Incomplete combustion produces a pollutant mixture that includes polycyclic aromatic Hydrocarbons (PAHs). Previous work by the Columbia centre for Children’s Environmental Health (CCCEH) and others linked exposure to PAH with symptoms of asthma and other adverse health effects in young children. Inhaled â2-adrenergic agonists are mainstays in the treatment of reactive airway diseases. These exogenous catecholamines engage membrane-bound â2-adrenergic receptors (â2AR) on airway epithelial and smooth muscle cells to cause airway dilation. The author hypothesised that exposure to PAH might similarly interfere with the function of â2AR in airway epithelial or smooth muscle cells, reducing the efficacy of a medication important for the treatment of asthma symptoms. A PAH mixture was devised, based on ambient levels measured prenatally among a cohort of pregnant women participating at the CCCEH. Primary airway epithelial and smooth muscle cells were exposed to varying concentrations of the PAH mixture and expression, function, and signalling of â2AR were assessed. Murine tracheal epithelial cells and human airway smooth muscle cells, after exposure to a PAH mixture exhibited reduced expression and function of â2AR.These findings support the authors’ hypothesis that environmentally relevant PAHs can impede â2AR-mediated airway relaxation, and suggest a new paradigm where air pollutants not only contribute to the pathogenesis of childhood asthma, but also diminish responsiveness to standard therapy.
Authors: Factor, Phillip; Akhmedov, Alexander T.; McDonald, Jacob D.; Qu, Anna; Wu, Jie; Jiang, Hong; Dasgupta, Trisha; Panettieri, Reynold A., Jr.; Perera, Frederica; Miller, Rachel L. ;Full Source: American Journal of Respiratory Cell and Molecular Biology [online computer file] 2011, 45(5), 1045-1049 (Eng) ;