**Is Insulin Resistance Work Related? Is Insulin Resistance Work Related?**

#### Marina Oțelea Marina Oțelea

Additional information is available at the end of the chapter Additional information is available at the end of the chapter

http://dx.doi.org/10.5772/66333

#### **Abstract**

Incidence of insulin resistance continues to grow, becoming a major public health con‐ cern worldwide. Besides the classical risk factors (obesity, unhealthy nutrition and lack of exercise), extensive research about some occupational hazards supports their asso‐ ciation with insulin resistance and metabolic syndrome. On the one hand, the classical risk factors for insulin resistance are augmented by the changes of the working condi‐ tions: the occupational level of physical activity has a tendency to decrease, reducing its contribution to the overall level of physical activity and favouring a sedentary lifestyle and the occupational stress became the second most common work‐related health issue, contributing to the increase of the maladaptive habits, such as unhealthy nutrition. On the other hand, some insulin resistance risk factors are primarily occupational hazards: desynchronization of the circadian rhythm and sleep disruption during the night shifts, workplace air pollution (particles, solvents), heavy metals (arsenic, mercury) or persis‐ tent organic pollutants exposure. Meantime, workplaces are excellent settings for health‐ promotion programmes and metabolic risk reduction, if there is managerial commitment and support. Therefore, assessment of the risk, screening and workplace intervention programmes to reduce insulin resistance incidence should be included in the occupa‐ tional health service provision.

**Keywords:** insulin resistance, occupational stress, sleep desynchronization, night shifts, sleep duration, indoor air pollution, persistent organic pollutants arsenic, mercury

#### **1. Introduction**

Insulin resistance (IR) is a complex pathophysiological state characterized by reduced target cells responsiveness to insulin. The variety of its manifestations correspond to the complex‐ ity of insulin actions in specific tissues; the IR state reduces glucose uptake in muscle and other insulin‐dependent tissues, increases lipolysis and fatty acids delivery from adipose tis‐ sue, increases hepatic glucose output and sodium retention, impairs uric acid metabolism,

© 2016 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. © 2017 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

enhances vascular endothelium vasoconstriction and inflammation—promoting atherosclero‐ sis and induces a systemic low grade metabolic inflammation. Two are the major clinical con‐ sequences of the IR: the cardio‐vascular disease and diabetes. There are also significant links between IR and other clinical conditions such as non‐alcoholic fatty liver disease, polycystic ovary syndrome and colorectal cancer. Cardiovascular diseases are already the leading cause of death in industrialized countries [1] and diabetes prevalence has doubled between 1980 and 2014. Diabetes is estimated to become the seventh leading cause of death in 2030 [2]. Taken together, all medical conditions related to IR are responsible for a high percentage of the total mortality rate. Therefore, prevention and early diagnosis is a major public health topic.

For many years, IR has been considered a complication of obesity but a non‐obese metabolic obese profile has been identified in the past few years, as up to 15–30% of the IR subjects are in the normal range value of the BMI. The complex pathogeny of IR has been explained by complementary or synergic interactions between genetic and epigenetic factors, gut microbiota and environmental factors. As the environmental factors are the modifiable ones, the interven‐ tion, including workplace interventions, became nowadays a major health prevention direction.

Insulin resistance is difficult to measure in clinical practice; therefore, surrogates are used for its assessment such as basal insulinemia, the homeostasis assessment index (HOMA‐IR), glucose ratio to insulin and the glucose tolerance test. Clinical markers for IR are lipid metab‐ olism impairment (increased triglycerides, reduced HDL cholesterol and increased LDL cholesterol), plasma uric acid increase, renal disease markers (albuminuria) and cardiovas‐ cular effects (hypertension and cardiac remodelling). As already mentioned, obesity, particu‐ larly the visceral deposition of the adipose tissue, is a risk factor. In different configurations, according to different scientific organizations, these factors define the metabolic syndrome, a more suitable clinical diagnostic. Although I fundamentally agree with those considering that metabolic syndrome is an 'artificial syndrome'—in fact is just a cluster of risk factors—and that diagnostic procedures should be developed for an easier clinical diagnostic of the IR syndrome, this article will have to rely on data accumulated under the metabolic syndrome entity, as it is much more frequently used in the medical literature.

Nutrition, lack of physical exercise are not occupational hazards that are traditionally IR risk factors. In recent research, there is more and more evidence accumulated on how particular occu‐ pational risks are involved in IR and this makes the subject of increasing interest for occupational physicians.
