**Appendices and nomenclatures (Optional)**

cell stress response (measurable by plasma/tissue H-index), reinforcing the chaperone bal-

If a short-term PM2.5 exposure promotes innumerous damages, long-term exposure may evidence chronic effects on human health. Xu et al. showed in experimental mice model that long-term PM2.5 exposure induces alterations on adipose tissue and leads to mitochondrial dysfunction. If PM2.5 exposure is associated with other risk factors for T2DM, such as inadequate eating behavior, it observed an increase in adiposity, body weight, and glucose intolerance [16], as well as increase in glucose and triacylglycerol plasma levels. Exposure to PM2.5 can markedly potentiate metabolic dysfunction in an already compromised organism, pro-

The implications to health of a link between PM2.5 pollutants exposure and T2DM are critical problems to public health since air pollution is a pervasive risk factor that affects many people worldwide. In this way, it is important to highlight that modest reduction of pollution exposure may provide substantial public health benefits [45]. The underlying mechanisms responsible for this adverse effect in response to ambient PM2.5 air pollution need to be further investigated [43]. Both experimental and epidemiologic studies suggest that environmental exposures to air pollutants can increase the risk of insulin resistance, which lead to a link

This chapter aimed to describe pathophysiological mechanisms of the association between exposure to atmospheric pollution by PM2.5 and T2DM development, which are being highlighted in experimental studies connected to epidemiological data. The highlighted mechanisms involve inflammation, oxidative stress, and a clear participation of impaired cell stress response observed by alterations on HSP70 levels. Finally, epidemiological together with experimental studies reinforce the complex nature of T2DM etiology and highlights the PM2.5

It is known that type 2 diabetes results from the interaction between genetic susceptibility, environmental factors, and lifestyle choices, commonly accepted causes for the development of T2DM. However, it is argued that these factors alone cannot fully explain the rapid rise in the prevalence of diabetes [45]. If the high prevalence of T2DM is a result of an association between several risk factors, and air pollution is one, environmental protection represented by prioritization of steps to minimize the air pollution levels may be considered as health strategy to avoid T2DM [44]. Given the enormous number of people exposed to air pollution as shown in **Figure 1**, even conservative reduction of PM2.5 emission would translate into a substantial decrease in the population attributable fraction of T2DM related to environmental factors [45]. In perspective, it is expected that future studies will describe molecular mechanisms involved, highlight the responsible pollutants and the role of combined exposures to mixtures, and susceptibility factors. These discoveries of metabolic effects of air pollution may help relevant public health guidelines discussion and government decision in this cur-

ance [([eHSP72]/[iHSP70]) status] as a biomarker of T2DM risk.

moting relevant alteration in cell stress response.

between air pollution and T2DM.

air pollution as a critical health problem.

rent context of global urbanization [59].

**4. Conclusion**

80 Diabetes and Its Complications

