**4. Conclusion**

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 air pollution as a critical health problem.

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 current context of global urbanization [59].
