A study to ascertain the potential inhalation hazard of toenail dust

Abstract

The use of the podiatric nail drill has become an acceptable way of reducing onychogryphotic nails in the clinical setting. The present study has demonstrated the presence of particles that are potentially dangerous to the human lung when they are contaminated with bacterial endotoxin (bacterial cell wall components that may cause an inflammatory response). Toenail dust collected from podiatric nail drills was examined for size, endotoxin content and the ability to stimulate release of IL-8 (IL- interleukins stimulate the release of other mediators in septic shock and inflammation) from macrophages and lung epithelial cells in vitro. The size distribution revealed a large number of particles that would deposit in the nose, airways and lung alveoli. Endotoxin was detected in extracts of nail particles and, interestingly, a component of these particles was able to stimulate substantial release of IL-8 from lung epithelial cells. Suspensions of toenail particles stimulated IL-8 release from monocyte-derived macrophages. Destruction of the endotoxin with the antibiotic polymyxin B still resulted in IL-8 release, suggesting that the particles themselves initiated the response and not necessarily the endotoxin. The authors conclude that podiatrists who routinely carry out nail reduction could be inhaling particles that could deposit throughout the respiratory tract, where they could contribute to inflammation by stimulating release of IL-8 from cells via the particles themselves and via endotoxin.sch_pod1. Davies R R, Savage M A, Dust extracting drills. The Chiropodist 1980; 35(1): 4-12. 2. Harvey C K, Comparison of the effectiveness of nail dust extractors. Journal of the American Podiatric Medical Association 1993; 83(12): 669-673. 3. Blair J, Burrow J G, Millar N A, Aidoo K, Efficiency and effectiveness of dust extraction systems of podiatric nail drills. British Journal of Podiatric Medicine 1999; 2(2): 53-60. 4. Abramson C, Wilton J, Inhalation of nail dust from onychomycotic toenails. Part I. Characterization of particles. Journal of the American Podiatric Medical Association 1985a; 75: 563-567. 5. Abramson C, Wilton J, Nail dust aerosols from onychomycotic toenails. Part II. Clinical and serologic aspects. Journal of the American Podiatric Medical Association 1985b; 75: 631-638. 6. Brown D M, Donaldson K,Wool and Grain dusts stimulate TNF secretion by alveolar macrophages in vitro. Occupational and Environmental Medicine 1996; 53: 387-393. 7. Davies R R, Human nail dust in chiropodial practice: irritant, allergen and source of antibodies to Trichophyton rubrum. Journal of the Royal Society of Health 1984; 104: 1-5. 8. Davies R R, Ganderton M A, Savage M A, Human nail dust and precipitating antibodies to Trichophyton rubrum in chiropodists. Clinical Allergy 1983; 13: 309-315. 9. Gatley, M, Human nail dust: hazard to chiropodists or merely nuisance? Journal of the Society of Occupational Medicine 1991; 41: 121- 125. 10. Ward P E, Atopy and reaction to nail dust inhalation. Clinics in Podiatric Medicine and Surgery 1995; 12(2): 275-278. 11. Health, Safety and Welfare of Patients. Guidelines - Podiatric Nail Drills. British Journal of Podiatric Medicine October 2000. 12. Millar N A, Burrow J G, Hay J, Stevenson R, Putative risks of ocular infection for chiropodists and podiatrists. British Journal of Podiatric Medicine 1996; 51(11): 158-160. 13. Brown D M, The mechanisms of wool and dust mediated inflammation and leukocyte activation in the rat lung. Submitted as part of a PhD thesis, 1993. 14. Ning Y, Imrich A, Goldsmith C A, Qin G, Kobzik L, Alveolar macrophage cytokine production in response to air particles in vitro: role of endotoxin. J Toxicol Environ Health 2000A; 59: 165-180. 15. Streiter RM, Kunkel S L, Chemokines. In Crystal RG, West JB (Eds) The Lung. Philadelphia: Scientific Foundations, Lippincott Raven 1997: 155-179. 16. Driscoll K E, Carter J M, Hassenbein D G, Howard B, Cytokines and particle-induced inflammatory cell recruitment. Environmental Health Perspectives 1997; 105: 1159-1164. 17. Gilmour P S, Rahman I, Hayashi S, Hogg J C, Donaldson K, MacNee W, Adenoviral E1A primes alveolar epithelial cells to PM(10)-induced transcription of interleukin-8. Am J Physiol Lung Cell Mol Physiol 2001; 281: L598-L606. 18. MacNee W, Donaldson K, Exacerbations of COPD: environmental mechanisms. Chest 2000; 117: 390-397.6pub622pub

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