Metabolic syndrome (MetS) is a cluster of major cardiovascular risk factors like glucose intolerance, dyslipidemia, and high blood pressure. The most important risk factor for MetS is abdominal obesity. Also, insulin resistance is considered as an underlying pathophysiology of MetS. Under the current paradigm, excess calorie intake and physical inactivity are major contributors to obesity and insulin resistance.
Meanwhile, many environmental chemicals have recently received attention as a significant contributor to obesity and obesity-related metabolic dysfunction. Among them, persistent organic pollutants (POPs) are closely linked to most components of MetS. POPs are various chemicals which share characteristics of high lipophilicity, the ability to accumulate in fat, and resistance to biodegradation. Although most chlorinated POPs such as polychlorinated biphenyls and organochlorine pesticides were banned several decades ago and the emission of dioxins are strictly regulated in most developed countries, the exposure to these chemicals in the general population still occurs because they have widely contaminated our food chain. Also, POPs accumulated in human adipose tissue have become an important source of internal exposure as POPs are slowly but continuously released from adipose tissue to the circulation.
A substantial number of cross-sectional and prospective epidemiological studies on POPs and components of MetS have been published in recent several years. Human findings on POPs and MetS are strongly supported by experimental findings as well. Animal experiments demonstrated that animals exposed to low dose mixed POPs developed abdominal obesity, hepatosteatosis, and insulin resistance, which are all MetS-related conditions. Interestingly there is human and experimental evidence on non-monotonic dose response relation, suggesting that high dose is not always more harmful than low dose. Even though POPs are well-known endocrine disrupting chemicals (EDCs), chronic depletion of glutathione and mitochondrial dysfunction may be more plausible mechanisms.
In conclusion, the chronic presence of lipophilic chemical mixtures like POPs in adipose tissue may be related to the recent epidemic of obesity-related metabolic dysfunctions like MetS. Even though the toxicodynamics of POPs could not be separated from the dynamics of adipose tissue in a real world, currently, almost all studies on MetS have not considered the role of adipose tissue as an important internal source of exposure to POPs. Future epidemiological and experimental studies should consider the very obvious fact, namely, that in modern society, adipose tissue is widely contaminated with POPs.