Abstract
Purpose
To assess changes in oxidative DNA damage and lung function amongst a group of foundry workers resulting from an engineering intervention to reduce air respirable dust in their working environment.
Methods
We studied all 22 workers recruited from a typical small Taiwanese iron foundry plant before and 3 months after improvements to air exhaust control. The effectiveness of the air exhaust intervention in reducing respirable dust and SiO2 was determined by personal breathing-zone air sampling. Initial baseline biomarker measurements were taken of lung function and urinary 8-hydroxy-deoxyguanosine (8-OHdG) in all of the workers, with follow-up measurements taken 3 months after the engineering control was put in place. Generalized estimating equations were used to assess the effect of the intervention on lung function and oxidative DNA damage.
Results
Following the intervention, respirable dust density decreased from 2.87 ± 1.38 mg/m3 to 1.60 ± 0.70 mg/m3 (p = 0.07), and SiO2 concentration decreased from 0.43 ± 0.25 mg/m3 to 0.18 ± 0.11 mg/m3 (p < 0.05). Compared to initial baseline, significant improvements were found in lung function (FVC, FEV1, FVC%pred and FEV1%pred) amongst the workers after the engineering intervention. A significant increase in concentration of urinary 8-OHdG was observed after the engineering intervention in smokers, but not in non-smokers.
Conclusions
These findings indicate that reductions in workplace respirable dust and SiO2 concentration can result in improved lung function amongst foundry workers.
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References
Chuang CY, Lee CC, Chang YK, Sung FC (2003) Oxidative DNA damage estimated by urinary 8-hydroxydeoxyguanosine: influence of taxi driving, smoking and areca chewing. Chemosphere 52:1163–1171
Ding M, Chen F, Shi X, Yucesoy B, Mossman B, Vallyathan V (2002) Diseases caused by silica: mechanisms of injury and disease development. Int Immunopharmacol 2:173–182
Forastiere F, Goldsmith DF, Sperati A, Rapiti E, Miceli M, Cavariani F et al (2002) Silicosis and lung function decrements among female ceramic workers in Italy. Am J Epidemiol 156:851–856
Fubini B, Hubbard A (2003) Reactive oxygen species (ROS) and reactive nitrogen species (RNS) generation by silica in inflammation and fibrosis. Free Radic Biol Med 34:1507–1516
Gamble JF, Hessel PA, Nicolich M (2004) Relationship between silicosis and lung function. Scand J Work Environ Health 30:5–20
Gromadzinska J, Wasowicz W (2003) Oxidative stress-inducing workplace agents. Comments Toxicol 9:23–37
Halliwell B (2002) Effect of diet on cancer development: is oxidative DNA damage a biomarker? Free Radic Biol Med 15:968–974
Hnizdo E, Vallyathan V (2003) Chronic obstructive pulmonary disease due to occupational exposure to silica dust: a review of epidemiological and pathological evidence. Occup Environ Med 60:237–243
IARC (1997) Monographs on the evaluation of the carcinogenic risk of chemicals to humans. Silca, some silicates, coal dust and para-aramid fibrils. Monograph 68, IARC, Lyon
Kelly FJ, Sandstrom T (2004) Air pollution, oxidative stress, and allergic response. Lancet 363:95–96
Kim JY, Mukherjee S, Ngo LC, Christiani DC (2004) Urinary 8-hydroxy-2′-deoxyguanosine as a biomarker of oxidative DNA damage in workers exposed to fine particulates. Environ Health Perspect 112:666–671
Knaapen AM, Albrecht C, Becker A, Hohr D, Winzer A, Haenen GR et al (2002) DNA damage in lung epithelial cells isolated from rats exposed to quartz: role of surface reactivity and neutrophilic inflammation. Carcinogenesis 23:1111–1120
Kuo HW, Chang CL, Liang WM, Chung BC (1999) Respiratory abnormalities among male foundry workers in central Taiwan. Occup Med (Lond) 49:499–505
Liou SH, Shih WY, Chen YP, Lee CC (1996) Pneumoconiosis and pulmonary function defects in silica-exposed fire brick workers. Arch Environ Health 51:227–233
Mukherjee S, Palmer LJ, Kim JY, Aeschliman DB, Houk RS, Woodin MA et al (2004) Smoking status and occupational exposure affects oxidative DNA injury in boilermakers exposed to metal fume and residual oil fly ash. Cancer Epidemiol Biomarkers Prev 13:454–460
Orman A, Kahraman A, Cakar H, Ellidokuz Hy, Serteser M (2005) Plasma malondialdehyde and erythrocyte glutathione levels in workers with cement dust-exposure silicosis. Toxicology 207:15–20
Pilger A, Germadnik D, Schaffer A, Theiler A, Pils P, Sluka F et al (2000) 8-Hydroxydeoxyguanosine in leukocyte DNA and urine of quartz-exposed workers and patients with silicosis. Int Arch Occup Environ Health 73:305–310
Porter DW, Millecchia L, Robinson VA, Hubbs A, Willard P, Pack D et al (2002) Enhanced nitric oxide and reactive oxygen species production and damage after inhalation of silica. Am J Physiol Lung Cell Mol Physiol 283:L485–L493
Porter DW, Hubbs AF, Mercer R, Robinson VA, Ramsey D, McLaurin J et al (2004) Progression of lung inflammation and damage in rats after cessation of silica inhalation. Toxicol Sci 79:370–380
Porter DW, Millecchia LL, Willard P, Robinson VA, Ramsey D, McLaurin J et al (2006) Nitric oxide and reactive oxygen species production causes progressive damage in rats after cessation of silica inhalation. Toxicol Sci 90:188–197
Rappaport SM, Goldberg M, Susi P, Herrick RF (2003) Excessive exposure to silica in the US construction industry. Ann Occup Hyg 47(2):111–122
Rosenman KD, Reilly MJ, Rice C, Hertzberg V, Tseng C-Y, Anderson HA (1996) Silicosis among foundry workers. Am J Epidemiol 144:890–900
Scabilloni JF, Wang L, Antonini JM, Roberts JR, Castranova V, Mercer RR (2005) Matrix metalloproteinase induction in fibrosis and fibrotic nodule formation due to silica inhalation. Am J Physiol Lung Cell Mol Physiol 288:L709–L717
Schins RP, Duffin R, Hohr D, Knaapen AM, Shi T, Weishaupt C et al (2002) Surface modification of quartz inhibits toxicity, particle uptake, and oxidative DNA damage in human lung epithelial cells. Chem Res Toxicol 15:1166–1173
Tokiwa H, Sera N, Nakanishi Y, Sagai M (1999) 8-Hydroxyguanosine formed in human lung tissues and the association with diesel exhaust particles. Free Radic Biol Med 27:1251–1258
Ulvestad B, Bakke B, Eduard W, Kongerud J, Lund MB (2001) Cumulative exposure to dust causes accelerated decline in lung function in tunnel workers. Occup Environ Med 58:663–669
Yang SC, Lin YF (2009) Airway function and respiratory resistance in Taiwanese coal workers with simple pneumoconiosis. Chang Gung Med J 32:438–446
Acknowledgments
This research was supported by a grant from the Institute of Occupational Safety and Health, Council of Labour Affairs, Taiwan, ROC and in part by P01-ES06052 from the National Institutes of Health, USA.
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The authors declare that they have no conflict of interest.
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Lin, MH., Liou, SH., Chang, CW. et al. An engineering intervention resulting in improvement in lung function and change in urinary 8-hydroxydeoxyguanosine among foundry workers in Taiwan. Int Arch Occup Environ Health 84, 175–183 (2011). https://doi.org/10.1007/s00420-010-0580-9
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DOI: https://doi.org/10.1007/s00420-010-0580-9