Epidemiologic and experimental studies suggest that environmental exposures to air pollutants can increase prevalence of metabolic and cardiorespiratory diseases. Among the risk factors, many studies have shown that air pollution, especially by fine particulate matter (PM2.5), can lead to the development of type 2 diabetes mellitus (T2DM) or make diabetics more susceptible to other health complications. This chapter aimed to discuss the pathophysiologic mechanisms evolved in susceptibility to cardiorespiratory PM2.5 effects in T2DM subjects, as well as the enhancing effect of PM2.5 exposure on development of T2DM. We discussed the pathophysiologic mechanisms of PM2.5 exposure and T2DM based on pro−/anti-inflammatory balance, metabolic regulation, redox status, and heat shock response, reinforcing the complex nature of T2DM etiology and highlighting the PM2.5 air pollution as a critical health problem.
Part of the book: Diabetes and Its Complications
Particulate matter (PM) is a mixture of solid particles and liquid droplets found in the air, and it is one of the most harmful air pollutants. When inhaled, it affects the pulmonary system, cardiovascular systems, and other tissues. The size, composition, and deposition of PM, mainly related to fine and ultrafine particulate matter, are factors that determine the harmful effects of exposure to particles. Among the main effects is the inducer of ROS production, and consequently oxidative tissue damage in target organs and other responses, mediated by inflammatory cytokines and cellular stress response. The main pathway through which particles are potent mediators of oxidative stress is the damage caused to DNA and lipid molecules, whereas the pro-inflammatory response involves an immune response against PM, which in turn, it is related to cell stress responses observed by heat shock proteins (HSPs) expression and release. Thus, the ability of an organism to respond to PM inhalation requires anti-oxidative, anti-inflammatory, and cellular stress defenses that can be impaired in susceptible subjects as people with chronic diseases as diabetes and obesity. In this chapter, we discuss the mechanistic aspects of PM effects on health and present some animal research models in particle inhalation studies.
Part of the book: Reactive Oxygen Species
The new coronavirus first appeared in December 2019 in Wuhan, China, being officially named severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) by the International Committee on Taxonomy of Viruses (ICTV), as well as the name of the disease has been described as COVID-19 (coronavirus disease 2019). In March 2020, the disease was considered a global pandemic, with currently more than 514 million cases worldwide, with 6.4 million deaths. Severe cases of COVID-19 progress to acute respiratory distress syndrome (ARDS), on average about 8–9 days after the onset of symptoms. It is also worth mentioning that the severity of the disease in patients is not only due to the viral infection but also due to the host response. This phase, called a cytokine storm, reflects a state of systemic immune activation, with high levels of cytokines, such as IL-6, IL-1b, IL-2, IL-12, IL-18, TNF, and interferon gamma (IFN-γ). In this sense, the management of the disease largely depends on symptomatic and supportive treatments. For severely or critically ill patients with acute respiratory distress syndrome (ARDS) and sepsis, in addition to supplemental oxygen, mechanical ventilation, and ARDS-specific therapies, antiviral and antibiotic treatments should also be considered. Thus, the purpose of this chapter is to describe the pathophysiology and treatment of SARS-CoV-2 infection.
Part of the book: COVID-19 Drug Development