Exposure to the non-phthalate plasticizer di-heptyl succinate is less disruptive to C57bl/6N mouse recovery from a myocardial infarction than DEHP, TOTM or related di-octyl succinate.

Phthalate plasticizers are incorporated into plastics to make them soft and malleable, but are known to leach out of the final product into their surroundings with potential detrimental effects to human and ecological health. The replacement of widely-used phthalate plasticizers, such as di-ethylhexyl phthalate (DEHP), that are of known toxicity, by the commercially-available alternative Tris(2-ethylhexyl) tri-mellitate (TOTM) is increasing. Additionally, several newly designed "green" plasticizers, including di-heptyl succinate (DHPS) and di-octyl succinate (DOS) have been identified as potential replacements.

Acute exposure to phthalates during recovery from a myocardial infarction induces greater inflammasome activation in male C57bl/6N mice.

Plasticizers escape from medical devices used in cardiac surgery into patient blood and tissues. Increased di-ethylhexyl phthalate (DEHP) exposure is correlated with chronic inflammation in vivo and increased cytokine release in exposed monocytes in vitro. To determine if acute phthalate exposure enhanced inflammation in a model of cardiac damage, we measured immune cell infiltration, inflammasome expression and cardiac function in male C57bl/6 N mice exposed to phthalates during recovery from a surgically-induced myocardial infarction (MI).

Emerging concepts and opportunities for endocrine disruptor screening of the non-EATS modalities.

Endocrine disrupting chemicals (EDCs) are ubiquitous in the environment and involve diverse chemical-receptor interactions that can perturb hormone signaling. The Organization for Economic Co-operation and Development has validated several EDC-receptor bioassays to detect endocrine active chemicals and has established guidelines for regulatory testing of EDCs. Focus on testing over the past decade has been initially directed to EATS modalities (estrogen, androgen, thyroid, and steroidogenesis) and validated tests for chemicals that exert effects through non-EATS modalities are less established.