Monday, 28 February 2011 23:59

Health Effects of Man-Made Fibres

Rate this item
(17 votes)

The industrial use of various types of man-made fibres has been increasing, particularly since restrictions were placed on the use of asbestos in view of its known health hazards. The potential for adverse health effects related to the production and use of man-made fibres is still being studied. This article will provide an overview of the general principles regarding the potential for toxicity related to such fibres, an overview of the various types of fibres in production (as listed in table 1) and an update regarding existing and ongoing studies of their potential health effects.

Table 1. Synthetic fibres

Man-made fibres

Aluminium oxide

Carbon/graphite

Kevlar® para-aramid

Silicon carbide fibres and
whiskers

 
Man-made vitreous fibres

Glass fibre

 

Mineral wool

 

Refractory ceramic fibre

Glass wool
Continuous glass filament
Special-purpose glass fibre

Rock wool
Slag wool

 

Toxicity Determinants

The primary factors related to potential for toxicity due to exposure to fibres are:

  1. fibre dimension
  2. fibre durability and
  3. dose to the target organ.

 

Generally, fibres that are long and thin (but of a respirable size) and are durable have the greatest potential for causing adverse effects if delivered to the lungs in sufficient concentration. Fibre toxicity has been correlated in short-term animal inhalation studies with inflammation, cytotoxicity, altered macrocyte function and biopersistence. Carcinogenic potential is most likely related to cellular DNA damage via formation of oxygen-free radicals, formation of clastogenic factors, or missegregation of chromosomes in cells in mitosis—alone or in combination. Fibres of a respirable size are those less than 3.0 to 3.5mm in diameter and less than 200μm in length. According to the “Stanton hypothesis,” the carcinogenic potential of fibres (as determined by animal pleural implantation studies) is related to their dimension (the greatest risk is associated with fibres less than 0.25μm in diameter and greater than 8mm in length) and durability (Stanton et al. 1981). Naturally occurring mineral fibres, such as asbestos, exist in a polycrystalline structure that has the propensity to cleave along longitudinal planes, creating thinner fibres with higher length-to-width ratios, which have a greater potential for toxicity. The vast majority of man-made fibres are non-crystalline or amorphous and will fracture perpendicularly to their longitudinal plane into shorter fibres. This is an important difference between asbestos and non-asbestos fibrous silicates and man-made fibres. The durability of fibres deposited in the lung is dependent upon the lung’s ability to clear the fibres, as well as the fibres’ physical and chemical properties. The durability of man-made fibres can be altered in the production process, according to end-use requirements, through the addition of certain stabilizers such as Al2O3. Because of this variability in the chemical constituents and size of man-made fibres, their potential toxicity has to be evaluated on a fibre-type by fibre-type basis.

Man-made Fibres

Aluminium oxide fibres

Crystalline aluminium oxide fibre toxicity has been suggested by a case report of pulmonary fibrosis in a worker employed in aluminium smelting for 19 years (Jederlinic et al. 1990). His chest radiograph revealed interstitial fibrosis. Analysis of the lung tissue by electron microscopy techniques demonstrated 1.3×109 crystalline fibres per gram of dry lung tissue, or ten times more fibres than the number of asbestos fibres found in lung tissue from chrysotile asbestos miners with asbestosis. Further study is needed to determine the role of crystalline aluminium oxide fibres (figure 1) and pulmonary fibrosis. This case report, however, suggests a potential for fibrization to take place when proper environmental conditions coexist, such as increased air flow across molten materials. Both phase-contrast light microscopy and electron microscopy with energy dispersion x-ray analysis should be used to identify potential airborne fibres in the work environment and in lung tissue samples in cases where there are clinical findings consistent with fibre-induced pneumoconiosis.

Figure 1. Scanning electron micrograph (SEM) of aluminium oxide fibres.

RES200F1

Courtesy of T. Hesterberg.

Carbon/Graphite Fibres

Carbonaceous pitch, rayon or polyacrylonitrile fibres heated to 1,200°C form amorphous carbon fibres, and when heated above 2,20 °C form crystalline graphite fibres (figure 2). Resin binders can be added to increase the strength and to allow moulding and machining of the material. Generally, these fibres have a diameter of 7 to 10μm, but variations in size occur due to the manufacturing process and mechanical manipulation. Carbon/graphite composites are used in the aircraft, automobile and sporting goods industries. Exposure to respirable-sized carbon/graphite particles can occur during the manufacturing process and with mechanical manipulation. Furthermore, small quantities of respirable-sized fibres can be produced when composites are heated to 900 to 1,10 °C. The existing knowledge regarding these fibres is inadequate to provide definite answers as to their potential for causing adverse health effects. Studies involving intratracheal injection of different graphite fibre composite dusts in rats produced heterogeneous results. Three of the dust samples tested produced minimal toxicity, and two of the samples produced consistent toxicity as manifested by cytotoxicity for alveolar macrophages and differences in the total number of cells recovered from the lung (Martin, Meyer and Luchtel 1989). Clastogenic effects have been observed in mutagenicity studies of pitch-based fibres, but not of polyacrylonitrile-based carbon fibres. A ten-year study of carbon fibre production workers, manufacturing fibres 8 to 10mm in diameter, did not reveal any abnormalities (Jones, Jones and Lyle 1982). Until further studies are available, it is recommended that exposure to respirable-sized carbon/graphite fibres be 1 fibre/ml (f/ml) or lower, and that exposure to respirable-sized composite particulates be maintained below the current respirable dust standard for nuisance dust.

Figure 2.   SEM of carbon fibres.

RES200F2

Kevlar para-aramid fibres

Kevlar para-aramid fibres are approximately 12μm in diameter and the curved ribbon-like fibrils on the surface of the fibres are less than 1mm in width (figure 3). The fibrils partially peel off the fibres and interlock with other fibrils to form clumps which are non-respirable in size. The physical properties of Kevlar fibres include substantial heat resistance and tensile strength. They have many different uses, serving as a reinforcing agent in plastics, fabrics and rubber, and as an automobile brake friction material. The eight-hour time-weighted average (TWA) of fibril levels during manufacturing and end-use applications ranges from 0.01 to 0.4 f/ml (Merriman 1989). Very low levels of Kevlar aramid fibres are generated in dust when used in friction materials. The only available health effects data is from animal studies. Rat inhalation studies involving one- to two-year time periods and exposures to fibrils at 25, 100 and 400 f/ml revealed alveolar bronchiolarization which was dose-related. Slight fibrosis and alveolar duct fibrotic changes also were noted at the higher exposure levels. The fibrosis may have been related to overloading of pulmonary clearance mechanisms. A tumour type unique to rats, cystic keratinizing squamous cell tumour, developed in a few of the study animals (Lee et al. 1988). Short-term rat inhalation studies indicate that the fibrils have low durability in lung tissue and are rapidly cleared (Warheit et al. 1992). There are no studies available regarding the human health effects of exposure to Kevlar para-aramid fibre. However, in view of the evidence of decreased biopersistence and given the physical structure of Kevlar, the health risks should be minimal if exposures to fibrils are maintained at 0.5 f/ml or less, as is now the case in commercial applications.

Figure 3. SEM of Kevlar para-aramid fibres.

RES200F5

Silicon carbide fibres and whiskers

Silicon carbide (carborundum) is a widely used abrasive and refractory material that is manufactured by combining silica and carbon at 2,400°C. Silicon carbide fibres and whiskers—figure 4 (Harper et al. 1995)—can be generated as by-products of the manufacture of silicon carbide crystals or can be purposely produced as polycrystalline fibres or monocrystalline whiskers. The fibres generally are less than 1 to 2μm in diameter and range from 3 to 30μm in length. The whiskers average 0.5μm in diameter and 10μm in length. Incorporation of silicon carbide fibres and whiskers adds strength to products such as metal matrix composites, ceramics and ceramic components. Exposure to fibres and whiskers can occur during the production and manufacturing processes and potentially during the machining and finishing processes. For example, short-term exposure during handling of recycled materials has been shown to reach levels up to 5 f/ml. Machining of metal and ceramic matrix composites have resulted in eight-hour TWA exposure concentrations of 0.031 f/ml and up to 0.76 f/ml, respectively (Scansetti, Piolatto and Botta 1992; Bye 1985).

Figure 4. SEMs of silicon carbide fibres (A) and whiskers (B).

A.

RES200F3

B.

RES200F4

Existing data from animal and human studies indicate a definite fibrogenic and possible carcinogenic potential. In vitro mouse cell culture studies involving silicon carbide whiskers revealed cytotoxicity equal to or greater than that resulting from crocidolite asbestos (Johnson et al. 1992; Vaughan et al. 1991). Persistent adenomatous hyperplasia of rat lungs was demonstrated in a subacute inhalation study (Lapin et al. 1991). Sheep inhalation studies involving silicon carbide dust revealed that the particles were inert. However, exposure to silicon carbide fibres resulted in fibrosing alveolitis and increased fibroblast growth activity (Bégin et al. 1989). Studies of lung tissue samples from silicon carbide manufacturing workers revealed silicotic nodules and ferruginous bodies and indicated that silicon carbide fibres are durable and can exist in high concentrations in lung parenchyma. Chest radiographs also have been consistent with nodular and irregular interstitial changes and pleural plaques.

Silicon carbide fibres and whiskers are respirable in size, durable, and have definite fibrogenic potential in lung tissue. A manufacturer of silicon carbide whiskers has set an internal standard at 0.2 f/ml as an eight-hour TWA (Beaumont 1991). This is a prudent recommendation based on currently available health information.

Man-made Vitreous Fibres

Man-made vitreous fibres (MMVFs) generally are classified as:

  1. glass fibre (glass wool or fibreglass, continuous glass filament and special-purpose glass fibre)
  2. mineral wool (rock wool and slag wool) and
  3. ceramic fibre (ceramic textile fibre and refractory ceramic fibre).

 

The manufacturing process begins with melting raw materials with subsequent rapid cooling, resulting in the production of non-crystalline (or vitreous) fibres. Some manufacturing processes allow for large variations in terms of fibre size, the lower limit being 1mm or less in diameter (figure 5). Stabilizers (such as Al2O3, TiO2 and ZnO) and modifiers (such as MgO, Li2O, BaO, CaO, Na2O and K2O) can be added to alter the physical and chemical properties such as tensile strength, elasticity, durability and thermal non-transference.

Figure 5. SEM of slag wool.

RES200F6

Rock wool, glass fibres and refractory ceramic fibres are identical in appearance.

Glass fibre is manufactured from silicon dioxide and various concentrations of stabilizers and modifiers. Most glass wool is produced through use of a rotary process resulting in 3 to 15μm average diameter discontinuous fibres with variations to 1μm or less in diameter. The glass wool fibres are bound together, most commonly with phenolic formaldehyde resins, and then put through a heat-curing polymerization process. Other agents, including lubricants and wetting agents, may also be added, depending on the production process. The continuous glass filament production process results in less variation from the average fibre diameter in comparison to glass wool and special-purpose glass fibre. Continuous glass filament fibres range from 3 to 25μm in diameter. Special-purpose glass fibre production involves a flame attenuation fibrization process that produces fibres with an average diameter of less than 3μm.

Slag wool and rock wool production involves melting and fibrizing slag from metallic ore and igneous rock, respectively. The production process includes a dish shaped wheel and wheel centrifuge process. It produces 3.5 to 7μm average diameter discontinuous fibres whose size may range well into the respirable range. Mineral wool can be manufactured with or without binder, depending on end-use applications.

Refractory ceramic fibre is manufactured through a wheel centrifuge or steam jet fibrization process using melted kaolin clay, alumina/silica, or alumina/silica/zirconia. Average fibre diameters range from 1 to 5μm. When heated to temperatures above 1,000°C, refractory ceramic fibres can undergo conversion to cristobalite (a crystalline silica).

MMVFs with different fibre diameters and chemical composition are used in over 35,000 applications. Glass wool is used in residential and commercial acoustical and thermal insulation applications, as well as in air handling systems. Continuous glass filament is used in fabrics and as reinforcing agents in plastics such as are employed in automobile parts. Special-purpose glass fibre is used in specialty applications, for instance in aircraft, that require high heat and acoustical insulation properties. Rock and slag wool without binder is used as blown insulation and in ceiling tiles. Rock and slag wool with a phenolic resin binder is used in insulation materials, such as insulation blankets and batts. Refractory ceramic fibre constitutes 1 to 2% of the worldwide production of MMVF. Refractory ceramic fibre is used in specialized high-temperature industrial applications, such as furnaces and kilns. Glass wool, continuous glass filament and mineral wool are manufactured in the greatest amounts.

MMVFs are thought to have less potential than naturally occurring fibrous silicates (such as asbestos) for producing adverse health effects because of their non-crystalline state and their propensity to fracture into shorter fibres. Existing data suggests that the most commonly utilized MMVF, glass wool, has the lowest risk of producing adverse health effects, followed by rock and slag wool, and then both special-purpose glass fibre with increased durability and refractory ceramic fibre. Special-purpose glass fibre and refractory ceramic fibre have the greatest potential for existing as respirable-sized fibres as they are generally less than 3mm in diameter. Special-purpose glass fibre (with increased concentration of stabilizers such as Al2O3) and refractory ceramic fibre are also durable in physiologic fluids. Continuous glass filaments are non-respirable in size and therefore do not represent a potential pulmonary health risk.

Available health data is gathered from inhalation studies in animals and morbidity and mortality studies of workers involved with MMVF manufacturing. Inhalation studies involving exposure of rats to two commercial glass wool insulation materials averaging 1μm in diameter and 20μm in length revealed a mild pulmonary cellular response which partly reversed following discontinuation of exposure. Similar findings resulted from an animal inhalation study of a type of slag wool. Minimal fibrosis has been demonstrated with animal inhalation exposure to rock wool. Refractory ceramic fibre inhalation studies resulted in lung cancer, mesothelioma and pleural and pulmonary fibrosis in rats and in mesothelioma and pleural and pulmonary fibrosis in hamsters at a maximum tolerated dose of 250 f/ml. At 75 f/ml and 120 f/ml, one mesothelioma and minimal fibrosis was demonstrated in rats, and at 25 f/ml, there was a pulmonary cellular response (Bunn et al. 1993).

Skin, eye, and upper and lower respiratory tract irritation can occur and depends on exposure levels and job duties. Skin irritation has been the most common health effect noted and can cause up to 5% of new MMVF manufacturing plant workers to leave their employment within a few weeks. It is caused by mechanical trauma to the skin from fibres greater than 4 to 5μm in diameter. It can be prevented with appropriate environmental control measures including avoiding direct skin contact with the fibres, wearing loose fitting, long-sleeved clothing, and washing work clothing separately. Upper and lower respiratory symptoms can occur in unusually dusty situations, particularly in MMVF product fabrication and end-use applications and in residential settings when MMVFs are not handled, installed or repaired correctly.

Studies of respiratory morbidity, as measured by symptoms, chest radiographs and pulmonary function tests among manufacturing plant workers generally have not found any adverse effects. However, an ongoing study of refractory ceramic fibre manufacturing plant workers has revealed an increased prevalence of pleural plaques (Lemasters et al. 1994). Studies in secondary production workers and end-users of MMVF are limited and have been hampered by the likelihood of the confounding factor of previous asbestos exposures.

Mortality studies of workers in glass fibre and mineral wool manufacturing plants are continuing in Europe and the United States. The data from the study in Europe revealed an overall increase in lung cancer mortality based upon national, but not local, mortality rates. There was an increasing trend of lung cancer in the glass and mineral wool cohorts with time since first employment but not with duration of employment. Using local mortality rates, there was an increase in lung cancer mortality for the earliest phase of mineral wool production (Simonato, Fletcher and Cherrie 1987; Boffetta et al. 1992). The data from the study in the United States demonstrated a statistically significant increased risk of respiratory cancer but failed to find an association between the development of cancer and various fibre exposure indices (Marsh et al. 1990). This is in accord with other case-control studies of slag wool and glass fibre manufacturing plant workers which have revealed an increased risk of lung cancer associated with cigarette smoking but not to the extent of MMVF exposure (Wong, Foliart and Trent 1991; Chiazze, Watkins and Fryar 1992). A mortality study of continuous glass filament manufacturing workers did not reveal an increased risk of mortality (Shannon et al. 1990). A mortality study involving refractory ceramic fibre workers is under way in the United States. Mortality studies of workers involved with product fabrication and end-users of MMVF are very limited.

In 1987, the International Agency for Research on Cancer (IARC) classified glass wool, rock wool, slag wool, and ceramic fibres as possible human carcinogens (group 2B). Ongoing animal studies and morbidity and mortality studies of workers involved with MMVF will help to further define any potential human health risk. Based on available data, the health risk from exposure to MMVF is substantially lower than what has been associated with asbestos exposure both from a morbidity and mortality perspective. The vast majority of the human studies, however, are from MMVF manufacturing facilities where exposure levels have generally been maintained below a 0.5 to 1 f/ml level over an eight-hour work day. The lack of morbidity and mortality data on secondary and end-users of MMVF makes it prudent to control respirable fibre exposure at or below these levels through environmental control measures, work practices, worker training and respiratory protection programmes. This is especially applicable with exposure to durable refractory ceramic and special purpose glass MMVF and any other type of respirable man-made fibre that is durable in biological media and that can therefore be deposited and retained in the pulmonary parenchyma.

 

Back

Read 20970 times Last modified on Saturday, 23 July 2022 19:57

" 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.