Proceedings of The Physiological Society

Physiology 2016 (Dublin, Ireland) (2016) Proc Physiol Soc 37, PCA089

Poster Communications

Does a 20-day exposure to aldehydes impair pulmonary function and structure?

W. A. Zin1, M. B. Abreu1, A. Candido-Neto2, G. C. Carvalho1, N. V. Casquilho1, N. Carvalho2, R. T. Okuro1, G. C. Motta-Ribeiro2, M. N. Machado1, A. N. Cardozo1, A. S. Silva1, T. Barboza1, L. R. Vasconcellos1, D. Rodrigues3, L. M. Camilo1, L. A. Carneiro3, F. Jandre2, A. V. Pino2, A. Giannella-Neto2, L. H. Travassos1, M. N. Souza2, A. R. Carvalho1

1. Institute of Biophysics, Federeal University of Rio de Janeiro, Rio de Janeiro, RJ, Brazil. 2. Biomedical Engineering Program, Alberto Luis Coimbra Institute of Post-Graduation and Research in Engineering, Federal University of Rio de Janeiro, Rio de Janeiro, RJ, Brazil. 3. Institute of Microbiology, Federal University of Rio de Janeiro, Rio de Janeiro, RJ, Brazil.


There are conflicting and scarce results on the lung outcomes of exposure to airborne aldehydes. They are not only by-products of fuel combustion but widespread materials can also continuously release them. Hence, we aimed to investigate the effects on mice lung and nasal epithelium of exposure (8 h/day, 20 days) to environmental relevant concentrations of formaldehyde (250 ppb, FA group), acetaldehyde (500 ppb, AC group), mixtures 1 (M1 group: 300 ppb FA + 1 ppm AC) or 2 (M2 group: 250 ppb FA + 4 ppm AC). The study was approved by the Ethics Committee on the Use of Animals, Federal University of Rio de Janeiro (license code: 187-05/16), and conducted in accordance to ARRIVE guidelines and national legislation. 108 male and 108 female C57BL/6 mice were randomly allocated to exposed groups (FA, AC, M1 and M2, n=36/group) and their respective controls (n=18/group). After a 20-day exposure, animals were anaesthetised (isoflurane 2.5% and midazolam 5 mg/kg), no podal reflex to nociceptive stimuli could be triggered. Then they were paralysed (pancuronium bromide 0.3 mg/kg) and lung mechanics was evaluated by the forced oscillation technique based on the constant-phase model. Hence, tissue damping and elastance, airway resistance, and inertance were determined. Total lung capacity and lung stiffness were calculated. The animals were quickly euthanised by sectioning of abdominal aorta and inferior vena cava under deep anaesthesia. The experiments lasted 20 min. Lung tissue then was collected and prepared for histological analyses (morphology and inflammatory cells counting) and determination of pro-inflammatory mediators [interleukin-1β (IL-1β), keratinocyte-derived cytokine (KC), tumour necrosis factor-α (TNF-α), interleukin-6 (IL-6), chemokine (C-C motif) ligand 2 (CCL2) and monocyte chemoattractant protein-1 (MCP-1)]. Lesion of the nasal epithelium was assessed by a lesion score (LS) and Fisher's exact test. After passing Kolmogorov-Smirnov and Levene tests, the remaining data were evaluated by Student's t-test. Data were expressed as mean±SEM, P<0.05 was considered significant. FA mice showed higher Il-1β and CCL-2 contents than their respective control group (56.73±9.64 vs. 28.77±4.91 and 13.69±2.06 vs. 7.35±1.19 pg/mg of tissue, respectively). AC group presented a larger TNF-a level than its control group (91.11±22.63 vs. 30.29±8.83 pg/mg of tissue, respectively). LS was higher in both FA and M2. No other changes were disclosed. In conclusion, the concentrations of formal- and acetaldehyde and their acetaldehyde-enriched mixture used in this study seem to be able to trigger an inflammatory burden to the respiratory tract in mice, as indicated by pro-inflammatory interleukins release and nasal epithelium alterations.

Where applicable, experiments conform with Society ethical requirements