title: Absence of proinflammatory cytokine gene expression in nasal biopsies from wood surface-coating industry workers.
abstract: Symptoms of nasal, pharyngeal and ocular discomfort have been reported among workers in the wood surface-coating industry. Symptoms were reported more often by workers using ultraviolet radiation-curable acrylate coatings (UV coatings), which contain potential chemical sensitizers, than by those using acid-curing coatings. Furthermore, increased levels of eosinophil cationic protein (ECP) and albumin, but not tryptase, in nasal lavage from workers exposed to UV coatings have been observed. To further examine whether air contaminants present in the UV-coating industry are causing the observed increase in symptoms, the inflammatory process in the nasal mucosa of workers exposed to UV coatings was investigated. Clinical and biochemical endpoints were selected to distinguish between specific and non-specific hypersensitivity and to test the hypothesis that the symptoms were consistent with Type IV hypersensitivity. The nasal lavage and nasal biopsy were performed under local anesthetic at the workplace during working hours after a minimum of 2 h of work in both the exposed and control groups. Albumin and ECP, and the cytokines tumor necrosis factor-alpha (TNF-alpha) and interleukin-8 (IL-8), were used as inflammatory markers. A multi-probe ribonuclease protection assay was used to attempt to detect cytokine variation in human nasal biopsies. The cytokine genes analyzed were TNF-alpha, GM-CSF, interferon-gamma, IL-2, IL-4 and IL-5. L32 and GAPDH were used as control genes for mRNA expression levels. Mucosal inflammation symptoms correlated with increased levels of albumin, but not with increased levels of ECP, secreted proinflammatory cytokines or cytokine gene mRNA expression. We conclude that the symptoms are non-specific and do not correlate with occupational exposure to UV coatings under the conditions of this investigation.
authors.affiliation: Department of Otorhinolaryngology, Huddinge University Hospital, Karolinska Institute, Sweden.
authors.forename: P
authors.initials: P
authors.lastname: Granstrand
authors.forename: L A
authors.initials: LA
authors.lastname: Nylander-French
authors.forename: G
authors.initials: G
authors.lastname: Lacks
authors.forename: M
authors.initials: M
authors.lastname: Holmström
authors.forename: J E
authors.initials: JE
authors.lastname: French
mesh_terms: D000418:Albumins / Q000378:metabolism; D001706:Biopsy; D002617:Chemical Industry; D016207:Cytokines / Q000235:genetics* / Q000276:immunology / Q000378:metabolism; D004804:Eosinophils / Q000276:immunology / Q000378:metabolism; D005260:Female; D015870:Gene Expression / Q000235:genetics*; D006801:Humans; D007249:Inflammation / Q000235:genetics / Q000276:immunology / Q000378:metabolism; D016209:Interleukin-8 / Q000235:genetics / Q000276:immunology / Q000378:metabolism; D008297:Male; D009296:Nasal Cavity / Q000473:pathology*; D017817:Nasal Lavage Fluid / Q000276:immunology; D009784:Occupational Diseases / Q000175:diagnosis; D016273:Occupational Exposure / Q000009:adverse effects; D010254:Paranasal Sinus Diseases / Q000175:diagnosis / Q000209:etiology; D010608:Pharyngeal Diseases / Q000175:diagnosis / Q000209:etiology; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000276:immunology / Q000378:metabolism; D014934:Wood
chemical_list: D000418:Albumins; D016207:Cytokines; D016209:Interleukin-8; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha