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AMERICAN JOURNAL OF INDUSTRIAL MEDICINE 30 :596-600 (1996)

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J0,~6238Pulmonary Fibrosis in a Carpenter WithLong-Lasting Exposure to Fiberglass

Toru Takahashi, MD, Mitsuru Munakata, MD, PhD, Hiroyuki Takekawa, MD,Yukihiko Homma, MD, PhD, and Yoshikazu Kawakami, MD . PhD

A 56.year-old male carpenter had a histon,of glass frber inhalation for 4l years n•ithout accprotective device. His chest radiograph showed small nodular opacities in lou•er lung fieldsand multiple e.tisric lesions and low attenuation areas in upper lung fields. Light and polar-izing microscopic examinations of his transbronchial lung biopsy .rpecimen revealed mildinterstitial fibrosis and mononuclear cell infiltration in alveolar walls without birefringentsubstances . However, widespread depositions of small glass fibers (<2 .5 ltm in length and0.3 Nrn in diameter) were detected by analytical electron microscopy, which suggested theirpossible contribution to the development of his pulmonary fibrosis . ® ro96, wile~-tasr. tnr.

KEY WORDS: glass fiber, inorganic dust, pulmonary jrbrosis, analytical electron micros-copy

INTRODUCTION

Recently, asbestos fibers were reported to have carci-nogenicity and fibrogenicity related to their structuralshape. This finding promoted the search for substitutes forinsulation work, and fiberglass is now often used . Althoughthe fragmentation of the material also results in fiber parti-cles, animal experiments suggest that fiberglass is a rela-tively inert material with no carcinogenic or fibrogenicproperties. We describe a patient with pulmonary fibrosiswho was exposed to fiberglass for 41 years. In a lung biopsyspecimen, the pulmonary parenchyma contained a largeamount of inorganic fibers, identified by electron micros-copy (EM) and analytical electron microscopy (AEM) .

CASE REPORT

A 56-year-old man was admitted to Hokkaido Univer-sity Hospital in December 1992 for the further investigation

Fvst Depar4nent of Medicine (T.T ., M.M ., H.T ., Y .K) and Medcal Admkidatra-flan CenOn (Y.H.), sdaol of Medicine, Hokkaitlo Utirersltr, Sapporo, Japan .

Address repriM requests to Toru TakahasAl, FYsI Deperhnent of MetAdne,School of Medidne, HoMkaido Ikeversity, N-1 s . W-7 . Kitaku, Sapporo 060. Japae.

Accepted for puhlicetian March 6 . 1996 .

of abnormal lung shadows and dyspnea on exertion . Hispast history included two previously treated episodes ofgastric ulcer. During 41 years as a carpenter, he had beenengaged in packing fiberglass into wall and roof spaces forthermal insulation. He had never used a dust mask and hadbeen inhaling a large amount of dust consisting of fiberglassas evidenced by glass fiber particles remaining in the mouthand nose after the daily work. He smoked 20 cigarettesdaily for 36 years. Chest auscultation revealed no rates ex-cept for a decreased respiratory sound over the upper lungsbilaterally . The remainder of the physical examination wasunremarkable . The chest radiograph on admission (Fig . 1)showed linear and ring shadows in whole lungs, pleuraladhesions with calcification in the upper lung fields, smallnodular shadows in the bilateral lower lung fields, and ir-regular diaphragm margins. A computed tomograph (CT) ofthe chest showed small nodular opacities spread throughoutthe lower lung fields (Fig . 2) . In the upper lung fields,multiple cystic lesions and low attenuation areas, suggestingcentrilobular emphysema, were recognized . Routine labo-ratory data revealed an increased erythrocyte sedimentationrate (49 mmlhr) but normal hematologic. hepatic, and renalfunctions. Serological examination showed no abnortnalitryin serum protein olectrophoresis and immunoglobulins . Theserum angiotensin-converting enzyme (ACE) level was nor .mal (7.8 mgldl). Autoimmune antibodies. including antinu-clear, anti-DNA, anti-SS-A, anti-SS-B, and Scl-70 antibod-

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Pulmonary Fibrosis With Fiberglass Exposure 597

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FIGURE 1 . Chest radiograph an adndssloq ahowNp Maear and rYq va0ona Inwhole lungs and small nodular sAadows n UYetersl bwer lag flNda.

FIGURE 2 Chest CT scan slqwng small nodular opacBies tNaughad lower luq fields aad muIBpb tyatic lesions aad

law attenuation areas, suggesgng centrilabular emphysema, in upper luup fxdds .


598 Takahashi et al .

FIGURE 3 . L'ght mlcroscoplc fmOwqe of TBLB specimen fr°m ryht 510, dqwpg nmapedfic lhiduning of elreolar septa

vritft mononuclear cells InfiltraUon .

ies, were all negative . Pulmonary functions were VC 3 .16 L(84% of predicted); FEVI 2.78 L (86%) ; FEVI/FVC 88% ;FRC3.8L(111%);TLC5.3L(89%);RV2.2L(112%);DLCO 11 .2 mVmin/mm Hg (53%) ; and DLCONA 2 .3 ml/minlmm Hg/L (48%) . Arterial blood gas analysis duringroom air breathing showed pH 7 .389; P02 87 mm Hg ; PcoZ43.1 mm Hg.

Transbronchial lung biopsy (TBLB) was performed atthe right basal segments (S° and S'°); microscopic exami-nation showed mild fibrosis with infiltration of lymphoidcells in the alveolar septa . No foreign body depositions orgranulations, such as giant cells or macrophages, could berecognized (Fig . 3) . With a polarizing microscope, no bire-fringent substance could be detected. However, EM exam-ination showed many nonstructural substances 0.5-2.5 pmin length and 0.3 µm in diameter (Fig . 4, top). Qualitativeanalysis of the substances with an AEM demonstrated Si, Aland Ti (Fig. 4, bottom), which are identical to the content ofglass fibers . Tho number of glass fibers was semiquantifiedaccording to the absestos fibers classification reported pre-

viously [Kohyama et al., 1993: Morinaga ct al., 1989] . Anaverage of 20 fibers in every two or three fields, randomlysampled from the entire specimen area under low magnifi-cation in EM, were found, and the number of glass fiberswere classified between grades ++ and +++ .

DISCUSSION

Fiberglass has been used increasingly for thermal andacoustic insulation, as well as in textiles and for plasticreinforcement . Recently, its use has expanded further, as itis substituted far asbestos minerals. In contrast to asbestosminerals, some researchers reported that fiberglass hasmuch less carcinogenicity and fibrogenicity . In large num-bers of reports, workers in the glass fiber plants have beenrecognized to have no demonstrable clinical and roentoge-nological pulmonary manifestations related to fiberglass ex-posures [Nasr et al., 19711. A cohon study of 6,586 workersin glass fiber production mills indicated no excesses of ma-lignant or nonmalignant respiratory disease [Morgan and


Pulmonary Fibrosis With Fiberglass Exposure 599

FIGI/RE 4 . EM 8ndnps of TBL8 spedrnens, slowin8 widespread rwnstrucluralfibers, <2.5 pm In length and 0 .3 µm h diameter (top) . OualitatWe analysis ofthe nonsbuc[wal fiber ueNp AEM, qtowinp the peaks of Si . AI . and Ti. The peakof Cu is derived from the tissue stand . Vertical axls shows the point twxnherswithin a t00-min point analygis (boCom) .

Kaplan, 19811 . However, in a recent review of the reportsrelating to carcinogenicity of fiberglass . Infante and asso-ciates [ 19941 suggested that carcinogenicity of fibrous glassis as potent as that of asbestos Fibers . In regard to chronicpulmonary diseases, based on comparison of dose-responsedata for certain asbestos pooled data and pooled U .S ./Eu-ropean man-made mineral fiber (MMMF) data, Goldsmith[ 1986] reported that MMMF appears to be at least as toxicas asbestos . [t was suggested that the important risk factorsare duration of exposure, cumulative exposure, fiber char-acteristics, exposure to other pollutants and smoking [Mer-chant, 1990] . In particular, the size of the fibers, whichpossibly determines the levels of exposure-because smallfibers deposit and large fibers are finally cleared-is spec-ulated to be an important factor in pulmonary injury. Work-ers involved in the production of smaller diameter (<I µm)glass wool fibers are known to have an increased risk ofsmall opacities on chest roentgenograms [Weill et al .,1983) .

From the results of the chest roentgenogram . CT scan,serum examination, and histology for TBLB specimens, this

patient was considered to have pulmonary fibrosis not dueto collagen disease, granulomatous lung disease, or hyper-sensitivity pneumonitis. Multiple cystic lesions and low at-tenuation areas and pleural thickening on his chest roent-genogram and CT scan suggested the coexistence ofpulmonary emphysema derived from long-term smokinghabits and healed pulmonary tuberculosis . He had a historyof long-term exposure to fiberglasses for 41 years withoutprotection. Light microscopy of his lung biopsy specimens,showed mild fibrosis and lymphocyte infiltration in alveolarsepta, but no birefringent material was detected . The EMfindings showed large amounts of inorganic compoundssurrounded by thickened elastic fibers. Mineral analysis ofthese compounds by AEM suggested glass fibers . The sizesof the glass particles were very small (0.5-2.5 pm in lengthand 0.3 pm in diameter). These findings suggest the possi-ble contribution of inhaled glass fiber particles to the de-velopment of pulmonary fibrosis. The coexistence of pul-monary fibrosis and emphysema in this patient who had aheavy smoking history may agree with previous reports sug-gesting that the same lung injury might result in either fi-brosis or emphysema, depending on connective tissue syn-thesis during the healing phase [Niewoehner and Hoidal,1982; Hiwatari et al ., 19931 . In this context, it seems pos-sible that his heavy smoking history, accompanied by heavyexposure to glass fiber particles, might contribute not onlyto the development of his pulmonary emphysema, but alsohis pulmonary fibrosis.

In this case, pulmonary deposition of glass fibers wasnot detected by either light microscope or polarizing micro-scope. The deposition and identification of glass fibers be-came possible only after the application of EM and AEM toexamine the TBLB specimens . To obtain an insight into thepossible cause of pulmonary fibrosis of unknown etiology,the application of these methods, even for small biopsyspecimens, is recommended .

REFERENCES

Goldsmith JR (1986): Comparative epidemiology of men exposed to as-hestus and man-made mineral fibers . Am 1 Ind Mad 10:543-552 .

Hiwatari N, Shimura s, Takishima T(1993): Pulmonary emphysema fnl-lowed by pulmonary fibrosis of undetennined cause. Respiration 60 :354-358.

Infame PF, Schumn LD, Dement J. Huff 1(1994): Fibrous glass andcancer . Am J Ind Med 26:559-584.

Kohyama N, Kyono H. Yokoyama K. Sera Y (1993): Evaluation of low-level asbestos exposure by aransbroncNal lung biopsy with analytical ekc-tron mieroscopy. J Elecorot Mic~ 42:315-327 .

Merchant JA (1990) : Human epidemiology: A review of fiber type andcharacteristics in the development of malignant and nonmalignant disease .Environ Heaah Perspecr 88287-293.

Morgan RW, Kaplan SD (1981) : Murtality study of fibrous glass produo-tion workera . Arch Fnviron Health 36: t79-183 .


600 Takahashi et al.

Morinaga K . Kohyama N. Yokoyama K. Yasui Y . Hara 1 . Sasaki M . Niewochner DE, Hoidal JR (1982): Lung fibrosis and emphysema: Diver.Suzuki,Y . Sera Y(1989) : Asbestos fibre comem of lung with mesothelio- gent responses m a common injury? Science 217 :359-360.mas in Osaka, Japan : A preliminary mpoe. In "Nonoccupational Exposureto Mineral Fibres." IARC Sci Publ . No . 90. Lyons : IARC, pp 438-443 . Weill H. Hughes 1M, Hammad YY. Glindmeyer WH Ill . Sharon G. Jones

Nasr ANM, Diuhek T, Schohens PA (1971) : The prevalence of radio- RN (1983); Respiratory health in workers exposed to man•made vitreous

graphip abnormalities in the chest of fiber glass workers . J Occup Med fibers . Am Rev Resp'v Dis 128 :104-112.

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