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ENVIRONMENTAL RESEARCH 16, 360 - 372 (1978) The Acute Effects of Chrysotile Asbestos Exposure on Lung Function1 Keith W. Harless,2 Suetaro Watanabe, and Attilio D. Renzetti, Jr.3 Pulmonary Division of the University of Utah College of Medicine, Salt Lake City, Utah S4I32 Received August 8. 1977 Lung function was determined in 23 men 1.5 months after an intense 5-month exposure to chrysotile asbestos using spirometry, plethysmography for determination of lung volumes and specific conductance, single breath nitrogen washout for determination of closing vol ume. and rest and postexercise arterial blood gas analysis. Although no man showed evi dence of restriction. 12 of the 23 had documented airflow obstruction. Eight months follow ing exposure. 16 of the 23 had a repeat pulmonary evaluation. This included the repetition of all previous testing and determination of the diffusion capacity for carbon monoxide and pulmonary compliance. Three men developed airflow obstruction, as determined by the closing volume, during the interval of study. Seventeen of the 23 had airflow obstruction documented on either the initial or follow-up study. Of these 17. 12 were nonsmokers, cur rent light smokers (less than 10 pack yearsl. or ex light smokers. It is concluded that acute intense chrysotile asbestos exposure causes airflow obstruction. INTRODUCTION Chronic exposure to asbestos fiber is a well-known health hazard. Such expo sure can cause a diffuse interstitial fibrosis (asbestosis) of the lung, carcinoma of the lung and gastrointestinal tract, mesothelioma, plaques, and calcifications of the pleura and asbestos corns of the skin (Becklake, 1976). Although these chronic effects of asbestos are recognized, we are not aware of any reports describing the effects of an acute and limited exposure to asbestos fibers. This report is concerned with studies of lung function of construction workers immediately following and 8 months after an intense 5-month exposure to chrys otile asbestos fibers. The results indicate that airflow obstruction may be an early manifestation of such exposure. MATERIALS AND METHODS Asbestos exposure. The exposure occurred during construction of the Automo tive Trades Building at the Utah Technical College in Orem, Utah between De cember 1975 and May 1976. The building is large, and inside finishing work was being completed during these months. Concrete asbestos Flexboard manufactured by the Johns-Mansville Corp. and containing 30% chrysotile asbestos was being used to cover all inside wails of the building for fire protection. The asbestos Flexboard was cut inside the building with an unventilated portable power saw for 1 Supported in part by the Parker B. Francis Foundation. 2 A Parker B. Francis Foundation Fellow in Pulmonary Research. Present address: Bend Memorial Clinic. 1501 Northeast Medical Center Drive. Bend. Oregon. 1 Author to whom requests for reprints should be sent. 0013-9351/78/0163 -0360S02.00/0 Copyright 1978 by Academic Press. Inc. All rights of reproduction in any form reserved. 360 ia,0000532 nri 1 n, c u ^ J- x,' o i acute asbestos exposure and lunc function 361 installation around electrical outlets, ventilation ducts, rafters, doors, and cor ners. Cutting occurred throughout the 5 months on most days. The building was kept closed because of the cold winter months. The concentration of asbestos in the air was not quantitated during the period of exposure. Workers stated it was always dusty, making it difficult at times to see across the building. Some workers reported leaving the building occasionally because of discomfort in breathing the dust. The chips and dust from the cutting were swept into piles periodically. Only one man reported occasionally wearing a protective respirator and observed no other workers doing so. Immediately following the job closure, air sampling was conducted by the Envi ronment Health Services Branch of the Utah State Division of Health and all workers were advised by their respective employers to be examined by a physi cian. The method used for the sampling was that stipulated in the Occupational Safety and Health Act (OSHA) (U.S. Occupational Health and Safety Administra tion. 1972) on 0.8-/xm membrane filters. The results of the air sampling activities are summarized in Table I. Additionally, grab samples of the dust on the floor of the building were analyzed and contained from 1 to 30% asbestos fiber. The OSHA standard for airborne asbestos exposure is 5.0 fibers greater than 0.5 ^im in length per cubic centimeter of air (tfcc) as an 8-hr time-weighted average and a 10 ficc maximum for any-time exposure. On July 1, 1976. the average limit was reduced to 2.0 ficc and the maximum exposure standard of 10 f/cc remained the same. Since the air samples were taken after job closure during simulated conditions (but without the asbestos Flexboard being cut or men actively working), the results in Table 1 are probably underestimates of the actual fiber density encoun tered by the men. TABLE 1 Asbestos Concentrations in the Air at Construction Site Where Recent Exposure Occurred" Date Activity during sampling Minutes of collection fibers/cc* 5-7-76 Sweeping and moving scaffolding Drilling holes in the Flexboard 20 3.84 14 6.18 25 0.57 5-25-76 After all cleaning completed Walking around on inspection 15 0.00 Slapping Flexboard walls 7 0.64 During collection of grab samples 74 0.06 Area sample 78 0.02 6-3-76 During installation of fiberglass insulation 28 0.15 " Sampling completed by the Utah State Division of Health. * Occupational Safety and Health Acts Standard is 2 asbestos fibers/cc of air as an 8-hr timeweighted average and 10 fibers/cc as an any-time exposure. 18-0000533 001952 362 HARLESS, WATANABE, AND RENZETTI Historical information from employers and from each examined man was used to estimate the duration of each man's exposure to the asbestos. The number of hours worked and exposed to the asbestos per day was multiplied by the number of working days and is reported as total hours for each man. For analysis, the exposures of the men were categorized as light (less than 199 hr), moderate (200 to 499 hr), and heavy (greater than 500 hr). Those men cutting the asbestos Flexboard were considered to have heavy exposure. Subjects. Approximately 79 men were exposed and 23 of these referred them selves for pulmonary evaluation. Their initial examination occurred an average of 45 days (21) after their last exposure day. This evaluation included a history, physical examination, pulmonary function testing, and standard chest radiog raphy. Seven months following the initial evaluation, 16 of the original 23 accepted a return invitation. History, physical examination, pulmonary function testing, and chest radiography were repeated with the additional measurements of carbon monoxide diffusing capacity (DLCO), and static, quasi-static, and dynamic pulmo nary compliance. The demographic data of the 23 workers (all men) initially evaluated are sum marized in Table 2. The length of the acute asbestos exposure was variable for individual men. The mean was 518 hr (344: range. 6 to 896 hr). The median was 623 hr and the mode was 896 hr. Four men had once been exposed to asbestos but considered it to be light exposure, i.e., less than 1 week. None of these four knew the fiber type(s) or density for their prior exposure. Eight men (35%) had never smoked cigarettes. Ten (43%) were smoking at the time of the study but six of these had smoked 10 pack-years or less. Five (22%) were ex-smokers, having smoked 10 pack-years or less in the past (average = 7.4 pack-years; range, 3 to 20: average time after quitting = 8 years; range, 2 to 19 years). Nine men (39%) had no prior history of respiratory symptoms or disease. Seven (30%) had a history of seasonal rhinitis. However, only one had ever consulted a physician because of symptoms and none of the seven had had symptoms for at least 5 months prior to testing. Four (17%) had chronic bronchitis, and three (13%) had a remote history of pneumonia. Only one man (No. 2) reported having continuous symptoms during the expo sure which were related to exacerbation of his asthma. Three others (Nos. 9, 12, and 23) experienced temporary difficulty breathing during their asbestos expo sure. One (No. 23) had acute pharyngitis associated with the exposure, causing him to quit work and following which he had a spontaneous recovery. All men were asymptomatic for acute respiratory infections at the time of their evaluation and had been so for at least the previous 2 months. Chest radiographs were interpreted by a board-certified radiologist without knowledge of the men's exposure history or lung function. Pulmonary function studies. The following procedures were done in the seated position: (1) Spirometric measurements were made with either a 13.5-liter Collins spirometer or a 13.5-liter waterless spirometer manufactured by Cardio-Pulmonary Instruments. The forced vital capacity (FVC), forced expired volume in 1 sec (FFV,). and the flow between 25 and 75% of the FVC (FF2S_T5c*) were measured 18-0000534 man was used 'he number of 'y the number analysis, the derate (200 to sbestos Flex- :ferred themtn average of Jd a history, hest radiog23 accepted tion testing, ts of carbon imic pulmo- :d are sumariable for ledian was bestos but four knew had never but six of s, having s, 3 to 20; Z)had no istory of cause of prior to history ie expo 9, 12, 5 expocausing of their without eated ollins ImoI sec ured acute asbestos exposure and lung function 363 If it go go x -o 3 1 .0 o 11 u <J a2 2(i <*<x o Z zocJj^Iozc zsc ux2z^cCx;xo2oz 1 2 (X i a zo : ii Zt > js i 31 5 ?' <h-> |. COS/3 (2-ft r--- * -w--~b ? *fS*| :. 3ox iZp. t _ ! 16g 5 --S *i ><S22n"l UEdr 2? as t$ So 5 Is S i8. zOz9 zozozozozoozC>U>zo zo ou9o Z>ZZ O9 ZZ J* "3 s= IjII UXOxf nM^2*z e u8Mt .5. SS " oe 00 -- IN -- IN G<t-O <^a Zw? M <> (OJ a0c > o .2 u|ul" <u S3S.*ai-c3Suh'<ScwJ3Cuu^* o, -S *1 .s ;is c-- w3Xa vt-'c'uo':ju0aV-- 2 * JS ui ^ 11w = m sm 2* m Jt *u33 J J3 2 2 fit X.w2* ^x* *' SS S N'' o $5*833*32 8 * -- I-* 91 5 2K W< 0m 2> a5. M* < 6 too f* ^^5B^oror**o*>o irn- rIs~- *r\ 0 *B0r2 --f* 22J^T ^ in wt*\i r> N" o nm aroi au 2$ o njuno.a<aza:-xz!tfjt a*. <n Z f3- o< QUJ m=j ^5 *3 0<. ^ 2 2 S ^13 m PS! > S> o o 3i CD * ppd, packs per day. * Ex-sm Ex-smoker.* r Number o f yean since stopping smoking 001354 364 HARLESS, WATANABE, AND RENZETTI manually from the spirometric record. The reported data are from the best test based upon the sum of FVC and EEV, of two or three spirometric records. Spirometric testing was completed before and after administration of 0.68 mg of aerosolized isoetharine with phenylephrine (Bronkometer). Normal values used were from the ITS Manual (Intermountain Thoracic Society, 1975). (2) Functional residual capacity {FRC). airway resistance (Raw), and thoracic gas volume (VTC) at which Raw was determined were measured by plethysmog raphy according to the methods of DuBois et al. (1956a. b) using a constant volume plethysmograph described by Schmidt and Cohn (1961). Specific conduc tance (SGaw) was calculated from Raw and VTC. (3) Total lung capacity (TLO was determined by adding the plethysmographically determined FRC to the spirometrically determined inspiratory capacity (/C). Normal values used for FRC and TLC were from the ITS Manual. (4) Closing volume of the lung (CV) was measured by the nitrogen method. The subject exhaled at a constant flow rate, approximately 0.5 liters/sec into a Fleisch No. 3 pneumotachograph after maximal inspiration of 100% oxygen initiated at residual volume (RV), the signal of which was displayed on an oscilloscope facing the subject, integrated through a Hewlett-Packard VR 4000 Digital Pneumotach, and recorded on the x axis of a Hewlett-Packard 7045A X-Y Recorder. The percentage nitrogen (N2) was measured at the mouth using an ionizing N2 meter (Cardio-Pulmonary Instruments Nitrogen Analyzer 410), the output of which was displayed on the y axis of the X-Y Recorder. The apparatus dead space between the mouth and oxygen source was about 40 ml. Closing volume was taken as that volume at which a sudden inflection in N2 concentration above the slope of the alveolar plateau occurred. It was expressed as CV!VC%. Closing capacity (CC) was obtained by adding residual volume (RV) to the CV and was expressed as CCITLC%. RV was obtained by subtracting the spirometrically determined ex piratory reserve volume (ERV) from the measured FRC. Closing volume tests were administered by the authors and all measurements were checked for accura cy by one of us. Normal values for the CV/VC% and the CC!TLC% were those of Buist and Ross (1973). At least two satisfactory tracings were obtained, each 5 min apart, and the mean of the CV measurements was taken as the final result. (5) Arterial blood gases before and immediately after exercise were determined with the Radiometer BMS3 Mk2 Blood Micro System blood gas analyzer. The exercise performed was 1 min of stepping up and down a 20-cm-high stool. (6) DiCO was determined using the single-breath technique described by Ogilvie et al. (1957). The expired gas sample was collected in a 2-liter bag and analyzed in a Beckman Medical gas analyzer LB-2 for CO. Normal values used were from the ITS Manual. (7) The pulmonary compliance was measured using an esophageal balloon (length, 10 cm; perimeter, 2.25 cm filled with 0.5 cc of air sealed over a polyethylene catheter, PE 200, i.d. = 1.40 mm) connected to a Statham PM131TC (i2.5 psid) transducer according to the method of Milic-Emili et al. (1964) and a Fleisch No. 3 pneumotachograph, whose signal was integrated for volume through a fast-responding integrator (Hewlett-Packard VR 4000). Pressure, volume, and flow were displayed on an oscilloscope and recorded on light-sensitive paper with the u pirat' meth tion 1 the c FRC Subjec No. Norm: I 6 S 10 11 i: i? u 15 16 17 18 19 :o :i :3 Average SD~ " Abt vital car and 75r7 capacity " Inter - Wat. * Norr Aste ' N ini Flov. * An a capacity O^6 .00 I-00105o m the best test netric records, i of 0.68 mg of >aJ values used ). ). and thoracic y plethysmogng a constant ecific conduc- hysmographi:apacity (/C). method. The ito a Fleisch i initiated at scope facing neumotach, -order. The g N2 meter which was ;e between ken as that ope of the acity (CO tressed as mined exume tests >r accura: those of ed, each d result, termined >zer. The tool. i by Ogilanalyzed ere from balloon over a 131TC 1 and a trough and r with acute asbestos exposure and lung function 365 the use of electronics manufactured by Electronics for Medicine. The static ex piratory compliance (Cst) was measured by a stepwise expiration from TLC by a method similar to that of Turner et al. (1968). The operator controlled the expira tion by periodically closing the airway for 3 sec while the subject relaxed against the closed airway. Measurements were made over a range of 0.750 liter above FRC. A quasi-static expiratory compliance was also measured by a slow expira- TABLE 3 Lung Volumes. Sirometry, Specific Conductance. Closing Volumes, and Closing Capacities in 23 Men After Recent Asbestos Exposure Subject No. 7XC> (%> FRC^ FEVj^. FEFk-j^ ^frc.m 'TVC^^FVC -^fvC (%) (%) (%) (%) SGait lliterslsec/cm of H,0/liter) CVIVC CC/TLC (%) (%) Normals 100 100 100 >70* >65* 1 > mm* * * mm 112 81 93 70 86 44 3 111 too 115 83 93 4 5 15m6 249 ** too 67 122 83 6 98 102 98 80 35' 92 76 7 105 134 98 92 120 8 139 188 123 70 49' 9 107 130 103 73 53 10 88 100 111 72 52 11 123 171 122 62 12 122 128 136 73 30' 54 13 81 100 79 73 81 14 107 107 120 82 80 15 120 140 114 75 62 16 106 102 121 68 106 17 132 161 107 68 43 18 98 125 120 89 110 19 96 123 98 76 59 20 107 137 114 75 59 21 94 90 93 87 112 22 109 123 its 79 75 23 116 148 118 87 106 Average SD 107 12 133 111 77 37 13 7 73 26 >0.127'- * * 0.127 0.121 0.225 0.177 0.107 0.191 0.113 0.119 0.210 0.232 0.190 0.205 0.239 0.134 0.208 0.190 0.146 0.248 0.161 0.240 0.180 0.044 N N N T* N N r t N t f N N N N N * N T N N N N _ -- N N N t N N T t t T t N N N T N** N t t N N N _ -- " Abbreviations used: TLC. total lung capacity: FRC. functional residual capacity: FVC. forced vital capacity: FEVt, forced espired volume in I sec; FEFn-nn,. average expiratory flow between 25 and 75% of the FVC; SGaw. specific conductance of the airways; CVIVC. closing volume per vital capacity: CCfTLC. closing capacity per TLC. * Intermountain Thoracic Society. 1975. * Watanabe et al.. 1974. * Normal values dependent upon age (Buist and Ross, 1973). * Asterisks (**) indicate study was not completed. ' N indicates normal result. * Flows improved at least 25% after administration of aerosolized isoetharine. * An arrow <f) indicates elevated closing volume;vital capacity (%) or closing capacity/total lung capacity (%) result. 18-0000537 366 HARLESS, WATANABE, AND RENZETTI tion from TLC. The dynamic compliance (Cdyn) was measured by the method of Mead and Whittenberger (1953). Dynamic compliance was measured at 15 and 60 breaths/min (Cdynti and Cdynm, respectively). The breathing frequencies were maintained voluntarily, being cued by a tape recording or by one of the authors. During the Cdyn maneuvers, the subject was instructed to maintain a constant tidal volume and to keep his FRC level constant. Static expiratory compliance, Cst. Cqst, and Cdyn were each determined after three slow vital capacity breaths. A mean of at least two different measurements for Cst and Cqst and eight breaths for Cdyn was used to express the final result reported. Static expiratory com pliance, Cqst, and Cdyn were expressed in cubic centimeters per centimeter of H20 and Cdyn was also expressed as a percentage of Cst (Cdyn/Cst%). Normal values for Cst and Cdyn used were from Begin et al. (1975). RESULTS The results of the initial pulmonary function studies are summarized in Table 3. No man had restrictive chest disease, as determined by FVC, FRC, or TLC. Twelve (50%) had airflow obstruction demonstrated. Most of these men had their airflow obstruction documented by two or more tests. All but one of these had an abnormal FEF25_7s<*. Of the twelve, three were nonsmokers and did not have a history of past respiratory symptoms or disease. Two were light smokers, and three were ex-smokers who smoked lightly in the past. Eleven (40%) did not manifest airflow obstruction, including five smokers, two ex-smokers, and four nonsmokers. There were no significant differences in the hours of asbestos expo sure for those with airflow obstruction (528 * 348 hr) and those without airflow obstruction (507 331 hr). Additionally, a dose response could not be dem onstrated in those with airflow obstruction. Seven had had heavy, one had moderate, and four had light asbestos exposure. The results of the arterial blood gas analysis before and after exercise, in gener al, showed the group had normal oxygenation of the arterial blood before and after exercise as well as normal ventilation and pH of the arterial blood. Five, who did not have a history of pulmonary disease, had mild hypoxemia at rest. Two of these had no other documented abnormality, whereas these others had airflow obstruc tion. Five others had a significant decrease in their arterial oxygen tension (PaO*) after exercise. Of these, three had airflow obstruction and two did not, although the latter two had smoked. Again, a dose-response relationship was not evident. The results of pulmonary function measurements in the 16 subjects who re turned for follow-up study were compared to the initial data given in Table 4. These follow-up studies were conducted an average of 1% days (23) after the initial examination. The asbestos exposure for this returning group averaged higher (656 290 hr) than that for the seven who did not return (203 209 hr), and this difference in exposure was significant (P < 0.005). Although the average change in weight between the initial and follow-up observations did not change significantly, three subjects gained more than 3 kg. It may be seen that the results of measurements of the FVC, FEV,, EEF25.7SRaw, TLC, and Pa02 at rest and after exercise did not change from the first to the second study for the group. Functional residual capacity decreased slightly and SCaw increased slightly for Time al Weight FVC (It: FVC'F\ FEV, (li FEVvF FEF FEF TLC ilit TLCi'TL FRC (lit FRC.FR SGau 11 CVIVC ' CC.'TLC PaO, at PaO, i! * The * The r Resu d Arte *P < the grc ume d (P < 0 The their ft the tes al.. 19change ume. ( were 1: respec asbest' The 6. All' for Cs judged subject smoke> 4.5 pac had qu The 23). Al 1.8-0000538 method of at 15 and 60 jencies were ' the authors, in a constant compliance, icity breaths, eight breaths liratory com:entimeter of .(%). Normal I i * id in Table 3. 7C. or TLC. nen had their these had an d not have a .mokers, and 40%) did not ers, and four sbestos expo- thout airflow not be demivy, one had rise, in generfore and after Five, who did Two of these flow obstrucension (PaO,) not. although not evident, jects who ren in Table 4. -23) after the oup averaged i 209 hr), and i the average id not change lat the results 03 at rest and or the group. :d slightly for \ j I | l I | 1 s ^ ACUTE ASBESTOS EXPOSURE AND LUNG FUNCTION 367 TABLE 4 Results of Pulmonary Function Measurements at 1.5 and 8 Months Following Asbestos Exposure in 16 Men* Time after exposure Initial measurement at 1.5 months Follow-up measurement at 8 months Weight (kg) FVC (liters)* FVCIFVCpm m FEV, (liters) FEV,/FVC (%) FFU_71, (LPS) FEFa.jyv'FVC (%) TLC (liters)r TLCITLCpm W FRC (liters)* FRCIFRCpm W SGair (liters/sec/ of H,CVliter)r CVIVC (%) CCfTLC (%) PaO, at rest (mmHg)11 PaO, with exercise (mmHg) 80.3 12.6 5.19 s 0.75 110 2 15 3.95 * 0.51 75 2 7 3.64 * 1.45 70 * 25 7.16 s 1.18 107 - 19 3.59 2 1.02 135 2 43 0.1667 2 0.0624 17.11 2 7.26 38.78 2 8.13 74 2 8 74 2 9 81.7 2 13.9 5.24 2 0.74 111 2 13 3.95 2 0.68 75 2 7 3.42 2 1.28 66 2 24 6.76 2 1.10 106 2 15 3.14 2 0.74 114 2 27 0.2005 2 0.0575 21.89 2 7.96* * 42.25 2 8.93 75 r 8 76 2 9 * The data are expressed as the mean 2 SD. * The abbreviations are the same as those given in Table 3. * Results in 13 men in whom measurements were made. * Arterial oxygen tension. * P < 0.05. the group, but neither change was significant. The group's average closing vol ume did show a significant increase from 17.11% 2:7.26% to 21.89% 7.%% (P < 0.05). The closing volume data are listed in Table 5 for the 16 returning men during their first and follow-up study. Assuming that there is a 2 to 3% variation during the testing and measuring Ducic ef al., 1975; McCarthy et al., 1975; Burki et al., 1975) plus a 0.5% increase due to the older age (about 1 year) and that larger changes are significant, seven men had significant increases in their closing vol ume. Of these, six (86%) either were nonsmokers at the time of both studies or were light smokers. Three (Nos. 8, 12, and 14) had gained 4.0, 6.5, and 6.0 kg, respectively. The others had gained 1 kg or less. Again, a dose response to the asbestos exposure could not be demonstrated. The results of the Z)LCO and lung compliance measurements are listed in Table 6. All values for the DLCO are within the normal range. All men had normal values for Cst. Nine demonstrated frequency dependence of compliance (Table 7), as judged by the results obtained from measurements in normal nonsmoking male subjects of comparable ages (Begin et al., 1975). Four (44%) of these had never smoked and had no prior history of lung disease. One was a smoker but for only 4.5 pack-years, and another was an ex-smoker who had smoked 1 pack-year and had quit 7 years previously. The radiographic examinations were abnormal in four men (Nos. 4, 11, 17 and 23). All were cigarette smokers and one (No. 23) had a history of possible pleural 00.1958 }_a_0000539 368 HARLESS, ATANABE, AND RENZETTI TABLE 5 Closing Volume Data at 1.5 and 8 Months Following Asbestos Exposure in 16 Men Subject No. 1.5 months (CV/VC%) 8 months <CV/VC%) I 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 Average SD 10.52 11.22 12.35 26,55 10.86 4.35 29.79 24.00 16.55 24.32 28.03 20.77 13.81 11.76 15.85 13.06 17.11 7.26 12.50 8.50 27.80 27.46 14.00 31.60 15.17 25.50 18.36 26.50 38.50 31.00 14.45 18.74 20.30 19.86 21.89 7.96 * The CVICV% measured at 8 months minus that measured at 1.5 months. Change* (CV/VC%) 1.98 -2.72 15.45 0.91 3.14 27.25 -14.62 1.50 1.81 2.18 10.47 10.23 0.64 6.98 4.45 6.80 and/or parenchymal lung disease. The changes observed were costophrenic angle blunting in the absence of pleural effusion (Nos. 4 and 23), lingular scarring (No. 17), and possible increase of the interstitial markings (No. 11). DISCUSSION This study demonstrates a high incidence of airway obstruction in the absence of restrictive defects after an acute 5-month exposure to chrysotile asbestos. The data given in Table 7 show that 17 of 23 men (74%) had airflow obstruction demonstrated at either the initial or follow-up study. AH but two of these had their obstruction documented by more than one test. Also documented in Table 7 are the interrelationships among the presence of airway obstruction, the intensity of asbestos exposure, and the incidence of other potential causes of obstruction in this group, namely, cigarette smoking and intrinsic pulmonary disease. In six (35%) of those men with obstruction no possible cause other than asbestos expo sure could be identified. Laboratory investigation by Burrows et al. (1977) and clinical observations suggest that less than 20 pack-years of smoking would rarely give rise to airflow obstruction. Using this criterion, 12 (71%) of the subjects in this study would be left with asbestos exposure as the probable major determinant of their airway obstruction. No obvious correlation exists between the intensity of asbestos ex posure and the occurrence of obstruction (Table 7). However, it must be recog nized that the estimates of intensity of exposure are very crude. Finally, since the 18-0000540 L Change* (CV/VC%) 1.98 -2.72 13.45 0.91 3.14 27.25 -14.62 1.50 1.81 2.18 10.47 10.23 0.64 6.98 4.45 6.80 I Phrenic angle scarring (No. i the absence sbestos. The obstruction >ese had their 0 Table 7 are 1 intensity of bstmetion in ease. 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E 2 <1a uuuvuvvttuuuvwuuQuOvuOOO i >s + +++ + I I + I ++++ I X III ++ + ++ I + ++ I I ++ M s: o ab TABLE 7 t o Sm o k in g H is t o r y , Pu lm o n a r y D isease, an d 2 Z2i--Z jjj'-Z2 ---: ^;s2z^c2 2 " z~ z~ Z " "Z :~zz~ z~ ~ z z zz 3t if Ux2 x: >1 <o -5 b IS V) 5z - z z z iz 2z z z aj z z ;Z I5ZZ.^ Z -- Z -- -- Z z z z z - z z z z z. ;z z z z z 2; z z z z z ; z z z zz z z z z i < i i i i i a2 iti 020 -- vi -- 0C**r*r-r >e *E <a ? uXjuXi 'O Sw* r--UX is uK 3 iO 8 '3 il: fi --M C w V Jj ff S 9 2 8- ^O 2a, 3a5 S 2-3 u 36 a .S >* t e il 2 I. Si il *= HyOi ^i*; i -2 a-a J3 JS5 3 av J; f &<J **2 oaE -eVc euO o u ? u 2 x XZ 5i e t355-s-x S*- 5 jt . xS s s .1 i 1 11 .>2 * ag -+ S 3 sX a5o s .a a3 a " 9 6 > < < i- < H u pulmons sureme r pliance. small pe The fi doin et i tion anc another in revie' of patie: cases. E niack ( McCau: fibrosis can be chrysot ways a' invests worker was no higher Of tl fall in . was nc that a abnorr The not sui Such d Thefe asbest Sine dard, stands asbesi risk d expos monii The Radiol' radiogi his rei Divisic technu t GG10G1 I r4J W UX ii s; S5 J2S I <s 3o i* *2 U= -Oc wS H 3-9 a i * ^T+ o-u* e--TJ ilC 3 Si E s5 -* UKJ <C ACUTE ASBESTOS EXPOSURE AND LUNG FUNCTION 371 pulmonary function test abnormalities observed most commonly were in the mea surements of the FF2s-tj<*. closing volume, and frequency dependence of com pliance, it seems likely that the site of airflow obstruction in this group is in the small peripheral airways. The finding of airflow obstruction is consistent with other published data. Jodoin et al. (1971) reported on the early effects of asbestos exposure on lung func tion and state that their findings support the possibility that asbestos dust is another cause of obstructive disease of the small airways. Becklake et al. (1976), in reviewing the published pulmonary function data obtained during the evaluation of patients with asbestosis, have suggested airflow obstruction may occur in some cases. Decreased airway conductance has been documented by Ostrow and Cherniack (1973) in interstitial lung diseases of other etiologies. Hourihane and McCaughey (1966) reported that the basic lesion in asbestosis is a peribronchial fibrosis which obliterates surrounding alveoli. These clinical and pathological data can be correlated with the findings of Peress et al. (1976), suggesting that chrysotile asbestos dust, representative of environmental dust, had the small air ways as one of the target sites as based upon closing volume data. Although other investigators (Murphy et al.. 1972) have shown in a study population of shipyard workers exposed to low concentrations of asbestos fiber that airflow obstruction was no more common than a matched control population, it is not clear what a higher dose would do. Of the 1(T men who had either arterial hypoxemia at rest or an exercise-induced fall in arterial PaO*, all but one had airflow obstruction. Furthermore, the DLCO was normal in all subjects in whom it was measured. Thus, there is no evidence that a defect in alveolar capillary gas diffusion played a role in the gas exchange abnormalities observed. The absence of any evidence of a restrictive defect in this group of subjects is not surprising when one considers the short interval between exposure and study. Such defects occur when there is pathologic and/or radiologic evidence of fibrosis. The few radiographic abnormalities noted in this study could not be related to the asbestos exposure. Since the exposure encountered by these men probably exceeded OSHA stan dard, we cannot predict the effects of an acute exposure that is less than the standard level. The OSHA standard is, however, intended as a protection against asbestosis and not necessarily malignancy. We would expect that these men may risk development of neoplastic disease in the future. We conclude that acute exposure to chrysotile asbestos dust causes airflow obstruction as early as 1.5 months after exposure. ACKNOWLEDGMENTS The authors wish to express their appreciation to Dr. John Armstrong, M.D.. Associate Professor of Radiology, University of Utah College of Medicine, Sait Lake City, Utah for interpreting the chest radiographs; Alan G. Barbour, M.D., Bureau of Disease Prevention. Utah State Division of Health for his referral of the workers studied; Mr. Jeff Throckmorton, Public Health Engineer, Utah State Division of Health for conducting the air sampling at the construction site; Ms. Angela Devito for her technical assistance; and Ms. Barbara Parker and Ms. Polly Detton for typing the manuscript. 18-0000543 nn i np \j x i/ 1/ kt 372 HARLESS, WATANABE, AND RENZETTI REFERENCES Becklake, M. R. (1976). 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