Cytopathology of the Nasal Mucosa in Chronic Exposure to Diesel Engine Emission: A Five-Year Survey of Swiss Customs Officers

Glück, Ulrich; Schütz, Rudolf-M.; Gebbers, Jan‐Olaf

doi:10.1289/ehp.4401

Cited by 20 publications

(15 citation statements)

References 25 publications

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“…Glück et al described chemical-induced rhinitis due to the exposure to diesel engine emission in nasal swabs with goblet cell hyperplasia, increased metaplastic and dysplastic epithelia and an increase in leukocytes [14].…”

Section: Discussionmentioning

confidence: 99%

Cytology of nasal mucosa, olfactometry and rhinomanometry in patients after CO2 laser mucotomy in inferior turbinate hypertrophy.

Olszewska

Sieśkiewicz²,

Kasacka³

et al. 2010

Folia Histochem Cytobiol.

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Abstract:To evaluate the cytology of nasal mucosa and sense of smell and nasal patency in patients underwent carbon dioxide laser turbinoplasty (CO 2 laser mucotomy) due to chronic nasal hypertrophy. 46 patients with inferior turbinate hypertrophy underwent complete laryngological examination, anterior rhinomanometry, olfactory measurements and cytology of nasal mucous which were performed before and 3 months after CO 2 laser mucotomy. Laser mucotomy was performed under local anesthesia. Cytograms revealed significant changes in cell proportion before and after the surgery. Goblet cells predominated in nasal smears before the laser mucotomy. An average percentage of eosinophils in evaluated cytograms before the surgery was 2.1%. Three months after laser mucotomy we observed decrease in goblet cells proportion (the mean range of goblet cells was 16.4%) in nasal cytology. We have also observed improvement in olfactory function, however only in 7 patients (20.6%). The mean value of total nasal airway resistance (NAR) before treatment was 0.98±0.24 Pa/cm 3 /s at 75 Pa. Rhinomanometry after 3 months showed a reduction in mean total resistance from the pretreatment level to 0.77 Pa/ cm 3 /s. We believe that CO 2 laser mucotomy is an efficacious, minimally invasive and easy to use treatment of inferior turbinate hypertrophy which is performed under local anesthesia with little discomfort for the patient and does not require hospitalization.

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Section: Discussionmentioning

confidence: 99%

Cytology of nasal mucosa, olfactometry and rhinomanometry in patients after CO2 laser mucotomy in inferior turbinate hypertrophy.

Olszewska

Sieśkiewicz²,

Kasacka³

et al. 2010

Folia Histochem Cytobiol.

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“…The cell types were assessed in percent. The normal percentage values have been published earlier [19] . Comet Assay.…”

Section: Methods Used To Study the Integrity Of The Nasal Mucosamentioning

confidence: 99%

A Clinical Study on the Tolerability of a Liposomal Povidone-Iodine Nasal Spray: Implications for Further Development

Glück¹,

Martin²,

Bosse³

et al. 2006

ORL

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Purpose of Study: This phase I study assessed tolerability and local effect of a liposome dispersion with povidone-iodine (polyvinylpyrrolidone-iodine, PVP-I) as nasal spray. Procedures: Three groups received liposomal dispersion with PVP-I (2.2, 4.4 and 0% as control) in single and repeated use (3 days, three times a day). A set of functional and cytological tests as well as safety assessments were performed. Results: No safety-relevant finding or serious adverse events were reported, no evidence for cyto- nor genotoxicity obtained. No clinically relevant changes in mucosa appearance, nor in olfactory sense, nor in ciliary activity (sensitive indicator of local tolerance) occurred and no complaints about nasal airflow obstruction were observed. All liposomal formulations had a positive effect on the nasal mucosa, challenged by allergy in some volunteers. Conclusions and Message: Application of liposomal PVP-I spray to the nasal mucosa does not result in any demonstrable limitation of the nasal function nor in detectable damage to the multilayer ciliated epithelium of the nose. Improvement of various parameters of nasal function under liposomal PVP-I suggest improved mucociliary clearance. Explanation could be humidification, improved surfactant (phospholipid) level and/or sufficient mucolytic activity of iodide due to local application of the constituents.

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“…In a study on human middle ear epithelial cells, exposure to DEPs increased the expression of MUC5AC, a secreted form of mucin [10]. Goblet cell hyperplasia of the nasal mucosa was also observed in a group of officers occupied with clearing diesel vehicles over 5 years [11]. …”

Section: Introductionmentioning

confidence: 99%

Diesel Exhaust Particles Enhance <b><i>MUC4</i></b> Expression in NCI-H292 Cells and Nasal Epithelial Cells via the p38/CREB Pathway

Park

Kang

Kim

et al. 2016

Int Arch Allergy Immunol

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Background: Diesel exhaust particles (DEPs), the major contributors to air pollution, induce inflammatory responses in the nasal epithelium. Overproduction of airway mucins is an important pathogenic finding in inflammatory airway diseases. Objective: The aims of the present study were to determine the effect of DEPs on the expression of the mucin gene MUC4 and to investigate the underlying mechanism of DEP-induced MUC4 expression in NCI-H292 cells and primary nasal epithelial cells (PNECs). Methods: NCI-H292 cells were stimulated for 24 h with DEPs. Messenger RNA (mRNA) and protein expression of MUC4 was determined by real-time reverse transcription (RT) polymerase chain reaction (PCR) and Western blotting. NCI-H292 cells were exposed to 3 mitogen-activated protein kinase inhibitors (U0126, SB203580, and SP600125) and a CREB (cAMP response element-binding protein) inhibitor prior to stimulation with DEPs, and MUC4 expression was examined by RT-PCR and Western blotting. PNECs were pretreated with a p38 inhibitor and CREB inhibitor prior to stimulation with DEPs, and MUC4 expression was then determined by RT-PCR and/or Western blotting. Results: DEPs significantly increased the expression of MUC4 mRNA and protein. MUC4 mRNA and protein expression was inhibited by pretreatment with p38 and CREB inhibitors in NCI-H292 stimulated with DEPs. p38 and CREB inhibitors also blocked the expression of MUC4 mRNA and protein in DEP-stimulated PNECs. Conclusions: We demonstrated that DEPs stimulated the expression of MUC4 via the p38/CREB pathway in NCI-H292 cells and PNECs. The results of the present study pave the way for further studies on the role of MUC4 in DEP-induced hypersecretion in airway epithelium.

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Cytopathology of the Nasal Mucosa in Chronic Exposure to Diesel Engine Emission: A Five-Year Survey of Swiss Customs Officers

Cited by 20 publications

References 25 publications

Cytology of nasal mucosa, olfactometry and rhinomanometry in patients after CO2 laser mucotomy in inferior turbinate hypertrophy.

Cytology of nasal mucosa, olfactometry and rhinomanometry in patients after CO2 laser mucotomy in inferior turbinate hypertrophy.

A Clinical Study on the Tolerability of a Liposomal Povidone-Iodine Nasal Spray: Implications for Further Development

Diesel Exhaust Particles Enhance <b><i>MUC4</i></b> Expression in NCI-H292 Cells and Nasal Epithelial Cells via the p38/CREB Pathway

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