Type 2 diabetes mellitus (T2DM) is a critical public health issue, with its prevalence expected to rise sharply worldwide. Recent evidence points to environmental pollution, specifically exposure to hazardous chemicals like styrene (STY) and ethylbenzene (ETB), as a contributing factor. Found in plastics, synthetic rubbers, and resins, these pollutants are pervasive in the environment and pose significant health threats. Addressing these challenges requires a deeper understanding of how environmental and genetic factors combine to influence T2DM risk. The study, followed 2,219 adults from the Wuhan-Zhuhai cohort over six years to investigate the effects of styrene and ethylbenzene exposure on T2DM development. Using urinary biomarkers and genetic risk scores, the study assessed the combined impact of environmental exposure and genetic predisposition.
The findings demonstrate that exposure to styrene and ethylbenzene significantly elevates the risk of T2DM. The research highlights that individuals with high exposure levels had a substantially increased risk, which was further intensified by genetic susceptibility. Participants with both high exposure and high genetic risk faced the greatest likelihood of developing T2DM, illustrating a potent additive interaction. This suggests that the joint impact of environmental pollutants and genetic factors on T2DM is more severe than their individual contributions, underscoring the need to control environmental exposures. As fundamental building blocks of materials like polystyrene and polyethylene, STY/ETB emissions persist in the environment due to the widespread use of related products, including plastics, synthetic rubbers, and various resins.
Additionally, STY/ETB are present in food packed using polystyrene and polyethylene materials and are also found in tobacco smoke, vehicle exhaust and sanitizers. The use of hand sanitizers containing STY/ETB has witnessed a significant increase during the global coronavirus pandemic as they aid in preventing viral spread. In conclusion, the investigation provided novel and potent evidence demonstrating significant associations between STY/ETB exposure and increased risks of both prevalent and incident T2DM. Moreover, we found that genetic predisposition factors exacerbated the adverse impact of styrene and ethyl-benzene on T2DM risk increment. On the other hand, metal exposure from environmental pollution is associated with increased calcium buildup in the coronary arteries at a level comparable to traditional risk factors like smoking and diabetes.
This is according to a study published today in JACC, the flagship journal of the American College of Cardiology. The findings support that metals in the body are associated with the progression of plaque buildup in the arteries and potentially provide a new strategy for managing and preventing atherosclerosis. Researchers used data from the Multi-Ethnic Study of Atherosclerosis (MESA) prospective cohort, tracking 6,418 men and women aged 45-84 from diverse racial backgrounds free from clinical CVD, to measure urinary metal levels at the beginning of the study in 2000-2002. They examined non-essential (cadmium, tungsten, uranium) and essential (cobalt, copper, zinc) metals, both common in U.S. populations and associated with CVD. Results provided evidence that metal exposure may be associated with atherosclerosis over 10 years by increasing coronary calcification.
Epidemiological studies show that exposure to lead, cadmium, or arsenic is associated with cardiovascular death mostly attributable to ischemic heart disease. Oxidative stress derived from biological reactions in cells and tissues are most likely responsible for the organic damages and the onset of complications. Public health measures reducing metal exposure are associated with reductions in cardiovascular disease death. Together with strengthening public health measures to prevent metal exposures, development of more sensitive and selective measurement modalities, clinical monitoring of metal exposures, and the development of metal chelation therapies could further diminish the burden of cardiovascular disease attributable to metal exposure.
- Edited by Dr. Gianfrancesco Cormaci, PhD, specialista in Clinical Biochemistry.
Scientific references
Yu L et al. Eco-Environ Health 2024 Aug 12; in press.
Pan Z, Gong T, Liang P. Circ Res. 2024; 134(9):1160-1178.
Lamas GA et al. J Amer Heart Assoc. 2023; 12(13):e029852.
Li R, Cai M et al. Sci Total Environ. 2022; 849:157838.