![]() Prior work has shown that increased concentrations of pro-inflammatory cytokines such as IL-6, IL-1β, and IL-17A are among the most important hallmarks of smoke-mediated lung inflammation ( Shan et al., 2009, 2014 Chang et al., 2014). Several human studies and pre-clinical models of smoke-induced emphysema have also confirmed that lymphocytes (T and B cells) and lung antigen presenting cells (APCs) play pathogenic roles in chronic lung inflammation in smokers ( Shan et al., 2009, 2014 Churg et al., 2012b). Innate immune cells such as alveolar macrophages and neutrophils are recruited to the lungs in response to cigarette smoke ( Salvi, 2014). Even less is known regarding the health-related inhalation effects of atmospheric and workplace airborne carbon particulates. While our understanding of the immune basis of smoke-induced sterile inflammation has increased, the molecular mechanism underlying emphysema and its persistence despite smoking cessation remains unclear ( Cosio et al., 2009 Kheradmand et al., 2012). Compounding this risk is particulate air pollution due to the combustion of organic materials including biomass fuels, slash and burn agriculture, and coal ( Furlaneto et al., 1969 Arif et al., 1993 Dadvand et al., 2014). ![]() Despite public awareness of the harmful effects of smoking, in many large developing countries the prevalence of smoking is growing ( Eriksen et al., 2014). Tobacco smoking is linked to a long and growing ( Barnes, 2014 Carter et al., 2015) list of fatal illnesses (e.g., emphysema, cancer, and stroke) and is the major preventable cause of human death. Such modifications could potentially protect people who are exposed to carbon black nanoparticles in the environment or in workplaces where carbon black is used, such as factories that produce automobile tires and other rubber products. then went on to show that nanoparticles of carbon black can be modified in a way that allows them to be cleared from the lungs. And because the nanoparticles cannot be cleared, they are released into the lung when cells die, which perpetuates lung inflammation and damage. also confirmed that nanoparticles of carbon black can cause emphysema in mice.Ĭloser examination of the lung damage caused by the nanoparticles revealed that they trigger breakages in DNA, which leads to inflammation of the lung. These nanoparticles are produced by the incomplete combustion of the cigarettes. have shown that this black substance is made of nano-sized particles of a material called carbon black (which is also known as elemental carbon). Now, by studying lung tissue taken from smokers with emphysema, You et al. Previously, little was known about the composition of the substance that causes this blackening, or its significance in the development of emphysema. One of the hallmarks of long-term smoking is a blackening of the lung tissue that persists even if someone stops smoking. Moreover, cigarette smoke also contains large numbers of small particles and relatively little is known about the role played by these particles in smoking-related disease. There are thousands of chemicals in cigarette smoke and many of them have been linked to the development of lung cancer, although it has been difficult to pinpoint those that are responsible for smoking-related emphysema. Smoking for many years damages the lungs and leads to a disease called emphysema that makes it difficult to breathe and is often deadly. Thus, nCB causes sterile inflammation, DSB, and emphysema and explains adverse health outcomes seen in smokers while implicating the dangers of nCB exposure in non-smokers. Increasing the polarity or size of CB mitigated many adverse effects. Delivered by smoking or intranasally, nCB persisted indefinitely in mouse lung, activated lung APCs, and promoted T helper 17 cell differentiation through double-stranded DNA break (DSB) and ASC-mediated inflammasome assembly in phagocytes. ![]() Likewise, nCB intranasal administration induced emphysema in mouse lungs. In this study, we show that insoluble nanoparticulate carbon black (nCB) accumulates in human myeloid dendritic cells (mDCs) from emphysematous lung and in CD11c + lung antigen presenting cells (APC) of mice exposed to smoke. The effect of carbon black (CB), a universal constituent of smoke derived from the incomplete combustion of organic material, in smokers and non-smokers is less known. Chronic inhalation of cigarette smoke is the major cause of sterile inflammation and pulmonary emphysema.
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