New IC3 study uncovers cause of Kawasaki disease in Japan linked to an environmental trigger contained in winds from agricultural regions in northeast China
Kawasaki disease may be caused by fungal particles or toxins carried on wind currents from dense croplands in northeastern China to Japan, according to our new study published in the Proceedings of the National Academy of Sciences of the United States of America. Kawasaki disease, the leading cause of acquired heart disease in children worldwide, inflames coronary arteries of affected young children and may lead to fatal heart disease. The causative agent of this disease, first observed in Japan in the 1960s and that has since then been recognized in other countries in the world, is yet unknown. Noting that the timing of Kawasaki disease outbreaks coincided with certain wind patterns from Asia, Xavier Rodó and colleagues simulated air currents and airborne particle transport in computer models on all days since 1977 and up to 2010, with high numbers of Kawasaki disease cases in Japan and using the vast epidemiologic database compiled by Nakamura and colleagues at Jichi Medical University in Japan. The thousands of model simulations conclusively suggested that the incidence of Kawasaki disease in many locations around Japan, in and out of epidemic years, peaked only when winds originated from a densely-cultivated region in northeastern China, characterized by vast extensions of cereal croplands. An aircraft campaign performed by IC3 scientists over Japan in 2011, in collaboration with Dr. Tanimoto from Tsukuba University and Dr. Brent Williams and Ian Lipkin at Columbia University, successfully isolated several Candida species as the dominant fungus aloft, demonstrating the potential for human disease in aerosols transported by wind currents.
Article PNAS-USA Number #14-00380: “Tropospheric winds from northeastern China carry the etiologic agent of Kawasaki disease from its source to Japan,” by Xavier Rodó et al.(http://www.pnas.org/content/111/22/7952.full.pdf+html).