Trace endotoxin in reclaimed water is only one of the risk sources in subchronic inhalation exposure.

Abstract

Pulmonary injury and inflammation have been detected in cases of subchronic inhalation exposure to reclaimed water, but the mechanism remains unclear. Endotoxin has been verified as the key risk factor in acute inhalation exposure through the TLR4 (Toll-like receptor 4) signalling pathway. In long-term exposure, endotoxin may also be a risk factor in reclaimed water, but the contribution of other health risk factors should not be underestimated. Wild-type C57BL/6J and TLR4-signalling-pathway-defective mice were used in this study to assess the risk of subchronic inhalation exposure to reclaimed water. Two types of reclaimed water, i.e., secondary effluent and MBR (membrane bioreactor) effluent, were found to induce pulmonary injury and inflammation in the wild-type mice and Tlr4-/- mutants. However, when both mice were exposed to the same concentrations of pure endotoxin in reclaimed water, only the wild-type mice that were treated with high-dose endotoxin showed pulmonary injury. In summary, non-TLR4 signalling pathways are related to lung inflammation caused by long-term exposure to reclaimed water. It is highly possible that pollutants in addition to endotoxin in the reclaimed water can induce chronic inflammation in the lung.