Lung effects of acute oral administration of bisphenol A-loaded low-density polyethylene microplastics

Abstract

Microplastics are emerging contaminants that ubiquitously occur in foods. Recent evidence in experimental animals indicated that microplastics can be absorbed and accumulated in different organs [1]. Functional plastics carry additives such as bisphenol A (BPA), known to be an endocrine disruptor and an oxidant/proinflammatory agent in its free form. The health impact of the additives occurring in marketed plastics is, however, still unknown.

To investigate the potential effects of free and microplastic-adsorbed BPA (average particle size of ca. 110 μm [2]) in rat lung.

20 Wistar female and male adult rats were gavaged with free BPA, polyethylene-adsorbed BPA (PE-BPA), or vehicles (n=4-6). BPA concentration was 2 mg/kg in both groups. Animals were sacrificed after 24 hours, and tissues were collected. Gene expression was analyzed by RT-PCR.

The administration of free BPA did not change the expression of markers of oxidative stress, inflammation, and tissue repair in the lung. By contrast, the administration of PE-BPA induced the expression of iNos (P<0.05). A trend towards increased Tnf-α (P=0.06) and decreased Il-10 (P=0.07) was observed in PE-BPA rats. Free BPA and PE-BPA effects in oxidative stress and inflammation markers were less prominent in the liver and adipose tissue than in the lung. Finally, PE-BPA induced the expression of Tfg-β (P<0.01) and collagen (P<0.05) in the lungs.

BPA-PE administration induced lung damage. PE might accumulate in the lungs thereby facilitating the deleterious effects of BPA. However, we cannot rule out that damage is triggered by PE itself.