Pulmonary phthalate exposure and asthma - is PPAR a plausible mechanistic link?

Authors

  • Anette Kocbach Bølling Division of Environmental Medicine, Norwegian Institute of Public Health, PO Box 4404 Nydalen, N-0403 Oslo, Norway
  • Jørn A Holme Division of Environmental Medicine, Norwegian Institute of Public Health, PO Box 4404 Nydalen, N-0403 Oslo, Norway
  • Carl Gustaf Bornehag University of Karlstad, 651-88, Karlstad, Sweden
  • Unni C Nygaard Division of Environmental Medicine, Norwegian Institute of Public Health, PO Box 4404 Nydalen, N-0403 Oslo, Norway
  • Randi J Bertelsen Division of Environmental Medicine, Norwegian Institute of Public Health, PO Box 4404 Nydalen, N-0403 Oslo, Norway
  • Eewa Nånberg University of Karlstad, 651-88, Karlstad, Sweden
  • Johanna Bodin Division of Environmental Medicine, Norwegian Institute of Public Health, PO Box 4404 Nydalen, N-0403 Oslo, Norway
  • Amrit Kaur Sakhi Division of Environmental Medicine, Norwegian Institute of Public Health, PO Box 4404 Nydalen, N-0403 Oslo, Norway
  • Cathrine Thomsen Division of Environmental Medicine, Norwegian Institute of Public Health, PO Box 4404 Nydalen, N-0403 Oslo, Norway
  • Rune Becher Division of Environmental Medicine, Norwegian Institute of Public Health, PO Box 4404 Nydalen, N-0403 Oslo, Norway

Keywords:

phthalates, asthma, Peroxisome Proliferation Activated Receptors, molecular mechanism

Abstract

Due to their extensive use as plasticisers in numerous consumer products, phthalates have become ubiquitous environmental contaminants. An increasing number of epidemiological studies suggest that exposure to phthalates may be associated with worsening or development of airway diseases. Peroxisome Proliferation Activated Receptors (PPAR)s, identified as important targets for phthalates in early studies in rodent liver, have been suggested as a possible mechanistic link. In this review we discuss the likelihood of an involvement of PPARs in asthma development and exacerbation due to pulmonary phthalate exposure. First, we go through the literature on indoor air levels of phthalates and pulmonary phthalate kinetics. These data are then used to estimate the pulmonary phthalate levels due to inhalation exposure. Secondly, the literature on phthalate-induced activation or modulation of PPARs is summarized. Based on these data, we discuss whether pulmonary phthalate exposure is likely to cause PPAR activation, and if this is a plausible mechanism for adverse effects of phthalates in the lung. It is concluded that the pulmonary concentrations of some phthalates may be sufficient to cause a direct activation of PPARs. Since PPARs mainly mediate anti-inflammatory effects in the lungs, a direct activation is not a likely molecular mechanism for adverse effects of phthalates. However, possible modulatory effects of phthalates on PPARs deserve further investigation, including partial antagonist effects and/or cross talk with other signalling pathways. Moreover other mechanisms, including interactions between phthalates and other receptors, could also contribute to possible adverse pulmonary effects of phthalates.

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Published

2013-08-20

How to Cite

Kocbach Bølling, A., Holme, J. A., Bornehag, C. G., Nygaard, U. C., Bertelsen, R. J., Nånberg, E., … Becher, R. (2013). Pulmonary phthalate exposure and asthma - is PPAR a plausible mechanistic link?. EXCLI Journal, 12, 733–759. Retrieved from https://www.excli.de/index.php/excli/article/view/1189

Issue

Vol. 12 (2013)

Section

Original articles

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