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DIVISION OF PULMONARY AND CRITICAL CARE MEDICINE August 30, 1 L nivcrsifv of Arkansas for Medical Sciences Department of Industrial Relations Division of Industrial Accidents Information and Assistance Bureau ATTENTION: Ms. Diane Bustillos 525 Golden Gate Avenue San Francisco, CA 94102 RE: r REDACTED Dear Ms. Bustillos: ,501) im as os 661-5525 was seen in our Chest Clinic on June 12, 1981 for evaluation of asbestosis as requested in your letter of March 26, 1981. related that he was first exposed to asbestos beginning in 1948 when he began working as a journeyman 3agger. The following year, he became a mechanic and remained in that occupation for 14 years during which time he had no asbestos exposure. From 1951 through 1956 he returned to his previous job as a lagger,continuing the same kind of exposure he had had previously. He joined Dupont in 1956, and had heavy^ primary exposure To asbestos until 1967. About two years agoflflfc --fa began having exertional dyspnea, which has been slowly progressing. Currently he states that he is able to ascend one flight of stairs, shovel dirt about five minutes, or walk about two blocks before being limited by dyspnea. He described his dyspnea as a feeling that he can move air appropriately, but "cannot get enough oxygen". He stated that his dyspnea resolved after about half hour of rest. He denied cough, sputum production, hemoptysis, and wheezing. He smoked approximately two packages of cigarettes daily for 30 years, stopping two years ago when he was informed of the high risk of malignancy due to smoking and asbestos exposure together. He-denied allergies. He had a past history of peptic ulcer disease, for-which he had taken cimetidine, but he was taking no medications at the time that he was seen. Physical examination revealed a well-developed, well-nourished white man who appeared to be his stated age and was in no distress. Examination of the chest revealed no adventitious sounds, normal breath sounds, and no abnormalities on percussion. The liver spanned 10 cenimeters to percussion, and there was mild right upper quadrant tenderness. The abdomen was otherwise normal. There was no clubbing of the fingers, cyanosis, nicotine staining of the fingers, or edema. There were no other abnormalities noted on physical examination. DUP 0947275 PA and lateral chest x-rays revealed an extensive area of thickened pleura on the,left, which had slightly increased in size in comparison with an x-ray made in 1979. There was a smalj approximately 14 x 4 - centimeter area of pleural thickening on the`right, and calcification of the diaphragm was visible on the right side. Resting arterial blood gases were Pa02 of 87 mmHg, PaC02 of 34 mmHg and pH of 7.41. Spirometry and lung volumes done by helium dilution are shown on the enclosed report. The lung volumes were normal; the FEVi/FVC ratio was slightly decreased to 73%. The studies were interpreted as showing a borderline obstructive defect. An electrocardiogram demonstrates incomplete right bundle branch block without other abnormalities. jal Opportunity Employer DU 038569 DIVISION OF PULMONARY AND CRITICAL CARE MEDICINE RE: Page 2 August 30, 1981 REDACTED An exercise test was performed on June 19, 1981 at Little Rock Veterans Administration Hospital by Dr. McKendree E. McNabb, a member of this Division. ^^OD^fthe report is enclosed. The pertinent findings were that ^^BHH^had normal cardiopulmonary function, including arterial oxygen saturation during exercise, and that he had a normal tolerance to exercise. During the exercise test he reached only 53% of the maximum breathing capacity predicted on the basis of the FEVi. It is notable that during initial steady state testing at low work 1 rates he had abnormally high ventilation, and that during subsequent testing at the same work rate he had normal ventilation. This suggests a phychogenic etiology for the initial hyperventilation. A single breath carbon monoxide diffusing capacity was performed at Little Rock Veterans Administration Hospital on June 19, 1981. The results was 26 ml/min/mmHg, the predicted value being 30. This is considered to be a normal value. Arterial blood gases drawn within two seconds of cessation of maximal exercise were as follows: Pa02 97 mmHg, PaC02 34 mmHg, and pH 7.41. The change from the resting blood gases represents a normal response to exercise. On the basis of his chest x-ray findings and his history, it is clear beyond any reasonable doubt thathas asbestosis. The slight decrease in FEVi/FVC ratio noted is more likely related to his long history of cigarette smoking than to his asbestosis exposure. In any case, that degree of obstructive spirometric defect would not be expected to result in disability or, indeed, in significant symptoms. I believe that WPWflPPil experiences the symptoms he describes, and \ that his life is significantly altered by them. Thorough evaluation \ does not reveal a physiologic basis. I believe that thev'~are TaratTv \ 3hychogenic in origin. anff~are~related^To^lWWWw,~Ts~ reaTTz3tfgrTthat ie nas asbestosis which he TTnflr~extremelv threatening. I think ni"s symptoms are probably increased by his relative~Tnactivities causing deconditioning, which, in turn, increases his symptoms. In summary, I I think his symptoms are due to his asbestos exposure and the resulting/ asbestosis, although I think the mechanism of symptom production is / psychologic, not physiologic. / I would recommend follow up examinations in the future, to primarily consist of chest x-ray's. Obviously, the reason for this is that mesotheleoma cannot be completely excluded ir> any point in time, and the only practical way to detect its occurrence would be to note a change on serial chest x-rays. In addition, it provides a means for detection of bronchogenic carcinoma, for which r is at increased risk. The only treatment other than tne follow up examinations I would recommend would be an effort to overcome the respiratory symptoms probably. I should think that the best way to approach this would be DUP 0947276 DU 038570 DIVISION OF PULMONARY AND CRITICAL CARE MEDICINE RE: Page 3 August 30, 1981 REDACTED through an exercise program combined with some incidential supportive therapy by a sympathetic physician. I have discussed this withflljiiifc is skeptical that he can be helped by an exercise program, out i have urged him to undertake one. It seems very likely that his exposure to asbestos between 1957 and 1967 was most significant in causing his asbestosis, since it was much larger in duration and degree than his previous exposure. If this does not adequately answer the questions of interest to you, please let me know. Sincerely yours. Assistant Professor of Medicine FJW/bas Enclosures cc: Hospital Chart Chest Clinic Corr. DUP 0947277 DU 038571 U , W.gt CLINICAL KECORD i'i. ruNcnoNS IFAOM. 6 >. ** II IJHl J CONSULTATION SHEET MQUESI _ w>4, %*, W EtfMi/f) OATS O/f NfcOOC/f'TT*V lxlkcisi: I'iiysrm.ocy i.v. uion: . luiuli'a c I. r l romeclijii i ra I cycle ei gome lei Inin Melaliolic Measurement Carl Siiuer 'Ui v .ms meter Mi ilaw mass sped romel or _ liew I ct i-I'a. k.ird ear oximeter Hew U lt-l'a.'kard Jigital pneumuiacli i'k u i:ri;m : '-_Aviuaicti valve beckman vaive s __ Mud! f ied Otia-MeKerrun valve Neoprene bags by ll-P _____ Mine Safely monoxolyzer ,. i'1' IV.Ileal a I work rates to maximum to ieranee; increments were melets per minute, work race was incremental eaeli minute. ___Sulim..a imum work rate, 6 minutes each _______ -00 J0O (.v 4U0 500 _______ 600 _ "700 800 1 "_900 I'.M'ii.Nr cui.'!>i:kai'ii)H:' 100 Kilograin- Good SUiiJCCl 1VL OliStiUVATION: < week _________chest pain __ weak Other__________________ ___ shortness of breath _dizzy COMMLNTS : Initially submaximal "constarit workr'ate"t'eTts^of dliu and" 400 kilcgT'ammuters per minute were performed. Observations made during the 5th and 6th minutes of these testSjWith an established physiologic steady state^revealed excessive ventilation, excessive respiratory frequency and abnormally low respiratory exchange ratio. Cardiac frequency was normal. The low respiratory exchange ratio was consistent with excessive ventilation and partial depletion of body C02 stores prior to initiation of exercise. Just before incrementing the workiate to determine maximum 02 consumption the patient was again 3sked to pedal 4 minutes at 200 kg-m/min followed by a 5th minute at 300 kg-m/min and a 6th minute at 400 kg-m/min. Of interest is that ventilation and breathing frequency fell significantly compared to that seen during the initial jiubmaximal testing at 200 kg-m/min. This suggests psychogenic rather than physiologic mediation of the excessive ventilation. Ventilation and respiratory frequency were increased relative to oxygen consumptio and tidal volume wan abnormally redu-'eci The heart rate was normally matched to oxygen consumption. Arterial tlxod ox 'pen saturation as estimated by ear oximetry was 96i resting and 96 to 97% throughout exei/ise. This was a normal response. He achieve an oxygen consumption of 2000 n.l ; s nm-ite (the predicted value is 2,568 with a normal range of 1,768 to 3,368 ml per r.inui... He expended only 53% of his breathing capacity (35 X 3,`jj = 136.5 liters per nunut- ) and 84% of cardiac chronotropic capacity. An arterial blood gas drawn withi ) 2 seconds of cessation of maximal exercise revealed no metabolic I'viNATuNl ANU TM-C M/hCLMPRrrr lATlLNT * IwCHTlA'Is. acidemia, PaO-> 97' PTCC' 4 nH 7.41^. bicarbonate 21. ^ . ~ (Conf an t*vr*9 *ta*) DA 'd. lOANTiriCATtON NO ONOANIZATION k munabb . M. D. 1 ()>p4o t tntJJJ* |'A. 4*f. ! e '24/81 Nn.m ,*t Aft, PULMONARY HtailTEN NO FUNCTION LABORATORY 1 WAND f3 '7i. C0NUIL1ATIQN SHUT Sun*4fd linn SU ill-iOo ac TJ O10 (J f A I V I * fc I I 4 I IP I 1 I $ I I t V*!-SX^XAV^v.sssy.ViV-y.v.,.w.v. vav.ViV.wVvV .w.w.vvy.v.v.v.sv- v -v| r~0o34 DU 038572 Tno fjcient indicated that tiredness of his legs kept him from co:.-.main i tiiu incremental exercise load. This is consistent with lack of ^pecifi ttairrinq and conditioning for the task of pedaling a cycle agur,.-: 1:. 'teasing resistance. In-.; ro,.-,ii.' : 1) Normal tolerance of heart and lungs to exercise i.e. normal aerobic capacity . While neurogenic stimuli from a diseased lung may cause ovessivc ventilation the tendency demonstrated here is more consistent with psychogenic hyperventilation. MCKENDREE E. MCNABB, M.D. Medical Director I DUP 0947279 aMMUU3KS DU 038573 Vi N ilW AIMING Tl DAI ' I; , jM:" 11 1 (l.M li.lll VUUIMI \ " a- ll. 1 . in i. / .1.1 n ! in i, i< i n IKI'ii | REDACTED. r' 7 0 C' /6- d> / j750 ^-70 f/od \%L> \ _ d_Zs= 1< h 5oO AV. / .73 / 3/, A SQ 7 |331/.- 9 ' ?5Tc) 9.5* ;fSZ> : O0 0 \ </7 0 \fWd b 70 . Vfd 770 . SOC /st)' 7/o jsAi o srs? i ,f fC/\ i; 031. 0-23 ' 0.23 4 oo jys \^r/.9,mp \ -,<k*Q. -dOO \(?oo ' 3f l\ l3.i '//- /vi'c' . $:so /<[ r IS7.3 ./A06 Ji-iO. U2. \70d i 32>- oi 7i: Ol/Aad/3>_9l //70 /*o i .t. t- > . - tod ;/7 ^'3_l/ipOt /6 761 /3/ .Vv;y |3`/3.. ^.0 3-7 zvO 0. 177 V \/MD ~r \/g/7>_J#T 4- i. J//<?o5 _!77../_ 3f--7.-n70^.Q& e-Zz &2l oM' 0-?sr 0.9/ Q,2. 0-95 'Ration i? o. L.OgUCTAKE MI RATION @ 1.00 L.OgUPTAKE I'A11 ENT MILD1CTED If.It 1.0 3.9of/, d yiTlUUOU g 1.50 L.{^UPTAKE ftTIAL VOLUME $ VENTILATION 30 l/min >: VI KA71. (? 0. L.O,UHAKE "tA*< NAT 1.0, .O^UPf/uC HEART kAT E(? ) , b i. ,0-pUPTAKE 'Sa Zr.llO. '2- tO l. i o.z. :-i7.. J 2," :J7L . Zle.btl.K' Aalltiss LB&12J- /O^LtSJ MlxltjA. C7 cD O 2 o0N5j .. * w ' n 'M/7/d. 0ArE /f/ ,i A* m 7& Ti i*, a fti-u i > jT> iTt i i i i I 'iiTv>Ti S< i * i.o fki t t *7 * >. `O** ** < * <,<*','< / I| 4 t tt . <4* 4. 1. t, * . - * 1' .' I I DU 038574 tur Oximetry ifatu Slieet , I/*/*: O.i te .it .'.suul w-..n;i iif tlii. Ml1 4 7 JO IA 11 cm il i i-,, lur eu. Ii minute. 0 i rii i.. i i - it 11 l 1 ii n i,. I . ,i. . i:, ioniiil_ Wuiktate Test:. 1 ncrenmntal 'lest kg--in/nitti - Rest " -- kg-in/mi n X Rest 'll ilUte 0 1 2 3 k 5 6 7 8 9 10 11 12 73 1 2 3 kg --rn/m in X Rest /< /i h oBo 4-uo stzvl) 9 (c 9<r to 9 Cc to to to L'oLiQ. 100 to ^oo /OoO - TToU Reac Rest . Rest to 97 392. 32. 77 J?2`J ?7- to co "0 O CO ho CO DU 038575 PULMONARY FUNCTIONS wncvs --- ---- .. _ 6-/i-Sji ' ! 1U--i|--3.qj * (cC*) ' --!--5-9----f-e-- \,--C--io--?--) . > *_7 / *< , _ _ _ _PRED. DATE 3.0 1 KV (L) \5.0t1! FRC (L) TLC (L) ___ I 1'1 ___ ___ PREDICT:--. REDi ^CTED ?1r). s 3.03 ! *! -3.0,0 (%)RV/TLC o 9o i 1 DLC0sb * (ml/min/mmCO) ! 30 ii______ XC t>c o u'i 'yxL CyflUAKoJC -XS "A? < In patients with anemia or polycythemia DlCO should be corrected, i.e. uncorrected t>i,CO ,, corrected DLCO (Am. Rev. Resp. Dis. 1V70,102,9651 .06at>S X Hgb (gm%) j i! PATIENT EFFORT iftOCaalstaQt INTERPRETATION: ABNORMAL BORDERLINE IMPAIRMENT: OBSTRUCTIVE RESTRICTIVE BOTH SEVERITY: MINI MAI, SLICIIT MODERATE MARKED comparison - previous studies: Ho previous teats. SEVERE lATE TIME Wk_ ~ M-3" i <k ~Sr Pa02 (mmHg) PaC02 (wnHg) pH H+ hco3 (NM/L) (MaQ/L) V 34- 74/ 2J. ,, J _ me. COMMENTS * f&cm Air y Tmnedta.ieJu after maxima/ ex ere) VAF 10-17(598) Feb. 1980 DUP DU 038576 VAKI 00 1 ut.'KK :ui i si is Uv-I.i (II III, 200 > ,IT 1 \h 1 M J M Ml . him i ' .01 | IT |' ` III 1 i Cl . 7(1(1 ':r-T i hvy i -.''ii >n< i *.\j>' > ! ,\i ai i ll ^ Uivt rv 'i In .A /min. I.NI 1 l..\! ION ' KK<U'I '.('V 1 ! DAI. V'lH.l'MI ; i/i.... r -- | [K11 ..in. - I .i i. i 1 | 0. W 9-J 2*) 18 1 U) l-ni.' .1: mi l f(( REDAC'TED 73^ 3V3 A un 1 .'(in 1 1 '<() 4-oo /oo D ?/0 (oo K.00 KiOO c/<3 33 O.V'i 1 10 13 All 1600 0/oo 69-7 9^0 1 .00 L2`> VI 20 2100 ------------- 4 IpAjUe AOL SZ)L a?z X} 4.7 3/. 9 77 L t DU 038577