehensive evaluation of
the dose through the various regions of the lung, taking into account
attached and unattached fractions and particle size distributions, has
recently been publiabed. 2 2
The table of background dose rates cited in Chapter IV is taken
fro National Co~ission on Radiation Protection and Measure~sents
{NCRP) Report 45, which assumes that the reference exposure atmosphere
for the United States is at about the concentration found in outdoor
sir, assumed to be radon-222 at 150 pCi/~3 in equilibrium with the
progeny. George and Brealin ~ ~ measured radon working levels in
cellars, fires-floor spaces, and outdoors for 21 houses in Hew York and
flew Jersey and found the ratio of firat-floor to outdoor average Annual
radon content to be 4.6, with median outdoor content of 180 pCt/a .
The firat-floor-to~outdoor waricing-level ratio was lower, 2.6' that
suggeeto a reduced equilibrium indoors, as eight be expected. The
annual Dean on the first floor Wee 0.004 if*. Bow representative these
are of the metropolitan Hew York area or other areas is rot known.
On the assu~tion that there was an 808 o`:cupancy factor in the
houses, with the 201 balance spent outdoors, the annual weighted
estimate for the New York-New Jersey study was 0.11 HTM~/yr. Over
70-yr life, that would produce roughly 8 Em.
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309
BIOLOGIC EFFECTS
This section deals with the estimation of potential risk to On
from inhalation exposure to radon progeny, the basis for the estimates
of risk, and the shortcomings in our knowledge related to the exposures
normally encountered.
Underground Miners
Much of our knowledge about the human health effects of radon and
its progeny is based on the experience of underground miners whose
exposures must be charac~cerized, in relation to environmental
characteristics, as having high dose rates (working levels ~ and high
cumulative doses (working-level months). Table VII-1 shows
representative values for underground mines and typical indoor
measurements in houses, to provide perspective or. the use of the term
~high. ~
In the general population, exposure to radon progeny occurs under
conditions rather different from those in underground mines, and it is
therefore necessary to consider the extent to which epidemiologic
studies in miners are germane to the general population. The
feasibility of conducting epidemiologic studies of nonmining
populations has recently been examined, and populations of health-spa
workers were identified as promising.4' There have been five major
reviews of results of studies on underground miners. The analysis here
draw" partly on those and on the reports cited in them. All five
reviews dealt with underground-mininq experience and with miners who
were, for the most part, adult males.
Conclusions patterned after those of Seltser derived from those
studies are as follows:
· There is no reason to doubt an excessive lung-cancer risk
among the early Bohemian uranic miners in Schneeberg and
Joachimatal, I' the U.S. uranium-miners at the Colorado Plateau, 27
and Czechoslovakian uraniu~miners. 2 ~ ~ ~ In addition, there were
increased occupational lung-cancer rates, relative to those of
equivalent smoking groups in the general population, among underground
miners with large exposures to radon and progeny in hematite,
fluorapar, and zinc miner in several countries. "
· It is clear that the respiratory tracts of the uranium-minere
received massive exposure from the alpha-emitting progeny, which are
responsible for much more of the radiation exposure than the parent
radon itself.
· There appears to be no convincing evidence that there are any
other components of the mine environment that are responsible for the
excess lung-cancer risk . Conversely, there is no evidence to rule out
a contributory role of other components of this unusual environment,
i.e., respirable silica dust and variable background dust
concentrations and size distributions.
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Representative terms from entire chapter:
cigarette smoke
310
. TABLE VI I-1
Reprelentat ive Exposures to Radon-222 Progeny
Sub Sects or
Location
Uranium minersC
Outdoors
Indoors
wLa
WIMa fib
1-20 100~10, 000
311
· There has been no definitive study in which a valid comparison
group for the highly selected occupational populations was used. The
observed-to-expected ratios have generally been expressed in relation
to the general population or to a selected portion of the general
population, and not to other underground miners. Such a comparison may
be difficult to obtain, because most underground mining involves
exposure to radon progeny at a higher-th.an-background concentration.
· Cigarette-smoking is clearly important, but not essential, in
the induction of lung cancer. Lung cancer is greatly increased in
these studies among uranium-miners who smoke, but is also higher among
non-cigarette-smoking miners. Inferences from both the human
epidemiologic work and the animal toxicologic studier are
contradictory: in each case, one can cite opposite conclusions on the
impor tance of smok ing .
Fundamentally, the existing information is insufficient for a
decision of whether radiation exposure multiplies the risk of lung
cancer associated with other factors, such as smoking, or whether it
produces a cancer risk that is proportional to the radiation exposure
and merely additive to these other risks. In this review, a model
based on the latter idea, the Absolute-risk model,. has been adopted,
although it must be kept in mind that it may not represent the true
situation. I'
Epidemiologic studies of carcinogenesis may be considered complete
if all the population at risk has died and the follownp is complete.
Thus what is usually measured is some cumulative tumor incidence in the
population up to the time of the analysis, which is lower than the
1 if etime excess r isk .
For such data, r isks may be def ined as cumulative incidence to time
t f rom exposures X . Or one may try to express the r isk in terms of
appearance per unit time (usually years), being careful to define the
period over which tumors appear. One must distinguish between latent
period and followup time of the study group. Sometimes, average risk
per year is found by dividing cumulative incidence to time t by the
followup time (i.e., as is done by UNSCEAR.S); but recently the
National Research Council Committee on the Biological Effects of
Ionizing Radiations (the BEIR Committee) excluded the latent period to
define the risk per year. Thus, risk estimates (in cancers/106
person-years per WLM) should not be directly compared with other
dimensionally equivalent risk estimates found for a different Period.
The method chosen here uses the cumulative incidence divided by the
followup time . In any event, the time over which a tzme-dependent r isk
estireate is derived is always specif led.
The results of studies of lung cancer in underground uranium-miners
in the United States and Czechoslovakia and non-uran~um-:niner" in
Sweden, Canada, and the United Kingdom, analyzed as a linear,
no~threshold phenomenon, are summarized in Table VII-2. The first
column shows the excess r is k In Terms of the number of expected
lung-cancer cases per working-level month per year; these range between
2.2 x 10-6 and 8 x ~ 0 6 . Column 1 is obtained by dividing the
observed number of lung cancers in the study group by the followap time
312
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fl id 1. 20 .~_~. .. 130 132 15. 1S'air~Onditioners,' .. 8. 163
and an evaporative cooler.'3 Bowever, their presence In a humidifier
doe. not imply dispersion in the air, ' 2. lt~ and airborne "xa may
differ from those commonly recovered from humidifier fluid.28
The pattern of symptom in those affected is related primarily to
the circumstances of exposure to the causal allergen. Those with
intermittent exposure to high concentrations of allergens, as occurs in
pigeon fanciers, develop recurrent episodes of breathlessness
accompanied by flulike symptoms of malaise, headache, ~algia, and
fever. Measurements of lung function during such an acute episode show
a restrictive ventilatory defect with a decrease in gas transfer. In
the absence of further exposure to the causal allergen, symptoms
resolve over a period of 7-10 d, with improvement in lung-function
measurements and chest-roentgenogram abnormalities over a month. With
further exposures, lung-function tests and radiographic abnormalities
can persist, and pulmonary f ibrosis develop.
Those who have more continuous exposure to low concentrations of
a Ilergen, such as those exposed to parakeet excrete in their homes,
often do not develop constitutional symptoms, but later, less
r eversible stages of the disease with increasing exertional dyspnea.
The abnormalities of lung function are similar deco those found in acute
disease: a restrictive ventilatory defect with impairment of gas
transfer. There may also be loss of volume of the upper lobes with
linear shadows and cystic change due to fibrosis.
A disease that is probably due to an allergic reaction in the
alveolar wall to contaminants of humidification systems, but which has
several important features that distinguish it from typical
hypersensitivity pneumonitis, has recently been described and called
dehumidifier fever. 37 The particular contaminants responsible are
unknown, but may be amebae growing in the water. Those affected have
recurrent episodes of flulike symptoms and fever that are often severe
enough to overshadow the associated breathlessness. Symptoms develop
4-6 h after the onset of exposure and resolve spontaneously, whether or
not exposure continues; and they recur only on reexposure after an
absence of several days from exposure. Lung-function measurements
during an attack show a restrictive ventilatory defect with impairment
of gas transfer that improves over a period of days with the resolution
of symptoms, despite continuing exposure. Unlike hypersensitivity
pneumonitis, it is not accompanied by abnormalities on the chest
roentgenogram during the acute attack, and pulmonary fibrosis does not
occur, even in those who have had recurrent episodes of the disease for
several years. Precipitins to an extract of the humidifier water or of
the ~jelly. growing in the humidifier are found in the serum of those
affected, but may also be found in the serum of other exposed persons
who do not get the disease. Immunofluorescent antibodies to various
species of amebae, particularly Neqleria qruberi and Acanthanoebae,
have been found in the serum of those with precipitins deco the
humidifier water, but the relationship of these antibodies to disease
remains unclear.
Concentrations of protozoa in interior air have not been
sytematically reported; however, their occurrence indoors from both
409
external and intramural sources nay be anticipated. Protozoa have been
recovered, in culture, f rom f ree air by several investigators, as
summarized by Schlichting, 127 although the indicated concentrations
have been well below those of pollens, algae, and fungal spores. Wind
scouring of dry soil has been favored an a source of airborne isolates,
although foams and such factors as sewage-proces~ing may contribute
locally. 127
Indoor fluid collections--such as aquariums, humidifier reservoirs,
and physiotherapy pools--are among the sites of potential colonization
by protozoa. Recoveries of an ameba (Hartmannella castellanii) from
air in a pediatr ic respiratory-care facility may implicate similar
sources; however, many strains of the same species, as well as
Nae~leria and SchizopYrenus, also were taken from outside air. "
Suspicion has also been cast on protozoa a. agents responsible for
humidifier fevers in office and factory workers.35 3' Some species
(i.e., Naeglerza fowler and Acanthamoeba spp.) are known to cause
dangerous necrologic infections, although aerial transmission has not
been demonstrated. 3 S
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