Recovery from Welding-Fume-Exposure-Induced Lung Fibrosis and Pulmonary Function Changes in Sprague Dawley Rats

Jae Hyuck Sung*, Byung-Gil Choi{dagger}, Seung-Hee Maeng*, Soo-Jin Kim*, Yong Hyun Chung*, Jeong Hee Han*, Kyung Seuk Song{ddagger}, Yong Hwan Lee§, Yong Bong Cho{dagger}, Myung-Haing Cho{ddagger}, Kwang Jong Kim*, Jin Suk Hyun* and Il Je Yu*,1

* Center for Occupational Toxicology, Occupational Safety & Health Research Institute, Daejeon, 305–380, Korea; {dagger} Department of Environmental Engineering, Yonsei University, Wonju, Korea; {ddagger} College of Veterinary Medicine, Seoul National University, Seoul, Korea; and § Department of Preventive Medicine, Kosin University, Pusan, Korea

Received July 7, 2004; accepted September 22, 2004


    ABSTRACT
 TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Welder's pneumoconiosis has generally been determined as benign based on the absence of pulmonary function abnormalities in welders with marked radiographic abnormalities. Yet, there have also been several reports on welders with respiratory symptoms, indicating lung function impairment, X-ray abnormalities, and extensive fibrosis. Accordingly, this study attempted to investigate the inflammatory responses and pulmonary function changes in rats during a 60-day welding-fume-inhalation exposure period to elucidate the process of fibrosis. The rats were exposed to manual metal-arc stainless-steel welding fumes (MMA-SS) with total suspended particulate concentrations of 64.8 ± 0.9 (low dose) and 107.8 ± 2.6 mg/m3 (high dose) for 2 h per day in an inhalation chamber for 60 days. Animals were sacrificed after the initial 2-h exposure and after 15, 30, and 60 days, and the pulmonary function was also measured every week after the daily exposure. Elevated cellular differential counts were also measured in the acellular bronchoalveolar lavage fluid of the rats exposed to the MMA-SS fumes for 60 days. Among the pulmonary function test parameters, only the tidal volume showed a statistically significant and dose-dependent decrease after 35 to 60 days of MMA-SS welding-fume exposure. When the rats exposed to the welding fumes were left for 60 days to recover their lung function and cellular differentiation, recovery was observed in both the high and low-dose rats exposed up to 30 days, resulting in the disappearance of inflammatory cells and restoration of the tidal volume. The rats exposed for 60 days at the low dose also recovered from the inflammation and tidal volume loss, yet the rats exposed for 60 days at the high dose did not fully recover even after a 60-day recovery period. Therefore, when taken together, the results of the current study suggest that a decrease in the tidal volume could be used as an early indicator of pulmonary fibrosis induced by welding-fume exposure in Sprague Dawley rats, and fibrosis would seem to be preventable if the exposure is short-term and moderate.

Key Words: welding fume; pulmonary function test; tidal volume; welder's pneumoconiosis; lung fibrosis.


    INTRODUCTION
 TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Chest X-rays of welders indicate an increased profusion of small opacities due to the chronic inhalation of welding fumes. Exposure to iron oxide fumes would appear to cause iron oxide pneumoconiosis (siderosis), a prominently abnormal chest film with no impairment of pulmonary function, attributable to welding fume exposure (Beckett, 1996Go; Buerke et al., 2002Go, 2003Go). Welders' pneumoconiosis has shown a gradual clearing of the X-ray identified effects following removal from exposure. In a 1978 survey of electric arc welders in Britain, 7% reported some degree of pneumoconiosis, yet none showed progressive massive fibrosis (Artfield and Ross, 1978Go). Yet, this benign welders' siderosis is histologically and clinically different from the serious clinical implications of the interstitial fibrosis suffered by welders after long-term heavy exposure to welding fumes (Morgenroth and Verhagen-Schröter, 1984Go; Müller and Verhoff, 2000Go; Stanulla and Liebtrau, 1984Go; Stern et al., 1983Go; Zober, 1981Go). However, although there have been several human studies on pulmonary function changes with welding fume exposure, there have been no studies using laboratory animals to assess the effects of inhaled welding fumes on pulmonary function.

Previously, the current authors developed a three-phase welding-fume-exposure-induced fibrosis animal model that was used to investigate the induction and recovery processes of lung fibrosis induced by welding-fume exposure based on rats exposed to welding fumes up to 90 days followed by a 90-day recovery period (Yu et al., 2001Go, 2003Go). The results revealed that the critical point for the induction and recovery of welding-fume-exposure-induced lung fibrosis was 30 days of welding-fume exposure at a high concentration, at which point early and delicate fibrosis was observed in the perivascular and peribronchiolar regions (Yu et al., 2003Go), accompanied by elevated inflammatory cells and markers (Yu et al., in press). However, the current study investigated the change of pulmonary function during 60 days of welding-fume exposure using manual metal arc stainless steel (MMA-SS) and a 60-day recovery period.


    MATERIALS AND METHODS
 TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Generation of MMA-SS welding fumes. The welding fumes were generated as described in previous reports (Yu et al., 2000Go, 2001Go), and the rats were exposed to the fumes in a whole-body-type exposure chamber (1.3 m3, Dusturbo, Seoul); that is, a rotating stainless disc (SUS 304, 500 mm diameter, 10 mm thickness) as the base metal and welding rod (KST 308, 2.6 and 3.2 x 300 mm) restrained in the welding rod holder support. When the welding rod was moved by the pulley (0.098 m/s) and approached the rotating disc (16 rpm), an arc was produced and the rod consumed, generating welding fumes. It took 5 min to process each welding rod, 3 min for the rod to move forward and be consumed while generating fumes, and a further 2 min for the holder to be returned and another welding rod installed.

Sampling and analysis of welding fumes. The welding fumes were collected using NIOSH method 0500 (NIOSH, 1999Go) and sampled with a personal sampler (MSA 484107, Pittsburgh) that contained a mixed cellulose ester filter (0.8 mm pore size, 37 mm diameter, Millipore AAWP 03700, Bedford) every 30 min for 2 h at a flow rate of 2 l/min. The welding fumes were analyzed for their metal composition using an atomic absorption spectrophotometer (SpectAA-800, Varian, Palo Alto) based on the NIOSH method (1999)Go. The gaseous fumes, O3, NO2, and nitrous fumes were measured using Dräger tubes (Cat. No. 6733181, CH 31001, and CH30001, respectively), and the gaseous fumes were sampled using a gas detector pump (6400000, Dräger, Lübeck), according to the manufacturer's direction, 1 h after initiating the welding-fume exposure. The metal concentrations and gaseous fractions of the welding fumes are shown in Table 1. The chemical composition of the welding fumes was not evenly separated between the low and high dose, which may have been attributable to other components, such as silicon oxide, titanium oxide, and calcium oxide, that were not analyzed and moisture in the fume particles captured during sampling.


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TABLE 1 Concentrations of MMA-SS Welding-Fume Components

 
Animals. Six-week-old male, specific pathogen-free Sprague Dawley (SD) rats, purchased from Biogenomics (Korea), were acclimated to a 12-h light, 12-h dark cycle with light from 0800 to 2000 h. The rats were fed Purina Chow 5001 (Ralston Purina Co., St Louis, MO) and tap water ad libitum for 1 week before initiating the experiment. The rats weighing 172.74 ± 0.63 g were randomly assigned to 7 groups per dose. Among the exposure groups, one group was sacrificed immediately after 2 h of exposure; then the other three groups were sacrificed after 15, 30, and 60 days of exposure, respectively. Meanwhile, the recovery groups were allowed to recover for 60 days after 15, 30, and 60 days of exposure, respectively, where each group consisted of four unexposed, four low-dose exposed, and four high-dose exposed rats. The time weighted average (TWA) concentrations in the exposure doses were 64.8 ± 0.9 mg/m3 (low dose) and 107.8 ± 2.6 mg/m3 (high dose) total suspended particulate for 2 h per day. The high dose was generated based on the consumption of 18 welding rods (3.2-mm diameter) per h, while the low dose was based on the consumption of 12 welding rods (2.6-mm diameter) per h. The experiment was carried out in accordance with the Guide of Animal Experimentation of the National Institute for Toxicological Research of Korea.

Pulmonary function test. Any change of pulmonary function in the rats exposed to welding fumes was evaluated every week during 60 days using a ventilated bias flow whole-body plethysmograph (WBP) (SFT3816, Buxco Electronics, Sharon, CT) consisting of a reference chamber and animal chamber interconnected by a pressure transducer (MAX1320, Buxco Electronics, Sharon, CT), thereby decreasing the errors due to anesthesia or trachea intubation. The parameters for the pulmonary function test included the tidal volume (TV, ml), minute volume (MV, ml/min), frequency (BPM, breath/min), inspiratory time (Ti, s), expiratory time (Te, s), peak inspiratory flow (PIF, ml/s), and peak expiratory flow (PEF, ml/s). After being exposed to the welding fumes for 2 h, the rats were put in the animal chamber, left for 40 min to stabilize, and the plethysmography was initiated by measuring the selected parameter values for 5 min.

Bronchoalveolar lavage (BAL). A BAL was performed on animals from each exposure group one day after the designated 2 h, 15, 30, and 60 days of welding-fume exposure and from each 60-day recovery group. The rats were deeply anesthetized with an overdose of sodium pentobarbital, then exsanguinated by severing the abdominal aorta. The lungs were lavaged 14 times with 3-ml aliquots of a warm calcium- and magnesium-free phosphate buffer solution (PBS), pH 7.4. The samples were also centrifuged for 7 min at 500 x g, and the cell-free BAL fluid was discarded. The cell pellets from all washes for each rat were then combined, washed, and resuspended in 1 ml of a PBS buffer and evaluated, as described below (Antonini et al., 1996Go, 1997Go; Lemaire and Ouellet, 1996Go).

BAL cell evaluation. The total cell numbers were determined using a hemocytometer. The cells were cultured for 40 min to attach a coverslip in a 24-well culture dish, then stained with Wright Giemsa Sure Stain (Adamson et al., 1995Go). Nonspecific esterase (NSE) staining to differentiate alveolar macrophages from granulocytes was also performed using an alpha-Naphthyl acetate esterase staining kit (Sigma, St. Louis, MO). The attached cells were fixed in a citrate-acetone-methanol fixative for 30 s at room temperature, washed with distilled water, and air-dried. The samples were then stained with a Trizmal buffer containing Fast blue RR salt (pH 7.6, maleate 1 M), alpha Naphthyl acetate, and ethylene glycol monomethyl ether for 30 min at 37°C. Thereafter, the samples were washed again with distilled water for 3 min, counterstained with Leukostat, and air-dried. The NSE-positive cells, mostly macrophages, were identifiable due to their black granulation, whereas granulocytes are NSE-negative.

Statistical analysis. All results are expressed as means ± standard error (SE). An analysis of variance (ANOVA) test and Duncan's multiple range tests were used to compare the body weight, brochoalveolar lavaged cell distribution, and parameters from the pulmonary function test obtained from the two dose groups with those obtained from the unexposed control rats. The level of significance was set at p < 0.05 and p < 0.01.


    RESULTS
 TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Body Weight Changes During Exposure and Recovery Periods
The rats exposed to the high concentration of welding fumes showed statistically significant changes in their body weights from 7 through 60 days (p < 0.05–0.01) (Fig. 1A). No statistically significant body weight changes were noted during the 60-day recovery period for the 2-h, 15-, 30-, and 60-day exposure groups (Fig. 1B). The decrease in the body weights observed during the 60-day exposure period was recovered during the 60-day recovery period. The animals did not show any distinct behavioral changes related to the welding-fume exposure.



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FIG. 1. Body weight change during 60-day exposure period. The error bars indicate the standard error (*p < 0.05; **p < 0.01 versus control). (A) 60 days exposure, (B) 60 days exposure and 60 days recovery.

 
Cellular Parameters of Lung Inflammation
The rats exposed to the welding fumes were studied for cell profile changes in the BAL fluid. Tables 2 and 3 show the differential counts of BAL cells among the 15-, 30-, and 60-day exposure groups and recovery groups, respectively. At all time points, the inhalation of MMA-SS welding fumes induced a dramatic and significant infiltration of cells into the lungs. When compared to the control group, all exposure groups, except for the 2-h low-dose group, had significantly elevated total cell numbers (p < 0.01–0.05). The alveolar macrophages (AM), polymorphonuclear cells (PMN), and lymphocyte numbers were also substantially elevated for the exposure groups at most time points when compared to the control groups (p < 0.01). The percentage of macrophages was over 80%, and the AM and PMN numbers increased dose-dependently for 15 days and time-dependently throughout the 60-day exposure period (Table 2). Although the 15 and 30-day exposure groups (including both the high and low dose) did not show any statistically significant increase of inflammatory cells during the 60-day recovery period, indicating recovery from the welding-fume-induced pulmonary damage, the 60-day high-dose exposure group showed a statistically significant increase in the total cell and AM numbers even after the 60-day recovery period (Table 3), indicating a macrophage-mediated pulmonary damage recovery process.


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TABLE 2 Bronchoalveolar Lavage Cell Distribution During 60-Day Exposure Period

 

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TABLE 3 Bronchoalveolar Lavage Cell Distribution During 60-Day Recovery Period

 
Pulmonary Function Test
Among the pulmonary function test parameters, only the tidal volume showed significant dose- and time-dependent decreases after 35 to 60 days of welding-fume exposure (p < 0.01) (Fig. 2A). Despite inconsistent effects on the pulmonary function during the recovery period, indicating various recovery features, the tidal volume decrease observed in the 15- and 30-day high and low-dose welding-fume exposure groups was completely restored after the 60-day recovery period (Figs. 2B and 2C). Only the 60-day high-dose welding-fume exposure group had difficulties in achieving a full tidal volume recovery, even after the 60-day recovery period (Fig. 2D).



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FIG. 2. Tidal volume change in lung function test after welding-fume exposure (*p < 0.05; **p < 0.01 versus control; ap < 0.05 low versus high dose; bp < 0.01 low versus high dose). (A) 60 days exposure, (B) 15 days exposure and 60 days recovery, (C) 30 days exposure and 60 days recovery, (D) 60 days exposure and 60 days recovery.

 

    DISCUSSION
 TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
The present study attempted to investigate the pulmonary function changes when animals were exposed to stainless steel arc welding (MMA-SS) fumes, which are known to have the highest toxicity, during 60 days of exposure and 60 days of recovery after certain designated exposure periods. Although the doses selected in the current study, 64.8 ± 0.9 mg/m3 (low dose) and 107.8 ± 2.6 mg/m3 (high dose), may seem to be too high to evaluate lung fibrosis, the concentrations are appropriate, as previous studies monitoring welding-fume exposure in the shipbuilding industry have reported on concentrations ranging from 6–73 mg/m3 (Geometric mean (GM), 16.6 mg/m3) to 0.3–91.16 mg/m3 (GM 5.59 mg/m3) (Choi et al., 1999Go; Kwag and Paik, 1997Go). However, since the exposure duration in the present study was only 2 h compared with 6 h in most other inhalation studies or 8 h in a real workplace, the actual doses used in this study were effectively 20–40 mg/m3. In addition, this welding fume exposure study presumed that the actual exposure to welding fumes in very confined workplaces, like shipbuilding or containers, could be 20–30 mg/m3 over nearly 10 years in a severe case (Yu et al., 2001Go, 2003Go). As such, the doses used in the current study do not reflect actual workplace concentrations, as the mass action effect and rate of deposition would be several fold higher when considering the ventilation rate and alveolar surface area differences between rats and humans. A previous study by the current authors clearly showed that the critical point for the induction and recovery of welding-fume-induced fibrosis is 30 days exposure. At this time, distinct peribronchiolar and perivascular fibrosis was observed with an increasing recruitment of inflammatory cells, including AM and PMN (Yu et al., 2001Go, 2003Go, in press). The pulmonary function, as indicated by the tidal volume in this study, also began to decrease at this time. When the exposure was stopped at this time (30 days) and the animals allowed to recover, fibrosis was preventable, as seen in a previous study (Yu et al., 2003Go) and evidenced in the present study by the elimination of the inflammatory cells from the BAL cells and pulmonary function recovery. In addition, this study also highlighted a decrease in the tidal volume as an early indicator of pulmonary fibrosis induced by welding-fume exposure that can be cured if exposure is stopped immediately.

Except for the tidal volume, none of the other pulmonary function parameters exhibited any noticeable change during the 60-day welding-fume exposure and recovery period (Sung et al., 2004Go). It should be noted that the time of the pulmonary function measurements may have resulted in no noticeable changes, except for the tidal volume, as the measurements were performed without exposure to any substances, such as metacholine or other inducers, seen in many obstructive pulmonary parameter changes in other studies (Arts et al., 2003Go; Michielsen et al., 2001Go).

Extensive studies have already investigated chronic effects on lung function. For example, welders exposed to welding fumes showed a significantly impaired lung function and, with advancing years, greater deterioration of lung function compared to controls (Akbar-Khanzadeh, 1980Go). Some of the main effects of welding-fume exposure on the pulmonary function are: (1) usual day-to-day welding exposure in the absence of acute inhalation injury does not necessarily not lead to a severe or apparent degree of lung function impairment (Sferlazza and Beckett, 1991Go); (2) a transient effect on the pulmonary function can occur at the time of exposure, yet this can be spontaneously reversed during the unexposed period before the next exposure (Beckett et al., 1996Go; Sferlazza and Beckett, 1991Go); and (3) stainless steel welders tend to have more significant across-shift reductions in lung function when compared with mild steel welders with similar exposure histories, while manual metal arc welders show a decreased across-shift in lung function compared with gas metal arc welders. However, it is still possible that heavily exposed or more susceptible workers could experience a different outcome from the above welders and control populations. Welders in confined and poorly ventilated spaces, like shipbuilding, have been found to exhibit more negative lung function effects than welders in well-ventilated areas (Akbar-Khanzadeh, 1980Go, 1993Go; Chinn et al., 1990Go; Mur et al., 1985Go; Oxhoj et al., 1979Go). Although interstitial lung fibrosis is usually conceived to have purely restrictive defects, a mixed pattern of obstructive and restrictive defects has also been seen. The lung function parameters for restrictive defects show a reduced lung volume, reflected in the vital capacity, residual volume, functional residual capacity, and total lung preserving FEV1/FVC ratio, and decreased DLCO (diffusing capacity for carbon monoxide) (Redlich, 1996Go). In the present study, only the tidal volume among the lung function parameters was significantly decreased in a dose-dependant manner from day 35 to day 60 during the exposure period and even after the 60-day recovery period, indicating fibrosis induction and progression after 30 days of exposure and that the diffusely progressed fibrosis after 60 days of exposure could not be eradicated even after a sufficient recovery period.


    NOTES
 

1 To whom correspondence should be addressed at Center for Occupational Toxicology, 104–8 Munji-dong, Yuseong-gu, Daejeon 305–380, Korea. Fax: +82-42-863-8361. E-mail: u1670916{at}chollian.net.


    REFERENCES
 TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Adamson, I. Y. R., Prieditis, H., and Hedgecock, C. (1995). Pulmonary response of mice to fiberglass: Cytokinetic and biochemical studies. J. Toxicol. Environ. Health 46, 411–424.[ISI][Medline]

Akbar-Khanzadeh, F. (1980). Long-term effects of welding fumes upon respiratory symptoms and pulmonary function. J. Occup. Med. 22, 337–341.[ISI][Medline]

Akbar-Khanzadeh, F. (1993). Short-term respiratory function changes in relation to work shift welding fume exposures. Int. Arch. Occup. Environ. Health 64, 393–397.[ISI][Medline]

Antonini, J. M., Krishna-Murthy, G. G., and Brain, J. D. (1997). Responses to welding fume: Lung injury inflammation and release of tumor necrosis factor-alpha and interleukin-1 beta. Exp. Lung. Res. 23, 205–227.[ISI][Medline]

Antonini, J. M., Krishna-Murthy, G. G., Rogers, R. A., Albert, R., Ulrich, G. D., and Brain, J. D. (1996). Pneumotoxicity and pulmonary clearance of different welding fumes after intratracheal instillation in the rat. Toxicol. Appl. Pharmacol. 114, 188–199.

Artfield, M. D., and Ross, D. S. (1978). Radiologic abnormalities in electric-arc welders. Br. J. Ind. Med. 35, 117–122.[ISI][Medline]

Arts, J. H. E., Bloksma, N., Leusink-Muis, T., and Kuper, C. F. (2003). Respiratory allergy and pulmonary irritation to trimellitic anhydride in Brown Norway rats. Toxicol. Appl. Pharm. 187, 38–49.[CrossRef][ISI][Medline]

Beckett, W. S. (1996). Industries associated with respiratory diseases. In Welding: Occupational and Environmental Respiratory Diseases (P. Harber, M. B. Schenker, and J. R. Balmes, Eds.), pp. 704–717. Mosby, St. Louis, MO.

Beckett, W. S., Pace, P. E., Sferlazza, S. J., Perman, G. D., Chen, A. H., and Xu, X. P. (1996). Airway reactivity in welders: A controlled prospective cohort study. J. Occup. Environ. Med. 38, 1229–1238.[CrossRef][ISI][Medline]

Buerke, U., Schneider, J., Muller, K. M., and Woitowitz, H. J. (2003). Interstitial pulmonary siderofibrosis: Requirements for acceptance as new occupational disease. Pneumologie 57, 9–14.[CrossRef][Medline]

Buerke, U., Schneider, J., Rösler, J., and Woitowitz, H. J. (2002). Interstitial pulmonary fibrosis after severe exposure to welding fumes. Am. J. Ind. Med. 41, 259–268.[CrossRef][ISI][Medline]

Chinn, D., Stevenson, I., and Cotes, J. (1990). Longitudinal respiratory survey of shipyard workers: Effects of trade and atopic status. Br. J. Ind. Med. 47, 83–90.[ISI][Medline]

Choi, H., Kim, K., Ahn, S. H., Park, W. M., Kim, S. J., Lee, Y. J., and Chung, K. C. (1999). Airborne concentrations of welding fume and metals of workers exposed to welding fume. Korean Ind. Hyg. Assoc. J. 9, 56–72.

Kwag, Y. S., and Paik, N. S. (1997). A study on airborne concentration on welding fumes and metals in confined spaces of a shipyard. Korean Ind. Hyg. Assoc. J. 7, 107–126.

Lemaire, I., and Ouellet, S. (1996). Distinctive profile of alveolar macrophage-derived cytokine release induced by fibrogenic and nonfibrogenic mineral dusts. J. Toxicol. Environ. Health 47, 465–478.[CrossRef][ISI][Medline]

Michielsen, C. P., Leusink-Muis, A., Vos, J. G., and Bloksma, N. (2001). Hexachlorobenzene-induced eosinophilic and granulomatous lung inflammation is associated with in vivo airways hyperresponsiveness in the Brown Norway rat. Tox. Appl. Pharm. 172, 11–20.[CrossRef][ISI][Medline]

Morgenroth, K., and Verhagen-Schröter, G. (1984). Light and electron microscopic examination and energy dispersive radiologic microanalysis of biopsy probes for the pathogenesis of arc-welders lung. Atemw-Lungenkrkh 10, 451–456.

Müller, K. M., and Verhoff, M. A. (2000). Graduation of sidero-pheumoconiosis. Atemw-Lungenkrkh 18, 428–436.

Mur, J. M., Teculescu, D., Pham, Q. T., Gaertner, M., Massin, N., Meyer-Bisch, C., Moulin, J. J., Diebold, F., and Pierre, F. (1985). Lung function and clinical findings in a cross sectional study of arc welders: An epidemiological study. Int. Arch. Occup. Environ. Health 57, 1–18.[CrossRef][ISI][Medline]

NIOSH, (1999). NIOSH manual of analytical methods, method No. 0500, 7300. National Institute for Occupational Health, Cincinnati.

Oxhoj, H., Bake, B., Wedel, H., and Wihelmsen, L. (1979). Effects of electric arc welding on ventilatory function. Arch. Environ. Health 34, 211–217.[ISI][Medline]

Redlich, C. A. (1996). Pulmonary fibrosis and interstitial lung diseases. In Occupational and Environmental Respiratory Diseases (P. Harber, M. B. Schenker, and J. R. Balmes, Eds.) pp. 216–227. Mosby, St. Louis, MO.

Sferlazza, S. J., and Beckett, W. S. (1991). The respiratory health of welders. Am. Rev. Respir. Dis. 143, 1134–1148.[ISI][Medline]

Stanulla, H., and Liebtrau, G. (1984). Electrowelder's lung. Prax. Klin. Pneumol. 38, 14–18.[Medline]

Stern, R. M., Pigott, G. H., and Abraham, J. L. (1983). Fibrogenic potential of welding fumes. J. Appl. Toxicol. 3, 18–30.[Medline]

Sung, J. H., Choi, B. G., Maeng, S. H., Kim, S. J., Chung, Y. H., Han, J. H., Hyun, J. S., Song, K. S., Cho, Y. B., and Yu, I. J. (2004). Changes of pulmonary function during 60 days of welding fume exposure period. J. Toxicol. Pub. Health 20(1), 55–61.

Yu, I. J., Kim, K. J., Chang, H. K., Song, K. S., Han, K. T., Han, J. H., Maeng, S. H., Chung, Y. H., Park, S. H., Chung, K. H., et al. (2000). Pattern of deposition of stainless welding fume particle inhaled into the respiratory systems of Sprague-Dawley rats exposed to a novel welding fume generating system. Toxicol. Lett. 116, 103–111.[CrossRef][ISI][Medline]

Yu, I. J., Song, K. S., Chang, H. K., Han, J. H., Chung, Y. H., Han, K. T., Chung, K. H., and Chung, H. K. (2003). Recovery from manual arc-stainless steel welding-fume exposure induced lung fibrosis in Sprague-Dawley rats. Toxicol. Lett. 143, 247–259.[CrossRef][ISI][Medline]

Yu, I. J., Song, K. S., Chang, H. K., Han, J. H., Kim, K. J., Chung, Y. H., Maeng, S. H., Park, S. H., Han, K. T., Chung, K. H., et al. (2001). Lung fibrosis in Sprague-Dawley rats. Induced by exposure to manual metal arc-stainless steel welding fumes. Toxicol. Sci. 63, 99–106.[Abstract/Free Full Text]

Yu, I. J., Song, K. S, Maeng, S. H., Kim, S. J., Sung, J. H., Han, J. H., Chung, Y. H., Cho, M. H., Chung, K. H., Han, K. T., et al. (2004). Inflammatory and genotoxic responses during 30-day welding-fume exposure period. Toxicol. Lett. 154, 105–115.[CrossRef][Medline]

Zober, A. (1981). Symptoms and finding at the bronchopulmonay system of electric arc welder. Zbl. Bakt. Mikrobiol. Hyg. 173, 92–119.





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