Effects For Air Pollution On Diabetes Mellitus Type 2

Effects for air pollution on diabetes mellitus type 2

Introduction

Air pollution is an important burden on public health, especially taking into account the high concentrations of pollutants, high population density and the penetrating nature of air pollution. (Rajagopalan 2012).

Traditionally it has been associated with air pollution with effects on respiratory and cardiovascular health of the population. Depending on the composition of pollutants, the dose and exposure time, the health effects of air pollution include: asthmatic crisis, respiratory infections, emphysema, lung cancer, obstruction of blood vessels, inhibition of hematopoiesis, andEven premature mortality (Kampa and Castaas, 2007). Studies conducted in recent years have shown that exposure to air pollution is associated with metabolic diseases, including type 2 diabetes mellitus (DM) (Pearson, 2010; Chuang, 2011; Wolf, 2016). 

Justification

Recently, studies have been published on the effect of air pollution on diabetes development. This has attracted the attention of those who design public health policies, due to the high proportion of the population exposed to high levels of pollutants for very long periods. Epidemiological studies are required on the association between air pollution and diabetes, as well as reviews that present in a summary way of possible physiological mechanisms that interact with the environment causing the development of DM.

Developing

Environmental pollution represents a constant threat to our health, well -being and quality of life.

Worldwide, only air pollution is the cause of about three million death a year in rural and urban areas, the most affected urban being (WHO, 2016).

The growing tendency in the prevalence of DM in Mexico may be due to population aging, the increase in the prevalence of obesity related to life styles (hypercaloric and sedentary lifestyle) and the exposure of environmental factors (Aguilar-Salinas, 2005). According to the latest air quality report in Mexico City in 2014, the average annual concentration of PM10 particulate material was 44 µg/m3, while the average annual concentration of PM2.5 was 22.8 µg/m3 (SMA-CDMX, 2015). PM2 composition.5 In Mexico City consists mainly of: bacteria, fungi and metals. These particles activate immune response and reactive species of oxygen ros causing a state of inflammation in the resident population (Calderón-Garcidueñas, 2015b)

PM particles are generated by human and natural sources. According to its origin there are primary (emitted by its direct source to the atmosphere) and secondary (formed in the atmosphere by chemical-physical transformation). The penetration of particles in the respiratory system is related to its size. They are classified as PM10, PM2.5 and PM0.1. PM10 are called thick fraction, with a diameter of 2.5 to 10 µm and deposit in the extrathoracic region (pharynx, nose). PM2.5 o Fine fraction have a diameter less than 2.5 µm and are deposited in the tracheobronchial region, being able to enter to the alveoli. And particles less than 0.1 µm or pm0.1 are the ultrafine fraction depositing mainly in alveoli. The particles that can enter the bloodstream after being inhaled are the PM2.5 and PM0.1, are distributed through systemic circulation reaching various organs even being able to enter the brain liquid. Its toxicity and health damage depend on the concentrations, sizes, number, physicochemical characteristics of them, and on the other hand it depends on the pulmonary immune integrity and the ventilatory patterns of the individual.

Atmospheric factors increase the risk of developing alteration in endothelial function, inflammatory response, in redox balance and cause oxidizing stress, which translates into an individual with alterations in DNA, proteins, lipids and carbohydrates that will be responsible for diseasesneurodegenerative, reproductive, eye, dermatological and metabolic.

DM is a metabolic disease that is characterized by hyperglycemia, insulin resistance and an altered insulin secretion by the β cells of the pancreas. Its etiology is multifactorial, and its main risk factors are genetic and environmental. Diabetes is the outcome of a process initiated several decades before diagnosis. A high percentage suffers arterial hypertension, abnormal cholesterol concentrations, triglycerides, HDL cholesterol, uric acid and develop insulin resistance before the appearance of hyperglycemia. Over time, blood glucose concentration increases, at first only after ingesting food, and years later even in a fast state (Aguilar-Salinas, 2005). When insulin resistance is present, insulin molecules cannot enter cells, glucose molecules remain inside the cells, unprocessed, and in the blood, giving rise to high levels of blood sugar. Beta cells in the pancreas, which produce insulin, respond to high blood glucose levels, and produce more insulin, which leads to high insulin levels, as well as blood sugar levels, also high, high. This is characteristic of type 2 diabetes. The processes for which exposure to atmospheric pollutants and the development of DM include: inflammation and oxidative stress. These processes increase insulin resistance.

The theoretical model proposed by Rajagopalan in 2012, tries to explain the origin of metabolic disease from exposure to air pollution. In addition to supercharging, atmospheric pollution mainly particulate material (PM) and ozone, cause directly or by the generation of biomolecules that begin and make an inflammatory response remain, DAMPS (Danger-Associated Molecular Patterns) Patterns). These patterns induce the immune mechanism with the activation of the TLRS (Toll Like Receivers) and the NLRS (Nucleotide-Binding Oligomena Domain-Like Receivers). Recent studies show that these receptors contribute to the development of insulin resistance associated with obesity. Oxidative stress leads to excess oxidants, also called free radicals. The oxidative response in this model is mediated by NADPH oxidase that is an enzyme that generates reactive species of ros (reactive oxygen speries) and reactive nitrogen species RNS (Reactive Nitrogen Species). Both can be produced by the organism or by exposure to the environment. The β cells of the pancreas are very sensitive to oxidative stress and could be destroyed by the ros and rns. Oxidative stress has been associated with insulin resistance.

In laboratory studies, it was observed that exposure to particulate material (PM) may be associated with high levels of systemic inflammation biomarkers: C-reactive protein, fibrinogen, IL-6, leukocytes, macrophages and cytokines. It has been observed that exposure to PM 2.5 is associated with macrophage levels in adipose tissue, increase in TNF-A and IL-6 and oxidative stress, it was also observed to be associated with fat formation, insulin resistance along with increases in levelsof leptin, due to decreased sensitivity to this hormone, called appetite inhibitor. Other researchers also found in laboratory studies, that long -term exposure to ozone lowers insulin levels and raises blood glucose levels. Both effects were reversed after exposure to ozone (Miller et al., 2016)

Some studies have found association between long -term exposure of PM10 and DM (Wang, 2014) and others have not been able to establish it (Park, 2015). The results have not been consistent due to the different characteristics of the populations, individual susceptibility, prevalence of DM, methodologies to evaluate the exposure, sources and types of exposure and degree and duration of the exposure. (Rajagopalan, 2012).

The individual inflammatory response to air pollutants depends on various factors, including age, gender, systemic antioxidants levels, and chronic diseases (Wittkopp et al., 2013). Additionally, it has been published that diabetics have greater susceptibility to some inflammation diseases (O’Neal, 2007).

In a study with young adults they observed systemic oxidative stress and inflammatory response dependent on the levels of atmospheric pollutants in Beijing (Huang, 2012).

Wolf and collaborators, in a study in Germany they found that the long -term exposure of PM10 was associated with an increase in insulin resistance. The average levels of PM10 (20 µg/m3) to which this population was exposed were lower than the standards established by the EPA, but higher than those recommended by WHO (Wolf, 2016). In another study it was found that exposure to PM2.5 It contributes to increasing the prevalence of DM in adults from the United States. (Pearson, 2010)

A study in Mexican Americans in California found that short -term exposure (up to 58 days) to PM2.5 was associated with an increase in insulin resistance, cholesterol levels and higher levels of glucose and insulin on an empty stomach. Long -term exposure (1 year) to PM2.5 was associated with higher levels of fasting glucose, greater insulin resistance and increased LDL cholesterol (Chen et al., 2016).

Conclusions

Atmospheric pollution, mainly by PM and O3, favors the development and permanence of inflammatory states and oxidative stress. Both are associated with insulin resistance. In some studies a clear association between long -term exposure of PMS and DT2 was found, while in others they could not be established.

In Mexico City studies were carried out in children exposed in the long -term.

We require studies in Mexico City on the burden of the consequences of air pollution, which inquire about the effects on metabolic diseases and their complications. It is necessary to implement follow -up programs that allow us to evaluate the effects of long -term pollution and allow the development of new primary and secondary prevention strategies.

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