Fukushima's lessons from the blue butterfly: A risk assessment of the human living environment in the post-Fukushima era : Lessons Learned from an Indicator Species, Post-Fukushima

Asthma is an inflammatory disorder caused by airway exposures to allergens and chemical irritants. Studies focusing on immune, smooth muscle, and airway epithelial function revealed many aspects of the disease mechanism of asthma. However, the limited efficacies of immune-directed therapies suggest the involvement of additional mechanisms in asthmatic airway inflammation. TRPA1 is an irritant-sensing ion channel expressed in airway chemosensory nerves. TRPA1-activating stimuli such as cigarette smoke, chlorine, aldehydes, and scents are among the most prevalent triggers of asthma. Endogenous TRPA1 agonists, including reactive oxygen species and lipid peroxidation products, are potent drivers of allergen-induced airway inflammation in asthma. Here, we examined the role of TRPA1 in allergic asthma in the murine ovalbumin model. Strikingly, genetic ablation of TRPA1 inhibited allergen-induced leukocyte infiltration in the airways, reduced cytokine and mucus production, and almost completely abolished airway hyperreactivity to contractile stimuli. This phenotype is recapitulated by treatment of wild-type mice with HC-030031, a TRPA1 antagonist. HC-030031, when administered during airway allergen challenge, inhibited eosinophil infiltration and prevented the development of airway hyperreactivity. Trpa1(-/-) mice displayed deficiencies in chemically and allergen-induced neuropeptide release in the airways, providing a potential explanation for the impaired inflammatory response. Our data suggest that TRPA1 is a key integrator of interactions between the immune and nervous systems in the airways, driving asthmatic airway inflammation following inhaled allergen challenge. TRPA1 may represent a promising pharmacological target for the treatment of asthma and other allergic inflammatory conditions.

The largest concern on the cesium-137 ((137)Cs) deposition and its soil contamination due to the emission from the Fukushima Daiichi Nuclear Power Plant (NPP) showed up after a massive quake on March 11, 2011. Cesium-137 ((137)Cs) with a half-life of 30.1 y causes the largest concerns because of its deleterious effect on agriculture and stock farming, and, thus, human life for decades. Removal of (137)Cs contaminated soils or land use limitations in areas where removal is not possible is, therefore, an urgent issue. A challenge lies in the fact that estimates of (137)Cs emissions from the Fukushima NPP are extremely uncertain, therefore, the distribution of (137)Cs in the environment is poorly constrained. Here, we estimate total (137)Cs deposition by integrating daily observations of (137)Cs deposition in each prefecture in Japan with relative deposition distribution patterns from a Lagrangian particle dispersion model, FLEXPART. We show that (137)Cs strongly contaminated the soils in large areas of eastern and northeastern Japan, whereas western Japan was sheltered by mountain ranges. The soils around Fukushima NPP and neighboring prefectures have been extensively contaminated with depositions of more than 100,000 and 10,000 MBq km(-2), respectively. Total (137)Cs depositions over two domains: (i) the Japan Islands and the surrounding ocean (130-150 °E and 30-46 °N) and, (ii) the Japan Islands, were estimated to be approximately 6.7 and 1.3 PBq, [corrected] respectively.We hope our (137)Cs deposition maps will help to coordinate decontamination efforts and plan regulatory measures in Japan.