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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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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 OCR for page 302
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

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312 ~ Y _ ~ ~ _ o o _ ~ o C o o sly =4' C ~ J C-) L) I I, ted ; dU .1 ~ ~ ~ ~ 80 O 1 t 1 1 1 v f t | / V ,x, ~ ~ O t 1 1 I K v ~ ' C| e c 0 " ~ ~ 1 ~ C C o c t: ~ a ~ :) 1 ~ ~ ~ Cal ,, ~ 31 X X 8 ~ O O ~ 3 X g 1 ~ ~ 1 1 1 In _ ~ ~ AL . ~ ~ ~ . o ~ ~ lo I J O ~ ~ I 0` ~ I t I E~ :^ 1 ~ 1 1 1 _ ~: ~ ^3 0 o0= _ C ~ ~ . 3 _. O - 10 to ~ ~ ~ : JO 4~` t8 O ~ 10 0 ~ ~ 8 . , , ~ ~ ~ 1 C c~ O 0 - 0 ~ ~ 3 X ~ X ~ _ ~ ~ 3 0 0 _' eo_ K ~ ~ ~ ~C ~ :: . 0 ~ ~ ~J ~_ ~ J ~ ~0 1 1 O O ~0 o K K O ~ ~

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408 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

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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 REFERENCES ~- 3. 4. 5. 1 . Ackermann, H . -W., B . Schmidt, and V. Lenk . Mycological studies of the outdoor and indoor air in Berlin. Myko~en 12:309-320, 1969. 2. Acosta, F., Jr., and G. W. Robertstad. Chrysosporium species as fungal air pollutants. Ann. Allergy 42:11-13, 1979. Adams, K. F., and H. A. Hyde. Pollen grains and fungal spores indoors and out at Cardiff. J. Palynol. (Lucknow) 1:67-69, 1965. Aisner, J., S. C. Schimpff, J. E. Bennett, V. M. Young, and P. H. Wiernik. Aspernillus infections in cancer patients. Association with fireproofing materials in a new hospital. J. An. Med. ASsoc. 235: 41}-412, 1976. Ar now, P . M., R. L . Anderson, P . D . Mainous , and E . J . Smith . Pulmonary aspergillosis during hospital renovation. Am. Rev. Respir . Dis . 118: 49-S3, 19?8. Austwick, P. K. C. Ecology of Asperqillus fureigatus and the pathogenic phycomycetes, pp. 644-6S1. In N. E. Gibbons, Ed. Recent Progress in Microbiology . Toronto: Univers ity of Toronto Press, 1963. Banaszak , E . F., J . Barbor iak , J . Fink , G . Scanlon, D. P. Schlueter, A. Sosman, W. miede, and G. Unger . Epidemiologic studies relating thermophilic fungi and hypersensitivity lung syndromes . Am. Rev. Respir . Dis . 110: 58S-591, 1974. Banaszak, E. F., W. H. Thiede, and J. N. Fink. Bypersensiti~rity pnewnonitis due to contamination of an air conditioner. N. Engl. J. Med . 283: 271-276, 1970. Baruah, a. K. The air spore of a cowshed. J. Gen. Microbial. 25:483-491, 1961. 1 0 . Benson , F . B ., J . J . Henderson , and D . E. Caldwell . Indoor- Outdoor Air Pollution Relationships: A Literature Review. U.S. Environmental Protection Agency, National Environmental Research

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