Geoengineering, Coal Fly Ash and the New Heart-Iron Connection: Universal Exposure to Iron Oxide Nanoparticulates

Globally, air pollution is the leading environmental cause of human disease and death, and it is a major contributor to cardiovascular disease. Air pollution damages the cardiovascular system by oxidative stress, inflammation, endothelial dysfunction, and pro-thrombotic changes. Ultrafine particulate matter from the combustion of fossil fuels delivers the most potent and harmful elements of air pollution. Coal fly ash is a rich source of nano-sized metal, iron oxide, and carbonaceous particles. Previous findings revealed that coal fly ash is widely utilized in undisclosed tropospheric aerosol geoengineering. Proper iron balance is central to human health and disease, and the harmful effects of iron are normallyprevented by tightly controlled processes of systemic and cellular iron homeostasis. Altered iron balance is linked to the traditional risk factors for cardiovascular disease. The iron-heart hypothesis is supported by epidemiological, clinical, and experimental studies. Biogenic magnetite (Fe3O4) serves essential life functions, but iron oxide nanoparticles from anthropogenic sources cause disease. The recent finding of countless combustion-type magnetic nanoparticles in damaged hearts of persons from highly polluted areas is definitive evidence of the connection between the iron oxide fraction of air pollution and cardiovascular disease. Spherical magnetic iron oxide particles found in coal fly ash and certain vehicle emissions match the exogenous iron pollution particles found in the human heart. Iron oxide nanoparticles cross the placenta and may act as seed material for future cardiovascular disease. The pandemic of non-communicable diseases like cardiovascular disease and also rapid global warming can be alleviated by drastically reducing nanoparticulate air pollution. It is crucial to halt tropospheric aerosol geoengineering, and to curb fine particulate emissions from industrial and traffic sources to avoid further gross contamination of the human race by iron oxide-type nanoparticles

Ambient particulate air pollution from vehicles promotes lipid peroxidation and inflammatory responses in rat lung

Oxidative stress plays a major role in the pathogenesis of particle-dependent lung injury. Ambient particle levels from vehicles have not been previously shown to cause oxidative stress to the lungs. The present study was conducted to a) determine whether short-term exposure to ambient levels of particulate air pollution from vehicles elicits inflammatory responses and lipid peroxidation in rat lungs, and b) determine if intermittent short-term exposures (every 4 days) induce some degree of tolerance. Three-month-old male Wistar rats were exposed to ambient particulate matter (PM) from vehicles (N = 30) for 6 or 20 continuous hours, or for intermittent (5 h) periods during 20 h for 4 consecutive days or to filtered air (PM <10 mum; N = 30). Rats continuously breathing polluted air for 20 h (P-20) showed a significant increase in the total number of leukocytes in bronchoalveolar lavage compared to control (C-20: 2.61 x 105 ± 0.51;P-20: 5.01 x 105 ± 0.81; P < 0.05) and in lipid peroxidation ([MDA] nmol/mg protein: C-20: 0.148 ± 0.01; P-20: 0.226 ± 0.02; P < 0.05). Shorter exposure (6 h) and intermittent 5-h exposures over a period of 4 days did not cause significant changes in leukocytes. Lipid damage resulting from 20-h exposure to particulate air pollution did not cause a significant increase in lung water content. These data suggest oxidative stress as one of the mechanisms responsible for the acute adverse respiratory effects of particles, and suggest that short-term inhalation of ambient particulate air pollution from street with high automobile traffic represents a biological hazard.

Health Effects of Ambient Particulate Pollutants / 예방의학회지

Recently, numerous studies have focused on the health effects of ambient particulate pollutants. Compared to earlier studies that focused on severe air pollution episodes, recent studies are more relevant to understanding the health effects of air pollution at levels common to contemporary cities. We reviewed recent epidemiologic studies that evaluated health effects of particulate air pollution and concluded that respirable particulate air pollution is an important contributing factor to acute mortality and morbidity. We observed increased respiratory and cardiovascular deaths, increased hospital admissions and visits, and decreased lung function. We also observed increased mortality and morbidity in a Korean population. Theses health effects were observed at levels below the current Ambient Air Quality Standard for particulate air pollution.