Monday, 28 February 2011 23:47

Respiratory System: The Variety of Pneumoconioses

Rate this item
(1 Vote)

This article is devoted to a discussion of pneumoconioses related to a variety of specific non-fibrous substances; exposures to these dusts are not covered elsewhere in this volume. For each material capable of engendering a pneumoconiosis upon exposure, a brief discussion of the mineralogy and commercial importance is followed by information related to the lung health of exposed workers.

Aluminium

Aluminium is a light metal with many commercial uses in both its metallic and combined states. (Abramson et al. 1989; Kilburn and Warshaw 1992; Kongerud et al. 1994.) Aluminium-containing ores, primarily bauxite and cryolite, consist of combinations of the metal with oxygen, fluorine and iron. Silica contamination of the ores is common. Alumina (Al2O3) is extracted from bauxite, and may be processed for use as an abrasive or as a catalyst. Metallic aluminium is obtained from alumina by electrolytic reduction in the presence of fluoride. Electrolysis of the mixture is carried out by using carbon electrodes at a temperature of about 1,000°C in cells known as pots. The metallic aluminium is then drawn off for casting. Dust, fume and gas exposures in pot rooms, including carbon, alumina, fluorides, sulphur dioxide, carbon monoxide and aromatic hydrocarbons, are accentuated during crust breaking and other maintenance operations. Numerous products are manufactured from aluminium plate, flake, granules and castings—resulting in extensive potential for occupational exposures. Metallic aluminium and its alloys find use in the aircraft, boat and automobile industries, in the manufacture of containers and of electrical and mechanical devices, as well as in a variety of construction and structural applications. Small aluminium particles are used in paints, explosives and incendiary devices. To maintain particle separation, mineral oils or stearin are added; increased lung toxicity of aluminium flakes has been associated with the use of mineral oil.

Lung health

Inhalation of aluminium-containing dusts and fumes may occur in workers involved in the mining, extraction, processing, fabrication and end-use of aluminium-containing materials. Pulmonary fibrosis, resulting in symptoms and radiographic findings, has been described in workers with several differing exposures to aluminium-containing substances. Shaver’s disease is a severe pneumoconiosis described among workers involved in the manufacture of alumina abrasives. A number of deaths from the condition have been reported. The upper lobes of the lung are most often affected and the occurrence of pneumothorax is a frequent complication. High levels of silicon dioxide have been found in the pot room environment as well as in workers’ lungs at autopsy, suggesting silica as a potential contributor to the clinical picture in Shaver’s disease. High concentrations of aluminium oxide particulate have also been observed. Lung pathology may show blebs and bullae, and pleural thickening is seen occasionally. The fibrosis is diffuse, with areas of inflammation in the lungs and associated lymph nodes.

Aluminium powders are used in making explosives, and there have been a number of reports of a severe and progressive fibrosis in workers involved in this process. Lung involvement has also occasionally been described in workers employed in the welding or polishing of aluminium, and in bagging cat litter containing aluminium silicate (alunite). However, there has been considerable variation in the reporting of lung diseases in relation to exposures to aluminium. Epidemiological studies of workers exposed to aluminium reduction have generally shown low prevalence of pneumoconiotic changes and slight mean reductions in ventilatory lung function. In various work environments, alumina compounds can occur in several forms, and in animal studies these forms appear to have differing lung toxicities. Silica and other mixed dusts may also contribute to this varying toxicity, as may the materials used to coat the aluminium particles. One worker, who developed a granulomatous lung disease after exposure to oxides and metallic aluminium, showed transformation of his blood lymphocytes upon exposure to aluminium salts, suggesting that immunologic factors might play a role.

An asthmatic syndrome has frequently been noted among workers exposed to fumes in aluminium reduction pot rooms. Fluorides found in the pot room environment have been implicated, although the specific agent or agents associated with the asthmatic syndrome has not been determined. As with other occupational asthmas, symptoms are often delayed 4 to 12 hours after exposure, and include cough, dyspnoea, chest tightness and wheeze. An immediate reaction may also be noted. Atopy and a family history of asthma do not appear to be risk factors for development of pot room asthma. After cessation of exposure, symptoms may be expected to disappear in most cases, although two-thirds of the affected workers show persistent non-specific bronchial responsiveness and, in some workers, symptoms and airway hyperresponsiveness continue for years even after exposure is terminated. The prognosis for pot room asthma appears to be best in those who are immediately removed from exposure when the asthmatic symptoms become manifest. Fixed airflow obstruction has also been associated with pot room work.

Carbon electrodes are used in the aluminium reduction process, and known human carcinogens have been identified in the pot room environment. Several mortality studies have revealed lung cancer excesses among exposed workers in this industry.

Diatomaceous Earth

Deposits of diatomaceous earth result from the accretion of skeletons of microscopic organisms. (Cooper and Jacobson 1977; Checkoway et al. 1993.) Diatomaceous earth may be utilized in foundries and in the maintenance of filters, abrasives, lubricants and explosives. Certain deposits comprise up to 90% free silica. Exposed workers may develop lung changes involving simple or complicated pneumoconiosis. The risk of death from both nonmalignant respiratory diseases and lung cancer has been related to the workers’ tenure in dusty work as well as to cumulative crystalline silica exposures during the mining and processing of diatomaceous earth.

Elemental Carbon

Aside from coal, the two common forms of elemental carbon are graphite (crystalline carbon) and carbon black. (Hanoa 1983; Petsonk et al. 1988.) Graphite is used in the manufacture of lead pencils, foundry linings, paints, electrodes, dry batteries and crucibles for metallurgical purposes. Finely ground graphite has lubricant properties. Carbon black is a partially decomposed form used in automotive tires, pigments, plastics, inks and other products. Carbon black is manufactured from fossil fuels through a variety of processes involving partial combustion and thermal decomposition.

Inhalation of carbon, as well as associated dusts, may occur during the mining and milling of natural graphite, and during the manufacture of artificial graphite. Artificial graphite is produced by the heating of coal or petroleum coke, and generally contains no free silica.

Lung health

Pneumoconiosis results from worker exposure to both natural and artificial graphite. Clinically, workers with carbon or graphite pneumoconiosis show radiographic findings similar to those for coal workers. Severe symptomatic cases with massive pulmonary fibrosis were reported in the past, particularly related to the manufacture of carbon electrodes for metallurgy, although recent reports emphasize that the materials implicated in exposures leading to this sort of condition are likely to be mixed dusts.

Gilsonite

Gilsonite, also known as uintaite, is a solidified hydrocarbon. (Keimig et al. 1987.) It occurs in veins in the western United States. Current uses include the manufacture of automotive body seam sealers, inks, paints and enamels. It is an ingredient of oil-well drilling fluids and cements; it is an additive in sand moulds in the foundry industry; it is to be found as a component of asphalt, building boards and explosives; and it is employed in the production of nuclear grade graphite. Workers exposed to gilsonite dust have reported symptoms of cough and phlegm production. Five of ninety-nine workers surveyed showed radiographic evidence of pneumoconiosis. No abnormalities in pulmonary function have been defined in relation to gilsonite dust exposures.

Gypsum

Gypsum is hydrated calcium sulphate (CaSO4·2H2O) (Oakes et al. 1982). It is used as a component of plasterboard, plaster of Paris and Portland cement. Deposits are found in several forms and are often associated with other minerals such as quartz. Pneumoconiosis has been observed in gypsum miners, and has been attributed to silica contamination. Ventilatory abnormalities have not been associated with gypsum dust exposures.

Oils and Lubricants

Liquids containing hydrocarbon oils are used as coolants, cutting oils and lubricants (Cullen et al. 1981). Vegetable oils are found in some commercial products and in a variety of foodstuffs. These oils may be aerosolized and inhaled when metals that are coated with oils are milled or machined, or if oil-containing sprays are used for purposes of cleaning or lubrication. Environmental measurements in machine shops and mills have documented airborne oil levels up to 9 mg/m3. One report implicated airborne oil exposure from the burning of animal and vegetable fats in an enclosed building.

Lung health

Workers exposed to these aerosols have occasionally been reported to develop evidence of a lipoid pneumonia, similar to that noted in patients who have aspirated mineral oil nose drops or other oily materials. The condition is associated with symptoms of cough and dyspnoea, inspiratory lung crackles, and impairments in lung function, generally mild in severity. A few cases have been reported with more extensive radiographic changes and severe lung impairments. Exposure to mineral oils has also been associated in several studies with an increased risk of respiratory tract cancers.

Portland Cement

Portland cement is made from hydrated calcium silicates, aluminium oxide, magnesium oxide, iron oxide, calcium sulphate, clay, shale and sand (Abrons et al. 1988; Yan et al. 1993). The mixture is crushed and calcined at high temperatures with the addition of gypsum. Cement finds numerous uses in road and building construction.

Lung health

Silicosis appears to be the greatest risk in cement workers, followed by a mixed dust pneumoconiosis. (In the past, asbestos was added to cement to improve its characteristics.) Abnormal chest radiographic findings, including small rounded and irregular opacities and pleural changes, have been noted. Workers have occasionally been reported to have developed pulmonary alveolar proteinosis after the inhalation of cement dust. Airflow obstructive changes have been noted in some, but not all, surveys of cement workers.

Rare Earth Metals

Rare earth metals or “lanthanides” have atomic numbers between 57 and 71. Lanthanum (atomic number 57), cerium (58), and neodymium (60) are the commonest of the group. The other elements in this group include praseodymium (59), promethium (61), samarium (62), europium (63), gadolinium (64), terbium (65), dysprosium (66), holmium (67), erbium (68), thulium (69), ytterbium (70) and lutetium (71). (Hussain, Dick and Kaplan 1980; Sabbioni, Pietra and Gaglione 1982; Vocaturo, Colombo and Zanoni 1983; Sulotto, Romano and Berra 1986; Waring and Watling 1990; Deng et al. 1991.) The rare earth elements are found naturally in monazite sand, from which they are extracted. They are used in a variety of alloy metals, as abrasives for polishing mirrors and lenses, for high-temperature ceramics, in fireworks and in cigarette lighter flints. In the electronics industry they are used in electrowelding and are to be found in various electronic components, including television phosphors, radiographic screens, lasers, microwave devices, insulators, capacitors and semiconductors.

Carbon arc lamps are used widely in the printing, photoengraving and lithography industries and were used for floodlighting, spotlighting and movie projection before the wide-scale adoption of argon and xenon lamps. The rare earth metal oxides were incorporated into the central core of carbon arc rods, where they stabilize the arc stream. Fumes which are emitted from the lamps are a mixture of gaseous and particulate material composed of approximately 65% rare earth oxides, 10% fluorides and unburnt carbon and impurities.

Lung health

Pneumoconiosis in workers exposed to rare earths has been exhibited primarily as bilateral nodular chest radiographic infiltrates. Lung pathology in cases of rare earth pneumoconiosis has been described as an interstitial fibrosis accompanied by an accumulation of fine granular dust particles, or granulomatous changes.

Variable pulmonary function impairments have been described, from restrictive to mixed restrictive-obstructive. However, the spectrum of pulmonary disease related to inhalation of rare earth elements is still to be defined, and data regarding the pattern and progression of disease and histological changes is available primarily only from a few case reports.

A neoplastic potential of the rare earth isotopes has been suggested by a case report of lung cancer, possibly related to ionizing radiation from the naturally occurring rare earth radioisotopes.

Sedimentary Compounds

Sedimentary rock deposits form through the processes of physical and chemical weathering, erosion, transport, deposition and diagenesis. These may be characterized into two broad classes: Clastics, which include mechanically deposited erosion debris, and chemical precipitates, which include carbonates, shells of organic skeletons and saline deposits. Sedimentary carbonates, sulphates and halides provide relatively pure minerals that have crystallized from concentrated solutions. Due to the high solubility of many of the sedimentary compounds, they are rapidly cleared from the lungs and are generally associated with little pulmonary pathology. In contrast, workers exposed to certain sedimentary compounds, primarily clastics, have shown pneumoconiotic changes.

Phosphates

Phosphate ore, Ca5(F,Cl)(PO4)3, is used in the production of fertilizers, dietary supplements, toothpaste, preservatives, detergents, pesticides, rodent poisons and ammunitions (Dutton et al. 1993). Extraction and processing of the ore may result in a variety of irritant exposures. Surveys of workers in phosphate mining and extraction have documented increased symptoms of cough and phlegm production, as well as radiographic evidence of pneumoconiosis, but little evidence of abnormal lung function.

Shale

Shale is a mixture of organic material composed mainly of carbon, hydrogen, oxygen, sulphur and nitrogen (Rom, Lee and Craft 1981; Seaton et al. 1981). The mineral component (kerogen) is found in the sedimentary rock called marlstone, which is of a grey-brown colour and a layered consistency. Oil shale has been used as an energy source since the 1850s in Scotland. Major deposits exist in the United States, Scotland and Estonia. Dust in the atmosphere of underground oil shale mines is of relatively fine dispersion, with up to 80% of the dust particles under 2 mm in size.

Lung health

Pneumoconiosis related to the deposition of shale dust in the lung is termed shalosis. The dust creates a granulomatous and fibrotic reaction in the lungs. This pneumoconiosis is similar clinically to coal workers’ pneumoconiosis and silicosis, and may progress to massive fibrosis even after the worker has left the industry.

Pathologic changes identified in lungs with shalosis are characterized by vascular and bronchial deformation, with irregular thickening of interalveolar and interlobular septa. In addition to interstitial fibrosis, lung specimens with shale pneumoconiosis have shown enlarged hilar shadows, related to the transport of shale dust and subsequent development of well-defined sclerotic changes in the hilar lymph nodes.

Shale workers have been found to have a prevalence of chronic bronchitis two and one-half times that of age-matched controls. The effect of shale dust exposures on lung function has not been studied systematically.

Slate

Slate is a metamorphic rock, made up of various minerals, clays and carbonaceous matter (McDermott et al. 1978). The major constituents of slate include muscovite, chlorite, calcite and quartz, along with graphite, magnetite and rutile. These have undergone metamorphosis to form a dense crystalline rock that possesses strength but is easily cleaved, characteristics which account for its economic importance. Slate is used in roofing, dimension stone, floor tile, flagging, structural shapes such as panels and window sills, blackboards, pencils, billiard tables and laboratory bench tops. Crushed slate is used in highway construction, tennis court surfaces and lightweight roofing granules.

Lung health

Pneumoconiosis has been found in a third of workers studied in the slate industry in North Wales, and in 54% of slate pencil makers in India. Various lung radiographic changes have been identified in slateworkers. Because of the high quartz content of some slates and the adjacent rock strata, slateworkers’ pneumoconiosis may have features of silicosis. The prevalence of respiratory symptoms in slateworkers is high, and the proportion of workers with symptoms increases with pneumoconiosis category, irrespective of smoking status. Diminished values of forced expiratory volume in one second (FEV1) and forced vital capacity (FVC) are associated with increasing pneumoconiosis category.

The lungs of miners exposed to slate dust reveal localized areas of perivascular and peribronchial fibrosis, extending to macule formation and extensive interstitial fibrosis. Typical lesions are fibrotic macules of variable configuration intimately associated with small pulmonary blood vessels.

Talc

Talc is composed of magnesium silicates, and is found in a variety of forms. (Vallyathan and Craighead 1981; Wegman et al. 1982; Stille and Tabershaw 1982; Wergeland, Andersen and Baerheim 1990; Gibbs, Pooley and Griffith 1992.)

Deposits of talc are frequently contaminated with other minerals, including both fibrous and non-fibrous tremolite and quartz. Lung health effects of talc-exposed workers may be related to both the talc itself as well as the other associated minerals.

Talc production occurs primarily in Australia, Austria, China, France and the United States. Talc is used as a component in hundreds of products, and is used in the manufacture of paint, pharmaceuticals, cosmetics, ceramics, automobile tires and paper.

Lung health

Diffuse rounded and irregular parenchymal lung opacities and pleural abnormalities are seen on the chest radiographs of talc workers in association with the talc exposure. Depending on the specific exposures experienced, the radiographic shadows may be ascribed to talc itself or to contaminants in the talc. Talc exposure has been associated with symptoms of cough, dyspnoea and phlegm production, and with evidence of airflow obstruction in pulmonary function studies. Lung pathology has revealed various forms of pulmonary fibrosis: granulomatous changes and ferruginous bodies have been reported, and dust-laden macrophages collected around the respiratory bronchioles intermingled with bundles of collagen. Mineralogical examination of lung tissue from talc workers is also variable and may show silica, mica or mixed silicates.

Since talc deposits may be associated with asbestos and other fibres, it is not surprising that an increased risk of bronchogenic carcinoma has been reported in talc miners and millers. Recent investigations of workers exposed to talc without associated asbestos fibres revealed trends for higher mortality from non-malignant respiratory disease (silicosis, silico-tuberculosis, emphysema and pneumonia), but the risk for bronchogenic cancer was not found to be elevated.

Hairspray

Exposure to hairsprays occurs in the home environment as well as in commercial hairdressing establishments (Rom 1992b). Environmental measurements in beauty salons have indicated the potential for respirable aerosol exposures. Several case reports have implicated hairspray exposure in the occurrence of a pneumonitis, thesaurosis, in heavily exposed individuals. Clinical symptoms in the cases were generally mild, and resolved with termination of exposure. Histology usually showed a granulomatous process in the lung and enlarged hilar lymph nodes, with thickening of alveolar walls and numerous granular macrophages in the airspaces. Macromolecules in hairsprays, including shellacs and polyvinylpyrrolidone, have been suggested as potential agents. In contrast to the clinical case reports, increased lung parenchymal radiographic shadows observed in radiological surveys of commercial hairdressers have not been conclusively related to hairspray exposure. Although the results of these studies do not allow definitive conclusions to be drawn, clinically important lung disease from typical hairspray exposures does appear to be an unusual occurrence.

 

Back

Read 6094 times Last modified on Saturday, 23 July 2022 19:44

" DISCLAIMER: The ILO does not take responsibility for content presented on this web portal that is presented in any language other than English, which is the language used for the initial production and peer-review of original content. Certain statistics have not been updated since the production of the 4th edition of the Encyclopaedia (1998)."

Contents

Respiratory System References

Abramson, MJ, JH Wlodarczyk, NA Saunders, and MJ Hensley. 1989. Does aluminum smelting cause lung disease? Am Rev Respir Dis 139:1042-1057.

Abrons, HL, MR Peterson, WT Sanderson, AL Engelberg, and P Harber. 1988. Symptoms, ventilatory function, and environmental exposures in Portland cement workers. Brit J Ind Med 45:368-375.

Adamson, IYR, L Young, and DH Bowden. 1988. Relationship of alveolar epithelial injury and repair to the indication of pulmonary fibrosis. Am J Pathol 130(2):377-383.

Agius, R. 1992. Is silica carcinogenic? Occup Med 42: 50-52.

Alberts, WM and GA Do Pico. 1996. Reactive airways dysfunction syndrome (review). Chest 109:1618-1626.
Albrecht, WN and CJ Bryant. 1987. Polymer fume fever associated with smoking and use of a mold release spray containing polytetraflouroethylene. J Occup Med 29:817-819.

American Conference of Governmental Industrial Hygienists (ACGIH). 1993. 1993-1994 Threshold Limit Values and Biological Exposure Indices. Cincinnati, Ohio: ACGIH.

American Thoracic Society (ATS). 1987 Standards for the diagnosis and care of patients with chronic obstructive pulmonary disease (COPD) and asthma. Am Rev Respir Dis 136:225-244.

—.1995. Standardization of Spirometry: 1994 update. Amer J Resp Crit Care Med 152: 1107-1137.

Antman, K and J Aisner. 1987. Asbestos-Related Malignancy. Orlando: Grune & Stratton.

Antman, KH, FP Li, HI Pass, J Corson, and T Delaney. 1993. Benign and malignant mesothelioma. In Cancer: Principles and Practice of Oncology, edited by VTJ DeVita, S Hellman, and SA Rosenberg. Philadelphia: JB Lippincott.
Asbestos Institute. 1995. Documentation center: Montreal, Canada.

Attfield, MD and K Morring. 1992. An investigation into the relationship between coal workers’ pneumoconiosis and dust exposure in US coal miners. Am Ind Hyg Assoc J 53(8):486-492.

Attfield, MD. 1992. British data on coal miners’ pneumoconiosis and relevance to US conditions. Am J Public Health 82:978-983.

Attfield, MD and RB Althouse. 1992. Surveillance data on US coal miners’ pneumoconiosis, 1970 to 1986. Am J Public Health 82:971-977.

Axmacher, B, O Axelson, T Frödin, R Gotthard, J Hed, L Molin, H Noorlind Brage, and M Ström. 1991. Dust exposure in coeliac disease: A case-referent study. Brit J Ind Med 48:715-717.

Baquet, CR, JW Horm, T Gibbs, and P Greenwald. 1991. Socioeconomic factors and cancer incidence among blacks and whites. J Natl Cancer Inst 83: 551-557.

Beaumont, GP. 1991. Reduction in airborne silicon carbide whiskers by process improvements. Appl Occup Environ Hyg 6(7):598-603.

Becklake, MR. 1989. Occupational exposures: Evidence for a causal association with chronic obstructive pulmonary disease. Am Rev Respir Dis. 140: S85-S91.

—. 1991. The epidemiology of asbestosis. In Mineral Fibers and Health, edited by D Liddell and K Miller. Boca Raton: CRC Press.

—. 1992. Occupational exposure and chronic airways disease. Chap. 13 in Environmental and Occupational Medicine. Boston: Little, Brown & Co.

—. 1993. In Asthma in the workplace, edited by IL Bernstein, M Chan-Yeung, J-L Malo and D Bernstein. Marcel Dekker.

—. 1994. Pneumoconioses. Chap. 66 in A Textbook of Respiratory Medicine, edited by JF Murray and J Nadel. Philadelphia: WB Saunders.

Becklake, MR and B Case. 1994. Fibre burden and asbestos-related lung disease: Determinants of dose-response relationships. Am J Resp Critical Care Med 150:1488-1492.

Becklake, MR. et al. 1988. The relationships between acute and chronic airways responses to occupational exposures. In Current Pulmonology. Vol. 9, edited by DH Simmons. Chicago: Year Book Medical Publishers.

Bégin, R, A Cantin, and S Massé. 1989. Recent advances in the pathogenesis and clinical assessment of mineral dust pneumoconioses: Asbestosis, silicosis and coal pneumoconiosis. Eur Resp J 2:988-1001.

Bégin, R and P Sébastien. 1989. Alveolar dust clearance capacity as determinant of individual susceptibility to asbestosis: Experimental oservations. Ann Occup Hyg 33:279-282.

Bégin, R, A Cantin, Y Berthiaume, R Boileau, G Bisson, G Lamoureux, M Rola-Pleszczynski, G Drapeau, S Massé, M Boctor, J Breault, S Péloquin, and D Dalle. 1985. Clinical features to stage alveolitis in asbestos workers. Am J Ind Med 8:521-536.

Bégin, R, G Ostiguy, R Filion, and S Groleau. 1992. Recent advances in the early diagnosis of asbestosis. Sem Roentgenol 27(2):121-139.

Bégin, T, A Dufresne, A Cantin, S Massé, P Sébastien, and G Perrault. 1989. Carborundum pneumoconiosis. Chest 95(4):842-849.

Beijer L, M Carvalheiro, PG Holt, and R Rylander. 1990. Increased blood monocyte procoagulant activity in cotton mill workers. J. Clin Lab Immunol 33:125-127.

Beral, V, P Fraser, M Booth, and L Carpenter. 1987. Epidemiological studies of workers in the nuclear industry. In Radiation and Health: The Biological Effects of Low-Level Exposure to Ionizing Radiation, edited by R Russell Jones and R Southwood. Chichester: Wiley.

Bernstein, IL, M Chan-Yeung, J-L Malo, and D Bernstein. 1993. Asthma in the Workplace. Marcel Dekker.

Berrino F, M Sant, A Verdecchia, R Capocaccia, T Hakulinen, and J Esteve. 1995. Survival of Cancer Patients in Europe: The EUROCARE Study. IARC Scientific Publications, no 132. Lyon: IARC.

Berry, G, CB McKerrow, MKB Molyneux, CE Rossiter, and JBL Tombleson. 1973. A study of the acute and chronic changes in ventilatory capacity of workers in Lancashire Cotton Mills. Br J Ind Med 30:25-36.

Bignon J, (ed.) 1990. Health-related effects of phyllosilicates. NATO ASI series Berlin: Springer-Verlag.

Bignon, J, P Sébastien, and M Bientz. 1979. Review of some factors relevant to the assessment of exposure to asbestos dusts. In The use of Biological Specimens for the Assessment of Human Exposure to Environmental Pollutants, edited by A Berlin, AH Wolf, and Y Hasegawa. Dordrecht: Martinus Nijhoff for the Commission of the European Communities.

Bignon J, J Peto and R Saracci, (eds.) 1989. Non-occupational exposure to mineral fibres. IARC Scientific Publications, no 90. Lyon: IARC.

Bisson, G, G Lamoureux, and R Bégin. 1987. Quantitative gallium 67 lung scan to assess the inflammatory activity in the pneumoconioses. Sem Nuclear Med 17(1):72-80.

Blanc, PD and DA Schwartz. 1994. Acute pulmonary responses to toxic exposures. In Respiratory Medicine, edited by JF Murray and JA Nadel. Philadelphia: WB Saunders.

Blanc, P, H Wong, MS Bernstein, and HA Boushey. 1991. An experimental human model of a metal fume fever. Ann Intern Med 114:930-936.

Blanc, PD, HA Boushey, H Wong, SF Wintermeyer, and MS Bernstein. 1993. Cytokines in metal fume fever. Am Rev Respir Dis 147:134-138.

Blandford, TB, PJ Seamon, R Hughes, M Pattison, and MP Wilderspin. 1975. A case of polytetrafluoroethylene poisoning in cockatiels accompanied by polymer fume fever in the owner. Vet Rec 96:175-178.

Blount, BW. 1990. Two types of metal fume fever: mild vs. serious. Milit Med 155:372-377.

Boffetta, P, R Saracci, A Anderson, PA Bertazzi, Chang-Claude J, G Ferro, AC Fletcher, R Frentzel-Beyme, MJ Gardner, JH Olsen, L Simonato, L Teppo, P Westerholm, P Winter, and C Zocchetti. 1992. Lung cancer mortality among workers in the European production of man-made mineral fibers-a Poisson regression analysis. Scand J Work Environ Health 18:279-286.

Borm, PJA. 1994. Biological markers and occupational lung dsease: Mineral dust-induced respiratory disorders. Exp Lung Res 20:457-470.

Boucher, RC. 1981. Mechanisms of pollutant induced airways toxicity. Clin Chest Med 2:377-392.

Bouige, D. 1990. Dust exposure results in 359 asbestos-using factories from 26 countries. In Seventh International Pneumoconiosis Conference Aug 23-26, 1988. Proceedings Part II. Washington, DC: DHS (NIOSH).

Bouhuys A. 1976. Byssinosis: Scheduled asthma in the textile industry. Lung 154:3-16.

Bowden, DH, C Hedgecock, and IYR Adamson. 1989. Silica-induced pulmonary fibrosis involves the reaction of particles with interstitial rather than alveolar macrophages. J Pathol 158:73-80.

Brigham, KL and B Mayerick. 1986. Endotoxin and Lung injury. Am Rev Respir Dis 133:913-927.

Brody, AR. 1993. Asbestos-induced lung disease. Environ Health Persp 100:21-30.

Brody, AR, LH Hill, BJ Adkins, and RW O’Connor. 1981. Chrysotile asbestos inhalation in rats: Deposition pattern and reaction of alveolar epithelium and pulmonary macrophages. Am Rev Respir Dis 123:670.

Bronwyn, L, L Razzaboni, and P Bolsaitis. 1990. Evidence of an oxidative mechanism for the hemolytic activity of silica particles. Environ Health Persp 87: 337-341.

Brookes, KJA. 1992. World Directory and Handbook of Hard Metal and Hard Materials. London: International Carbide Data.

Brooks, SM and AR Kalica. 1987. Strategies for elucidating the relationship between occupational exposures and chronic air-flow obstruction. Am Rev Respir Dis 135:268-273.

Brooks, SM, MA Weiss, and IL Bernstein. 1985. Reactive airways dysfunction syndrome (RADS). Chest 88:376-384.

Browne, K. 1994. Asbestos-related disorders. Chap. 14 in Occupational Lung Disorders, edited by WR Parkes. Oxford: Butterworth-Heinemann.

Brubaker, RE. 1977. Pulmonary problems associated with the use of polytetrafluoroethylene. J Occup Med 19:693-695.

Bunn, WB, JR Bender, TW Hesterberg, GR Chase, and JL Konzen. 1993. Recent studies of man-made vitreous fibers: Chronic animal inhalation studies. J Occup Med 35(2):101-113.

Burney, MB and S Chinn. 1987. Developing a new questionnaire for measuring the prevalence and distribution of asthma. Chest 91:79S-83S.

Burrell, R and R Rylander. 1981. A critical review of the role of precipitins in hypersensitivity pneumonitis. Eur J Resp Dis 62:332-343.

Bye, E. 1985. Occurrence of airborne silicon carbide fibers during industrial production of silicon carbide. Scand J Work Environ Health 11:111-115.

Cabral-Anderson, LJ, MJ Evans, and G Freeman. 1977. Effects of NO2 on the lungs of aging rats I. Exp Mol Pathol 27:353-365.

Campbell, JM. 1932. Acute symptoms following work with hay. Brit Med J 2:1143-1144.

Carvalheiro MF, Y Peterson, E Rubenowitz, R Rylander. 1995. Bronchial activity and work-related symptoms in farmers. Am J Ind Med 27: 65-74.

Castellan, RM, SA Olenchock, KB Kinsley, and JL Hankinson. 1987. Inhaled endotoxin and decreased spirometric values: An exposure-response relation for cotton dust. New Engl J Med 317:605-610.

Castleman, WL, DL Dungworth, LW Schwartz, and WS Tyler. 1980. Acute repiratory bronchiolitis - An ultrastructural and autoradiographic study of epithelial cell injury and renewal in Rhesus monkeys exposed to ozone. Am J Pathol 98:811-840.

Chan-Yeung, M. 1994. Mechanism of occupational asthma due to Western red cedar. Am J Ind Med 25:13-18.

—. 1995. Assessment of asthma in the workplace. ACCP consensus statement. American College of Chest Physicians. Chest 108:1084-1117.
Chan-Yeung, M and J-L Malo. 1994. Aetiological agents in occupational asthma. Eur Resp J 7:346-371.

Checkoway, H, NJ Heyer, P Demers, and NE Breslow. 1993. Mortality among workers in the diatomaceous earth industry. Brit J Ind Med 50:586-597.

Chiazze, L, DK Watkins, and C Fryar. 1992. A case-control study of malignant and non-malignant respiratory disease among employees of a fibreglass manufacturing facility. Brit J Ind Med 49:326-331.

Churg, A. 1991. Analysis of lung asbestos content. Brit J Ind Med 48:649-652.

Cooper, WC and G Jacobson. 1977. A twenty-one year radiographic follow-up of workers in the diatomite industry. J Occup Med 19:563-566.

Craighead, JE, JL Abraham, A Churg, FH Green, J Kleinerman, PC Pratt, TA Seemayer, V Vallyathan and H Weill. 1982. The pathology of asbestos associated diseases of the lungs and pleural cavities. Diagnostic criteria and proposed grading system. Arch Pathol Lab Med 106: 544-596.

Crystal, RG and JB West. 1991. The Lung. New York: Raven Press.

Cullen, MR, JR Balmes, JM Robins, and GJW Smith. 1981. Lipoid pneumonia caused by oil mist exposure from a steel rolling tandem mill. Am J Ind Med 2: 51-58.

Dalal, NA, X Shi, and V Vallyathan. 1990. Role of free radicals in the mechanisms of hemolysis and lipid peroxidation by silica: Comparative ESR and cytotoxicity studies. J Tox Environ Health 29:307-316.

Das, R and PD Blanc. 1993. Chlorine gas exposure and the lung: A review. Toxicol Ind Health 9:439-455.

Davis, JMG, AD Jones, and BG Miller. 1991. Experimental studies in rats on the effects of asbestos inhalation couples with the inhalation of titanium dioxide or quartz. Int J Exp Pathol 72:501-525.

Deng, JF, T Sinks, L Elliot, D Smith, M Singal, and L Fine. 1991. Characterisation of respiratory health and exposures at a sintered permanent magnet manufacturer. Brit J Ind Med 48:609-615.

de Viottis, JM. 1555. Magnus Opus. Historia de gentibus septentrionalibus. In Aedibus Birgittae. Rome.

Di Luzio, NR. 1985. Update on immunomodulating activities of glucans. Springer Semin Immunopathol 8:387-400.

Doll, R and J Peto. 1985. Effects on health of exposure to asbestos. London, Health and Safety Commission London: Her Majesty’s Stationery Office.

—. 1987. In Asbestos-Related Malignancy, edited by K Antman and J Aisner. Orlando, Fla: Grune & Stratton.

Donelly, SC and MX Fitzgerald. 1990. Reactive airways dysfunction syndrome (RADS) due to acute chlorine exposure. Int J Med Sci 159:275-277.

Donham, K, P Haglind, Y Peterson, and R Rylander. 1989. Environmental and health studies of farm workers in Swedish swine confinement buildings. Brit J Ind Med 46:31-37.

Do Pico, GA. 1992. Hazardous exposure and lung disease among farm workers. Clin Chest Med 13: 311-328.

Dubois, F, R Bégin, A Cantin, S Massé, M Martel, G Bilodeau, A Dufresne, G Perrault, and P Sébastien. 1988. Aluminum inhalation reduces silicosis in a sheep model. Am Rev Respir Dis 137:1172-1179.

Dunn, AJ. 1992. Endotoxin-induced activation of cerebral catecholamine and serotonin metabolism: Comparison with Interleukin.1. J Pharmacol Exp Therapeut 261:964-969.

Dutton, CB, MJ Pigeon, PM Renzi, PJ Feustel, RE Dutton, and GD Renzi. 1993. Lung function in workers refining phosphorus rock to obtain elementary phosphorus. J Occup Med 35:1028-1033.

Ellenhorn, MJ and DG Barceloux. 1988. Medical Toxicology. New York: Elsevier.
Emmanuel, DA, JJ Marx, and B Ault. 1975. Pulmonary mycotoxicosis. Chest 67:293-297.

—. 1989. Organic dust toxic syndrome (pulmonary mycotoxicosis) - A review of the experience in central Wisconsin. In Principles of Health and Safety in Agriculture, edited by JA Dosman and DW Cockcroft. Boca Raton: CRC Press.

Engelen, JJM, PJA Borm, M Van Sprundel, and L Leenaerts. 1990. Blood anti-oxidant parameters at different stages in coal worker’s pneumoconiosis. Environ Health Persp 84:165-172.

Englen, MD, SM Taylor, WW Laegreid, HD Liggit, RM Silflow, RG Breeze, and RW Leid. 1989. Stimulation of arachidonic acid metabolism in silica-exposed alveolar macrophages. Exp Lung Res 15: 511-526.

Environmental Protection Agency (EPA). 1987. Ambient Air Monitoring reference and equivalent methods. Federal Register 52:24727 (July l, 1987).

Ernst and Zejda. 1991. In Mineral Fibers and Health, edited by D Liddell and K Miller. Boca Raton: CRC Press.

European Standardization Committee (CEN). 1991. Size Fraction Definitions for Measurements of Airborne Particles in the Workplace. Report No. EN 481. Luxembourg: CEN.

Evans, MJ, LJ Cabral-Anderson, and G Freeman. 1977. Effects of NO2 on the lungs of aging rats II. Exp Mol Pathol 27:366-376.

Fogelmark, B, H Goto, K Yuasa, B Marchat, and R Rylander. 1992. Acute pulmonary toxicity of inhaled (13)-B-D-glucan and endotoxin. Agents Actions 35:50-56.

Fraser, RG, JAP Paré, PD Paré, and RS Fraser. 1990. Diagnosis of Diseases of the Chest. Vol. III. Philadelphia: WB Saunders.

Fubini, B, E Giamello, M Volante, and V Bolis. 1990. Chemical functionalities at the silica surface determining its reactivity when inhaled. Formation and reactivity of surface radicals. Toxicol Ind Health 6(6):571-598.

Gibbs, AE, FD Pooley, and DM Griffith. 1992. Talc pneumoconiosis: A pathologic and mineralogic study. Hum Pathol 23(12):1344-1354.

Gibbs, G, F Valic, and K Browne. 1994. Health risk associated with chrysotile asbestos. A report of a workshop held in Jersey, Channel Islands. Ann Occup Hyg 38:399-638.

Gibbs, WE. 1924. Clouds and Smokes. New York: Blakiston.

Ginsburg, CM, MG Kris, and JG Armstrong. 1993. Non-small cell lung cancer. In Cancer: Principles & Practice of Oncology, edited by VTJ DeVita, S Hellman, and SA Rosenberg. Philadelphia: JB Lippincott.

Goldfrank, LR, NE Flomenbaum, N Lewin, and MA Howland. 1990. Goldfrank’s Toxicologic Emergencies. Norwalk, Conn.: Appleton & Lange.
Goldstein, B and RE Rendall. 1987. The prophylactic use of polyvinylpyridine-N-oxide (PVNO) in baboons exposed to quartz dust. Environmental Research 42:469-481.

Goldstein, RH and A Fine. 1986. Fibrotic reactions in the lung: The activation of the lung fibroblast. Exp Lung Res 11:245-261.
Gordon, RE, D Solano, and J Kleinerman. 1986. Tight junction alterations of respiratory epithelia following long term NO2 exposure and recovery. Exp Lung Res 11:179-193.

Gordon, T, LC Chen, JT Fine, and RB Schlesinger. 1992. Pulmonary effects of inhaled zinc oxide in human subjects, guinea pigs, rats, and rabbits. Am Ind Hyg Assoc J 53:503-509.

Graham, D. 1994. Noxious gases and fumes. In Textbook of Pulmonary Diseases, edited by GL Baum and E Wolinsky. Boston: Little, Brown & Co.

Green, JM, RM Gonzalez, N Sonbolian, and P Renkopf. 1992. The resistance to carbon dioxide laser ignition of a new endotracheal tube. J Clin Anesthesiaol 4:89-92.

Guilianelli, C, A Baeza-Squiban, E Boisvieux-Ulrich, O Houcine, R Zalma, C Guennou, H Pezerat, and F MaraNo. 1993. Effect of mineral particles containing iron on primary cultures of rabbit tracheal epithelial cells: Possible implication of oxidative stress. Environ Health Persp 101(5):436-442.

Gun, RT, Janckewicz, A Esterman, D Roder, R Antic, RD McEvoy, and A Thornton. 1983. Byssinosis: A cross-sectional study in an Australian textile factory. J Soc Occup Med 33:119-125.

Haglind P and R Rylander. Exposure to cotton dust in an experimental cardroom. Br J Ind Med 10: 340-345.

Hanoa, R. 1983. Graphite pneumoconiosis. A review of etiologic and epidemiologic aspects. Scand J Work Environ Health 9:303-314.

Harber, P, M Schenker, and J Balmes. 1996. Occupational and Environmental Respiratory Disease. St. Louis: Mosby.

Health Effects Institute - Asbestos Research. 1991. Asbestos in Public and Commercial Buildings: A Literature Review and Synthesis of Current Knowledge. Cambridge, Mass.: Health Effects Institute.

Heffner, JE and JE Repine. 1989. Pulmonary strategies of antioxidant defense. Am Rev Respir Dis 140: 531-554.

Hemenway, D, A Absher, B Fubini, L Trombley, P Vacek, M Volante, and A Cabenago. 1994. Surface functionalities are related to biological response and transport of crystalline silica. Ann Occup Hyg 38 Suppl. 1:447-454.

Henson, PM and RC Murphy. 1989. Mediators of the Inflammatory Process. New York: Elsevier.

Heppleston, AG. 1991. Minerals, fibrosis and the Lung. Environ Health Persp 94:149-168.

Herbert, A, M Carvalheiro, E Rubenowiz, B Bake, and R Rylander. 1992. Reduction of alveolar-capillary diffusion after inhalation of endotoxin in normal subjects. Chest 102:1095-1098.

Hessel, PA, GK Sluis-Cremer, E Hnizdo, MH Faure, RG Thomas, and FJ Wiles. 1988. Progression of silicosis in relation to silica dust exposure. Am Occup Hyg 32 Suppl. 1:689-696.

Higginson, J, CS Muir, and N Muñoz. 1992. Human cancer: Epidemiology and environmental causes. In Cambridge Monographs on Cancer Research. Cambridge: Cambridge Univ. Press.

Hinds, WC. 1982. Aerosol Technology: Properties, Behavior, and Measurement of Airborne Particles. New York: John Wiley.

Hoffman, RE, K Rosenman, F Watt, et al. 1990. Occupational disease surveillance: Occupational asthma. Morb Mortal Weekly Rep 39:119-123.

Hogg, JC. 1981. Bronchial mucosal permeability and its relationship to airways hyperreactivity. J Allergy Clin immunol 67:421-425.

Holgate, ST, R Beasley, and OP Twentyman. 1987. The pathogenesis and significance of bronchial hyperresponsiveness in airways disease. Clin Sci 73:561-572.

Holtzman, MJ. 1991. Arachidonic acid metabolism. Implications of biological chemistry for lung function and disease. Am Rev Respir Dis 143:188-203.

Hughes, JM and H Weil. 1991. Asbestosis as a precursor of asbestos related lung cancer: Results of a prospective mortality study. Brit J Ind Med 48: 229-233.

Hussain, MH, JA Dick, and YS Kaplan. 1980. Rare earth pneumoconiosis. J Soc Occup Med 30:15-19.

Ihde, DC, HI Pass, and EJ Glatstein. 1993. Small cell lung cancer. In Cancer: Principles and Practice of Oncology, edited by VTJ DeVita, S Hellman, and SA Rosenberg. Philadelphia: JB Lippincott.

Infante-Rivard, C, B Armstrong, P Ernst, M Peticlerc, L-G Cloutier, and G Thériault. 1991. Descriptive study of prognostic factors influencing survival of compensated silicotic patients. Am Rev Respir Dis 144:1070-1074.

International Agency for Research on Cancer (IARC). 1971-1994. Monographs on the Evaluation of Carcinogenic Risks to Humans. Vol. 1-58. Lyon: IARC.

—. 1987. Monographs on the Evaluation of Carcinogenic Risks to Humans, Overall Evaluations of Carcinogenicity: An Updating of IARC
Monographs. Vol. 1-42. Lyon: IARC. (Supplement 7.)

—. 1988. Man-made mineral fibres and radon. IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, No. 43. Lyon: IARC.

—. 1988. Radon. IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, No. 43. Lyon: IARC.

—. 1989a. Diesel and gasoline engine exhausts and some nitroarenes. IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, No. 46. Lyon: IARC.

—. 1989b. Non-occupational exposure to mineral fibres. IARC Scientific Publications, No. 90. Lyon: IARC.

—. 1989c. Some organic solvents, resin monomers and related compounds, pigments and occupational exposure in paint manufacture and painting. IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, No. 47. Lyon: IARC.

—. 1990a. Chromium and chromium compounds. IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, No. 49. Lyon: IARC.

—. 1990b. Chromium, nickel, and welding. IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, No. 49. Lyon: IARC.

—. 1990c. Nickel and nickel compounds. IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, No. 49. Lyon: IARC.

—. 1991a. Chlorinated drinking-water; Chlorination by-products; Some other halogenated compounds; Cobalt and cobalt compounds. IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, No. 52. Lyon: IARC.

—. 1991b. Occupational exposures in spraying and application of insecticides and some pesticides. IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, No. 53. Lyon: IARC.

—. 1992. Occupational exposures to mists and vapours from sulfuric acid, other strong inorganic acids and other industrial chemicals. IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, No. 54. Lyon: IARC.

—. 1994a. Beryllium and beryllium compounds. IARC Monographs on the Evaluationof Carcinogenic Risks to Humans, No. 58. Lyon: IARC.

—. 1994b. Beryllium, cadmium and cadmium compounds, mercury and the glass industry. IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, No. 58. Lyon: IARC.

—. 1995. Survival of cancer patients in Europe: The EUROCARE study. IARC Scientific Publications, No.132. Lyon: IARC.

International Commission on Radiological Protection (ICRP). 1994. Human Respiratory Tract Model for Radiological Protection. Publication No. 66. ICRP.

International Labour Office (ILO). 1980. Guidelines for the use of ILO international classification of radiographs of pneumoconioses. Occupational Safety and Health Series, No. 22. Geneva: ILO.

—. 1985. Sixth International Report on the Prevention and Suppression of Dust in Mining, Tunnelling and Quarrying 1973-1977. Occupational Safety and Health Series, No.48. Geneva: ILO.

International Organization for Standardization (ISO). 1991. Air Quality - Particle Size Fraction Definitions for Health-Related Sampling. Geneva: ISO.

Janssen, YMW, JP Marsh, MP Absher, D Hemenway, PM Vacek, KO Leslie, PJA Borm, and BT Mossman. 1992. Expression of antioxidant enzymes in rat lungs after inhalation of asbestos or silica. J Biol Chem 267(15):10625-10630.

Jaurand, MC, J Bignon, and P Brochard. 1993. The mesothelioma cell and mesothelioma. Past, present and future. International Conference, Paris, Sept. 20 to Oct. 2, 1991. Eur Resp Rev 3(11):237.

Jederlinic, PJ, JL Abraham, A Churg, JS Himmelstein, GR Epler, and EA Gaensler. 1990. Pulmonary fibrosis in aluminium oxide workers. Am Rev Respir Dis 142:1179-1184.

Johnson, NF, MD Hoover, DG Thomassen, YS Cheng, A Dalley, and AL Brooks. 1992. In vitro activity of silicon carbide whiskers in comparison to other industrial fibers using four cell culture systems. Am J Ind Med 21:807-823.

Jones, HD, TR Jones, and WH Lyle. 1982. Carbon fibre: Results of a survey of process workers and their environment in a factory producing continuous filament. Am Occup Hyg 26:861-868.

Jones, RN, JE Diem, HW Glindmeyer, V Dharmarajan, YY Hammad, J Carr, and H Weill. 1979. Mill effect and dose-response relationships in byssinosis. Br J Ind Med 36:305-313.

Kamp, DW, P Graceffa, WA Prior, and A Weitzman. 1992. The role of free radicals in asbestos-induced diseases. Free Radical Bio Med 12:293-315.

Karjalainen, A, PJ Karhonen, K Lalu, A Pentilla, E Vanhala, P Kygornen, and A Tossavainen. 1994. Pleural plaques and exposure to mineral fibres in a male urban necropsy population. Occup Environ Med 51:456-460.

Kass, I, N Zamel, CA Dobry, and M Holzer. 1972. Bronchiectasis following ammonia burns of the respiratory tract. Chest 62:282-285.

Katsnelson, BA, LK Konyscheva, YEN Sharapova, and LI Privalova. 1994. Prediction of the comparative intensity of pneumoconiotic changes caused by chronic inhalation exposure to dusts of different cytotoxicity by means of a mathematical model. Occup Environ Med 51:173-180.

Keenan, KP, JW Combs, and EM McDowell. 1982. Regeneration of hamster tracheal epithelium after mechanical injury I, II, III. Virchows Archiv 41:193-252.

Keenan, KP, TS Wilson, and EM McDowell. 1983. Regeneration of hamster tracheal epithelium after mechanical injury IV. Virchows Archiv 41:213-240.
Kehrer, JP. 1993. Free radicals as mediators of tissue injury and disease. Crit Rev Toxicol 23:21-48.

Keimig, DG, RM Castellan, GJ Kullman, and KB Kinsley. 1987. Respiratory health status of gilsonite workers. Am J Ind Med 11:287-296.

Kelley, J. 1990. Cytokines of the Lung. Am Rev Respir Dis 141:765-788.

Kennedy, TP, R Dodson, NV Rao, H Ky, C Hopkins, M Baser, E Tolley, and JR Hoidal. 1989. Dusts causing pneumoconiosis generate OH and product hemolysis by acting as fenton catalysts. Arch Biochem Biophys 269(1):359-364.

Kilburn, KH and RH Warshaw. 1992. Irregular opacities in the lung, occupational asthma, and airways dysfunction in aluminum workers. Am J Ind Med 21:845-853.

Kokkarinen, J, H Tuikainen, and EO Terho. 1992. Severe farmer’s lung following a workplace challenge. Scand J Work Environ Health 18:327-328.

Kongerud, J, J Boe, V Soyseth, A Naalsund, and P Magnus. 1994. Aluminium pot room asthma: The Norwegian experience. Eur Resp J 7:165-172.

Korn, RJ, DW Dockery, and FE Speizer. 1987. Occupational exposure and chronic respiratory symptoms. Am Rev Respir Dis 136:298-304.

Kriebel, D. 1994. The dosimetric model in occupational and environmental epidemiology. Occup Hyg 1:55-68.

Kriegseis, W, A Scharmann, and J Serafin. 1987. Investigations of surface properties of silica dusts with regard to their cytotoxicity. Ann Occup Hyg 31(4A):417-427.

Kuhn, DC and LM Demers. 1992. Influence of mineral dust surface chemistry on eicosanoid production by the alveolar macrophage. J Tox Environ Health 35: 39-50.

Kuhn, DC, CF Stanley, N El-Ayouby, and LM Demers. 1990. Effect of in vivo coal dust exposure on arachidonic acid metabolism in the rat alveolar macrophage. J Tox Environ Health 29:157-168.

Kunkel, SL, SW Chensue, RM Strieter, JP Lynch, and DG Remick. 1989. Cellular and molecular aspects of granulomatous inflammation. Am J Respir Cell Mol Biol 1:439-447.

Kuntz, WD and CP McCord. 1974. Polymer fume fever. J Occup Med 16:480-482.

Lapin, CA, DK Craig, MG Valerio, JB McCandless, and R Bogoroch. 1991. A subchronic inhalation toxicity study in rats exposed to silicon carbide whiskers. Fund Appl Toxicol 16:128-146.

Larsson, K, P Malmberg, A Eklund, L Belin, and E Blaschke. 1988. Exposure to microorganisms, airway inflammatory changes and immune reactions in asymptomatic dairy farmers. Int Arch Allergy Imm 87:127-133.

Lauweryns, JM and JH Baert. 1977. Alveolar clearance and the role of the pulmonary lymphatics. Am Rev Respir Dis 115:625-683.

Leach, J. 1863. Surat cotton, as it bodily affects operatives in cotton mills. Lancet II:648.

Lecours, R, M Laviolette, and Y Cormier. 1986. Bronchoalveolar lavage in pulmonary mycotoxicosis (organic dust toxic syndrome). Thorax 41:924-926.

Lee, KP, DP Kelly, FO O’Neal, JC Stadler, and GL Kennedy. 1988. Lung response to ultrafine kevlar aramid synthetic fibrils following 2-year inhalation exposure in rats. Fund Appl Toxicol 11:1-20.

Lemasters, G, J Lockey, C Rice, R McKay, K Hansen, J Lu, L Levin, and P Gartside. 1994. Radiographic changes among workers manufacturing refractory ceramic fiber and products. Ann Occup Hyg 38 Suppl 1:745-751.

Lesur, O, A Cantin, AK Transwell, B Melloni, J-F Beaulieu, and R Bégin. 1992. Silica exposure induces cytotoxicity and proliferative activity of type II. Exp Lung Res 18:173-190.

Liddell, D and K Millers (eds.). 1991. Mineral fibers and health. Florida, Boca Raton: CRC Press.
Lippman, M. 1988. Asbestos exposure indices. Environmental Research 46:86-92.

—. 1994. Deposition and retention of inhaled fibres: Effects on incidence of lung cancer and mesothelioma. Occup Environ Med 5: 793-798.

Lockey, J and E James. 1995. Man-made fibers and nonasbestos fibrous silicates. Chap. 21 in Occupational and Environmental Respiratory Diseases, edited by P Harber, MB Schenker, and JR Balmes. St.Louis: Mosby.

Luce, D, P Brochard, P Quénel, C Salomon-Nekiriai, P Goldberg, MA Billon-Galland, and M Goldberg. 1994. Malignant pleural mesothelioma associated with exposure to tremolite. Lancet 344:1777.

Malo, J-L, A Cartier, J L’Archeveque, H Ghezzo, F Lagier, C Trudeau, and J Dolovich. 1990. Prevalence of occupational asthma and immunological sensitization to psyllium among health personnel in chronic care hospitals. Am Rev Respir Dis 142:373-376.

Malo, J-L, H Ghezzo, J L’Archeveque, F Lagier, B Perrin, and A Cartier. 1991. Is the clinical history a satisfactory means of diagnosing occupational asthma? Am Rev Respir Dis 143:528-532.

Man, SFP and WC Hulbert. 1988. Airway repair and adaptation to inhalation injury. In Pathophysiology and Treatment of Inhalation Injuries, edited by J Locke. New York: Marcel Dekker.

Markowitz, S. 1992. Primary prevention of occupational lung disease: A view from the United States. Israel J Med Sci 28:513-519.

Marsh, GM, PE Enterline, RA Stone, and VL Henderson. 1990. Mortality among a cohort of US man-made mineral fiber workers: 1985 follow-up. J Occup Med 32:594-604.

Martin, TR, SW Meyer, and DR Luchtel. 1989. An evaluation of the toxicity of carbon fiber composites for lung cells in vitro and in vivo. Environmental Research 49:246-261.

May, JJ, L Stallones, and D Darrow. 1989. A study of dust generated during silo opening and its physiologic effect on workers. In Principles of Health and Safety in Agriculture, edited by JA Dosman and DW Cockcroft. Boca Raton: CRC Press.

McDermott, M, C Bevan, JE Cotes, MM Bevan, and PD Oldham. 1978. Respiratory function in slateworkers. B Eur Physiopathol Resp 14:54.

McDonald, JC. 1995. Health implications of environmental exposure to asbestos. Environ Health Persp 106: 544-96.

McDonald, JC and AD McDonald. 1987. Epidemiology of malignant mesothelioma. In Asbestos-Related Malignancy, edited by K Antman and J Aisner. Orlando, Fla: Grune & Stratton.

—. 1991. Epidemiology of mesothelioma. In Mineral Fibres and Health. Boca Raton: CRC Press.

—. 1993. Mesothelioma: Is there a background? In The Mesothelioma Cell and Mesothelioma: Past, Present and Future, edited by MC Jaurand, J Bignon, and P Brochard.

—. 1995. Chrysotile, tremolite, and mesothelioma. Science 267:775-776.

McDonald, JC, B Armstrong, B Case, D Doell, WTE McCaughey, AD McDonald, and P Sébastien. 1989. Mesothelioma and asbestos fibre type. Evidence from lung tissue analyses. Cancer 63:1544-1547.

McDonald, JC, FDK Lidell, A Dufresne, and AD McDonald. 1993. The 1891-1920 birth cohort of Quebec chrystotile miners and millers: mortality 1976-1988. Brit J Ind Med 50:1073-1081.

McMillan, DD and GN Boyd. 1982. The role of antioxidants and diet in the prevention or treatment of oxygen-induced lung microvascular injury. Ann NY Acad Sci 384:535-543.

Medical Research Council. 1960. Standardized questionnaire on respiratory symptoms. Brit Med J 2:1665.

Mekky, S, SA Roach, and RSF Schilling. 1967. Byssinosis among winders in the industry. Br J Ind Med 24:123-132.

Merchant JA, JC Lumsden, KH Kilburn, WM O’Fallon, JR Ujda, VH Germino, and JD Hamilton. 1973. Dose response studies in cotton textile workers. J Occup Med 15:222-230.

Meredith, SK and JC McDonald. 1994. Work-related respiratory disease in the United Kingdom, 1989-1992. Occup Environ Med 44:183-189.

Meredith, S and H Nordman. 1996. Occupational asthma: Measures of frequency of four countries. Thorax 51:435-440.

Mermelstein, R, RW Lilpper, PE Morrow, and H Muhle. 1994. Lung overload, dosimetry of lung fibrosis and their implications to the respiratory dust standard. Ann Occup Hyg 38 Suppl. 1:313-322.

Merriman, EA. 1989. Safe use of Kevlar aramid fiber in composites. Appl Ind Hyg Special Issue (December):34-36.

Meurman, LO, E Pukkala, and M Hakama. 1994. Incidence of cancer among anthophyllite asbestos miners in Finland. Occup Environ Med 51:421-425.

Michael, O, R Ginanni, J Duchateau, F Vertongen, B LeBon, and R Sergysels. 1991. Domestic endotoxin exposure and clinical severity of asthma. Clin Exp Allergy 21:441-448.

Michel, O, J Duchateau, G Plat, B Cantinieaux, A Hotimsky, J Gerain and R Sergysels. 1995. Blood inflammatory response to inhaled endotoxin in normal subjects. Clin Exp Allergy 25:73-79.

Morey, P, JJ Fischer, and R Rylander. 1983. Gram-negative bacteria on cotton with particular reference to climatic conditions. Am Ind Hyg Assoc J 44: 100-104.

National Academy of Sciences. 1988. Health risks of radon and other internally deposited alpha-emitters. Washington, DC: National Academy of Sciences.

—. 1990. Health effects of exposure to low levels of ionizing radiation. Washington, DC: National Academy of Sciences.

National Asthma Education Program (NAEP). 1991. Expert Panel Report: Guidelines for the Diagnosis and Management of Asthma. Bethesda, Md: National Institutes of Health (NIH).

Nemery, B. 1990. Metal toxicity and the respiratory tract. Eur Resp J 3:202-219.

Newman, LS, K Kreiss, T King, S Seay, and PA Campbell. 1989. Pathologic and immunologic alterations in early stages of beryllium disease. Reexamination of disease definition and natural history. Am Rev Respir Dis 139:1479-1486.

Nicholson, WJ. 1991. In Health Effects Institute-Asbestos Research: Asbestos in Public and Commercial Buildings. Cambrige, Mass: Health Effects Institute-Asbestos Research.

Niewoehner, DE and JR Hoidal. 1982. Lung Fibrosis and Emphysema: Divergent responses to a common injury. Science 217:359-360.

Nolan, RP, AM Langer, JS Harrington, G Oster, and IJ Selikoff. 1981. Quartz hemolysis as related to its surface functionalities. Environ Res 26:503-520.

Oakes, D, R Douglas, K Knight, M Wusteman, and JC McDonald. 1982. Respiratory effects of prolonged exposure to gypsum dust. Ann Occup Hyg 2:833-840.

O’Brodovich, H and G Coates. 1987. Pulmonary Clearance of 99mTc-DTPA: A noninvasive assessment of epithelial integrity. Lung 16:1-16.

Parkes, RW. 1994. Occupational Lung Disorders. London: Butterworth-Heinemann.

Parkin, DM, P Pisani, and J Ferlay. 1993. Estimates of the worldwide incidence of eighteen major cancers in 1985. Int J Cancer 54:594-606.

Pepys, J and PA Jenkins. 1963. Farmer’s lung: Thermophilic actinomycetes as a source of “farmer’s lung hay” antigen. Lancet 2:607-611.

Pepys, J, RW Riddell, KM Citron, and YM Clayton. 1962. Precipitins against extracts of hay and molds in the serum of patients with farmer’s lung, aspergillosis, asthma and sarcoidosis. Thorax 17:366-374.

Pernis, B, EC Vigliani, C Cavagna, and M Finulli. 1961. The role of bacterial endotoxins in occupational diseases caused by inhaling vegetable dusts. Brit J Ind Med 18:120-129.

Petsonk, EL, E Storey, PE Becker, CA Davidson, K Kennedy, and V Vallyathan. 1988. Pneumoconiosis in carbon electrode workers. J Occup Med 30: 887-891.

Pézerat, H, R Zalma, J Guignard, and MC Jaurand. 1989. Production of oxygen radicals by the reduction of oxygen arising from the surface activity of mineral fibres. In Non-occupational exposure to mineral fibres, edited by J Bignon, J Peto, and R Saracci. IARC Scientific Publications, no.90. Lyon: IARC.

Piguet, PF, AM Collart, GE Gruaeu, AP Sappino, and P Vassalli. 1990. Requirement of tumour necrosis factor for development of silica-induced pulmonary fibrosis. Nature 344:245-247.

Porcher, JM, C Lafuma, R El Nabout, MP Jacob, P Sébastien, PJA Borm, S Hannons, and G Auburtin. 1993. Biological markers as indicators of exposure and pneumoconiotic risk: Prospective study. Int Arch Occup Environ Health 65:S209-S213.

Prausnitz, C. 1936. Investigations on respiratory dust disease in operatives in cotton industry. Medical Research Council Special Report Series, No. 212. London: His Majesty’s Stationery Office.

Preston, DL, H Kato, KJ Kopecky, and S Fujita. 1986. Life Span Study Report 10, Part 1. Cancer Mortality Among A-Bomb Survivors in Hiroshima and Nagasaki, 1950-1982. Technical Report. RERF TR.

Quanjer, PH, GJ Tammeling, JE Cotes, OF Pedersen, R Peslin and J-C Vernault. 1993. Lung volumes and forced ventilatory flows. Report of Working Party, Standardization of Lung Function Tests, European Community for Steel and Coal. Official Statement of the European Respiratory Society. Eur Resp J 6(suppl 16): 5-40.

Raabe, OG. 1984. Deposition and clearance of inhaled particles. In Occupational Lung Disease, edited by BL Gee, WKC Morgan, and GM Brooks. New York: Raven Press.

Ramazzini, B. 1713. De Moribis Artificium Diatriba (Diseases of Workers). In Allergy Proc 1990, 11:51-55.

Rask-Andersen A. 1988. Pulmonary reactions to inhalation of mould dust in farmers with special reference to fever and allergic alveolitis. Acta Universitatis Upsalienses. Dissertations from the Faculty of Medicine 168. Uppsala.

Richards, RJ, LC Masek, and RFR Brown. 1991. Biochemical and Cellular Mechanisms of Pulmonary Fibrosis. Toxicol Pathol 19(4):526
-539.

Richerson, HB. 1983. Hypersensitivity pneumonitis – pathology and pathogenesis. Clin Rev Allergy 1: 469-486.

—. 1990. Unifying concepts underlying the effects of organic dust exposures. Am J Ind Med 17:139-142.

—. 1994. Hypersensitivity pneumonitis. In Organic Dusts - Exposure, Effects, and Prevention, edited by R Rylander and RR Jacobs. Chicago: Lewis Publishing.

Richerson, HB, IL Bernstein, JN Fink, GW Hunninghake, HS Novey, CE Reed, JE Salvaggio, MR Schuyler, HJ Schwartz, and DJ Stechschulte. 1989. Guidelines for the clinical evaluation of hypersensitivity pneumonitis. J Allergy Clin immunol 84:839-844.

Rom, WN. 1991. Relationship of inflammatory cell cytokines to disease severity in individuals with occupational inorganic dust exposure. Am J Ind Med 19:15-27.

—. 1992a. Environmental and Occupational Medicine. Boston: Little, Brown & Co.

—. 1992b. Hairspray-induced lung disease. In Environmental and Occupational Medicine, edited by WN Rom. Boston: Little, Brown & Co.

Rom, WN, JS Lee, and BF Craft. 1981. Occupational and environmental health problems of the developing oil shale industry: A review. Am J Ind Med 2: 247-260.

Rose, CS. 1992. Inhalation fevers. In Environmental and Occupational Medicine, edited by WN Rom. Boston: Little, Brown & Co.

Rylander R. 1987. The role of endotoxin for reactions after exposure to cotton dust. Am J Ind Med 12: 687-697.

Rylander, R, B Bake, J-J Fischer and IM Helander 1989. Pulmonary function and symptoms after inhalation of endotoxin. Am Rev Resp Dis 140:981-986.

Rylander R and R Bergström 1993. Bronchial reactivity among cotton workers in relation to dust and endotoxin exposure. Ann Occup Hyg 37:57-63.

Rylander, R, KJ Donham, and Y Peterson. 1986. Health effects of organic dusts in the farm environment. Am J Ind Med 10:193-340.

Rylander, R and P Haglind. 1986. Exposure of cotton workers in an experimental cardroom with reference to airborne endotoxins. Environ Health Persp 66:83-86.

Rylander R, P Haglind, M Lundholm 1985. Endotoxin in cotton dust and respiratory function decrement among cotton workers. Am Rev Respir Dis 131:209-213.

Rylander, R and PG Holt. 1997. Modulation of immune response to inhaled allergen by co-exposure to the microbial cell wall components (13)-B-D-glucan and endotoxin. Manuscript.

Rylander, R and RR Jacobs. 1994. Organic Dusts: Exposure, Effects, and Prevention. Chicago: Lewis Publishing.

—. 1997. Environmental endotoxin – A criteria document. J Occup Environ Health 3: 51-548.

Rylander, R and Y Peterson. 1990. Organic dusts and lung disease. Am J Ind Med 17:1148.

—. 1994. Causative agents for organic dust related disease. Am J Ind Med 25:1-147.

Rylander, R, Y Peterson, and KJ Donham. 1990. Questionnaire evaluating organic dust exposure. Am J Ind Med 17:121-126.

Rylander, R, RSF Schilling, CAC Pickering, GB Rooke, AN Dempsey, and RR Jacobs. 1987. Effects after acute and chronic exposure to cotton dust - The Manchester criteria. Brit J Ind Med 44:557-579.

Sabbioni, E, R Pietra, and P Gaglione. 1982. Long term occupational risk of rare-earth pneumoconiosis. Sci Total Environ 26:19-32.

Sadoul, P. 1983. Pneumoconiosis in Europe yesterday, today and tomorrow. Eur J Resp Dis 64 Suppl. 126:177-182.

Scansetti, G, G Piolatto, and GC Botta. 1992. Airborne fibrous and non-fibrous particles in a silicon carbide manufacturing plant. Ann Occup Hyg 36(2):145-153.

Schantz, SP, LB Harrison, and WK Hong. 1993. Tumours of the nasal cavity and paranasal sinuses, nasopharynx, oral cavity,and oropharynx. In Cancer: Principles & Practice of Oncology, edited by VTJ DeVita, S Hellman, and SA Rosenberg. Philadelphia: JB Lippincott.

Schilling, RSF. 1956. Byssinosis in cotton and other textile workers. Lancet 2:261-265.

Schilling, RSF, JPW Hughes, I Dingwall-Fordyce, and JC Gilson. 1955. An epidemiological study of byssinosis among Lancashire cotton workers. Brit J Ind Med 12:217-227.

Schulte, PA. 1993. Use of biological markers in occupational health research and practice. J Tox Environ Health 40:359-366.

Schuyler, M, C Cook, M Listrom, and C Fengolio-Preiser. 1988. Blast cells transfer experimental hypersensitivity pneumonitis in guinea pigs. Am Rev Respir Dis 137:1449-1455.

Schwartz DA, KJ Donham, SA Olenchock, WJ Popendorf, D Scott Van Fossen, LJ Burmeister and JA Merchant. 1995. Determinants of longitudinal changes in spirometric function among swine confinement operators and farmers. Am J Respir Crit Care Med 151: 47-53.

Science of the total environment. 1994. Cobalt and Hard Metal Disease 150(Special issue):1-273.

Scuderi, P. 1990. Differential effects of copper and zinc on human peripheral blood monocyte cytokine secretion. Cell Immunol 265:2128-2133.
Seaton, A. 1983. Coal and the lung. Thorax 38:241-243.

Seaton, J, D Lamb, W Rhind Brown, G Sclare, and WG Middleton. 1981. Pneumoconiosis of shale miners. Thorax 36:412-418.

Sébastien, P. 1990. Les mystères de la nocivité du quartz. In Conférence Thématique. 23 Congrès International De La Médecine Du Travail Montréal: Commission international de la Médecine du travail.

—. 1991. Pulmonary Deposition and Clearance of Airborne Mineral Fibers. In Mineral Fibers and Health, edited by D Liddell and K Miller. Boca Raton: CRC Press.

Sébastien, P, A Dufresne, and R Bégin. 1994. Asbestos fibre retention and the outcome of asbestosis with or without exposure cessation. Ann Occup Hyg 38 Suppl. 1:675-682.

Sébastien, P, B Chamak, A Gaudichet, JF Bernaudin, MC Pinchon, and J Bignon. 1994. Comparative study by analytical transmission electron microscopy of particles in alveolar and interstitial human lung macrophages. Ann Occup Hyg 38 Suppl. 1:243-250.

Seidman, H and IJ Selikoff. 1990. Decline in death rates among asbestos insulation workers 1967-1986 associated with diminution of work exposure to asbestos. Annals of the New York Academy of Sciences 609:300-318.

Selikoff, IJ and J Churg. 1965. The biological effects of asbestos. Ann NY Acad Sci 132:1-766.

Selikoff, IJ and DHK Lee. 1978. Asbestos and Disease. New York: Academic Press.

Sessions, RB, LB Harrison, and VT Hong. 1993. Tumours of the larynx, and hypopharynx. In Cancer: Principles and Practice of Oncology, edited by VTJ DeVita, S Hellman, and SA Rosenberg. Philadelphia: JB Lippincott.

Shannon, HS, E Jamieson, JA Julian, and DCF Muir. 1990. Mortality of glass filament (textile) workers. Brit J Ind Med 47:533-536.

Sheppard, D. 1988. Chemical agents. In Respiratory Medicine, edited by JF Murray and JA Nadel. Philadelphia: WB Saunders.

Shimizu, Y, H Kato, WJ Schull, DL Preston, S Fujita, and DA Pierce. 1987. Life span study report 11, Part 1. Comparison of Risk Coefficients for Site-Specific Cancer Mortality based on the DS86 and T65DR Shielded Kerma and Organ Doses. Technical Report. RERF TR 12-87.

Shusterman, DJ. 1993. Polymer fume fever and other flourocarbon pyrolysis related syndromes. Occup Med: State Art Rev 8:519-531.

Sigsgaard T, OF Pedersen, S Juul and S Gravesen. Respiratory disorders and atopy in cotton wool and other textile mill workers in Denmark. Am J Ind Med 1992;22:163-184.

Simonato, L, AC Fletcher, and JW Cherrie. 1987. The International Agency for Research on Cancer historical cohort study of MMMF production workers in seven European countries: Extension of the follow-up. Ann Occup Hyg 31:603-623.

Skinner, HCW, M Roos, and C Frondel. 1988. Asbestos and Other Fibrous Minerals. New York: Oxford Univ. Press.

Skornik, WA. 1988. Inhalation toxicity of metal particles and vapors. In Pathophysiology and Treatment of Inhalation Injuries, edited by J Locke. New York: Marcel Dekker.

Smith, PG and R Doll. 1982. Mortality among patients with ankylosing sponchylitis after a single treatment course with X-rays. Brit Med J 284:449-460.

Smith, TJ. 1991. Pharmacokinetic models in the development of exposure indicators in epidemiology. Ann Occup Hyg 35(5):543-560.

Snella, M-C and R Rylander. 1982. Lung cell reactions after inhalation of bacterial lipopolysaccharides. Eur J Resp Dis 63:550-557.

Stanton, MF, M Layard, A Tegeris, E Miller, M May, E Morgan, and A Smith. 1981. Relation of particle dimension to carcinogenicity in amphibole asbestoses and other fibrous minerals. J Natl Cancer Inst 67:965-975.

Stephens, RJ, MF Sloan, MJ Evans, and G Freeman. 1974. Alveolar type I cell response to exposure to 0.5 ppm 03 for short periods. Exp Mol Pathol 20:11-23.

Stille, WT and IR Tabershaw. 1982. The mortality experience of upstate New York talc workers. J Occup Med 24:480-484.

Strom, E and O Alexandersen. 1990. Pulmonary damage caused by ski waxing. Tidsskrift for Den Norske Laegeforening 110:3614-3616.

Sulotto, F, C Romano, and A Berra. 1986. Rare earth pneumoconiosis: A new case. Am J Ind Med 9: 567-575.

Trice, MF. 1940. Card-room fever. Textile World 90:68.

Tyler, WS, NK Tyler, and JA Last. 1988. Comparison of daily and seasonal exposures of young monkeys to ozone. Toxicology 50:131-144.

Ulfvarson, U and M Dahlqvist. 1994. Pulmonary function in workers exposed to diesel exhaust. In Encyclopedia of Environmental Control Technology New Jersey: Gulf Publishing.

US Department of Health and Human Services. 1987. Report on cancer risks associated with the ingestion of asbestos. Environ Health Persp 72:253-266.

US Department of Health and Human Services (USDHHS). 1994. Work-Related Lung Disease Surveillance Report. Washington, DC: Public Health Services, Center for Disease Control and Prevention.

Vacek, PM and JC McDonald. 1991. Risk assessment using exposure intensivity: An application to vermiculite mining. Brit J Ind Med 48:543-547.

Valiante, DJ, TB Richards, and KB Kinsley. 1992. Silicosis surveillance in New Jersey: Targeting workplaces using occupational disease and exposure surveillance data. Am J Ind Med 21:517-526.

Vallyathan, NV and JE Craighead. 1981. Pulmonary pathology in workers exposed to nonasbestiform talc. Hum Pathol 12:28-35.

Vallyathan, V, X Shi, NS Dalal, W Irr, and V Castranova. 1988. Generation of free radicals from freshly fractured silica dust. Potential role in acute silica-induced lung injury. Am Rev Respir Dis 138:1213-1219.

Vanhee, D, P Gosset, B Wallaert, C Voisin, and AB Tonnel. 1994. Mechanisms of fibrosis in coal workers’ pneumoconiosis. Increased production of platelet-derived growth factor, insulin-like growth factor type I, and transforming growth-factor beta and relationship to disease severity. Am J Resp Critical Care Med 150(4):1049-1055.

Vaughan, GL, J Jordan, and S Karr. 1991. The toxicity, in vitro, of silicon carbide whiskers. Environmental Research 56:57-67.
Vincent, JH and K Donaldson. 1990. A dosimetric approach for relating the biological response of the lung to the accumulation of inhaled mineral dust. Brit J Ind Med 47:302-307.

Vocaturo, KG, F Colombo, and M Zanoni. 1983. Human exposure to heavy metals. Rare earth pneumoconiosis in occupational workers. Chest 83:780-783.

Wagner, GR. 1996. Health Screening and Surveillance of Mineral Dust Exposed Workers. Recommendation for the ILO Workers Group. Geneva: WHO.

Wagner, JC. 1994. The discovery of the association between blue asbestos and mesotheliomas and the aftermath. Brit J Ind Med 48:399-403.

Wallace, WE, JC Harrison, RC Grayson, MJ Keane, P Bolsaitis, RD Kennedy, AQ Wearden, and MD Attfield. 1994. Aluminosilicate surface contamination of respirable quartz particles from coal mine dusts and from clay works dust. Ann Occup Hyg 38 Suppl. 1:439-445.

Warheit, DB, KA Kellar, and MA Hartsky. 1992. Pulmonary cellular effects in rats following aerosol exposures to ultrafine Kevlar aramid fibrils: Evidence for biodegradability of inhaled fibrils. Toxicol Appl Pharmacol 116:225-239.

Waring, PM and RJ Watling. 1990. Rare deposits in a deceased movie projectionist. A new case of rare earth pneumoconiosis? Med J Austral 153:726-730.

Wegman, DH and JM Peters. 1974. Polymer fume fever and cigarette smoking. Ann Intern Med 81:55-57.

Wegman, DH, JM Peters, MG Boundy, and TJ Smith. 1982. Evaluation of respiratory effects in miners and millers exposed to talc free of asbestos and silica. Brit J Ind Med 39:233-238.

Wells, RE, RF Slocombe, and AL Trapp. 1982. Acute toxicosis of budgerigars (Melopsittacus undulatus) caused by pyrolysis products from heated polytetrafluoroethylene: Clinical study. Am J Vet Res 43:1238-1248.

Wergeland, E, A Andersen, and A Baerheim. 1990. Morbidity and mortality in talc-exposed workers. Am J Ind Med 17:505-513.

White, DW and JE Burke. 1955. The Metal Beryllium. Cleveland, Ohio: American Society for Metals.

Wiessner, JH, NS Mandel, PG Sohnle, A Hasegawa, and GS Mandel. 1990. The effect of chemical modification of quartz surfaces on particulate-induces pulmonary inflammation and fibrosis in the mouse. Am Rev Respir Dis 141:11-116.

Williams, N, W Atkinson, and AS Patchefsky. 1974. Polymer fume fever: Not so benign. J Occup Med 19:693-695.

Wong, O, D Foliart, and LS Trent. 1991. A case-control study of lung cancer in a cohort of workers potentially exposed to slag wool fibres. Brit J Ind Med 48:818-824.

Woolcock, AJ. 1989. Epidemiology of Chronic airways disease. Chest 96 (Suppl): 302-306S.

World Health Organization (WHO) and International Agency for Research on Cancer (IARC). 1982. IARC Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Lyon: IARC.

World Health Organization (WHO) and Office of Occupational Health. 1989. Occupational Exposure Limit for Asbestos. Geneva: WHO.


Wright, JL, P Cagle, A Shurg, TV Colby, and J Myers. 1992. Diseases of the small airways. Am Rev Respir Dis 146:240-262.

Yan, CY, CC Huang, IC Chang, CH Lee, JT Tsai, and YC Ko. 1993. Pulmonary function and respiratory symptoms of portland cement workers in southern Taiwan. Kaohsiung J Med Sci 9:186-192.

Zajda, EP. 1991. Pleural and airway disease associated with mineral fibers. In Mineral Fibers and
Health, edited by D Liddell and K Miller. Boca Raton: CRC Press.

Ziskind, M, RN Jones, and H Weill. 1976. Silicosis. Am Rev Respir Dis 113:643-665.