Abstract
Fine particulate matter (PM(2.5)) has become an important risk factor threatening human health. Epidemiological and toxicological investigations have revealed that PM(2.5) not only leads to cardiovascular dysfunction, but it also gives rise to various adverse health effects on the human body, such as cardiovascular and cerebrovascular diseases, cancers, neurodevelopmental disorders, depression and autism. PM(2.5) is able to penetrate both respiratory and placental barriers, thereby resulting in negative effects on fetal development. A large body of epidemiological evidences has suggested that gestational exposure to PM(2.5) increases the incidence of congenital diseases in offspring, including congenital heart defects. In addition, animal model studies have revealed that gestational exposure to PM(2.5) can disrupt normal heart development in offspring, although the potential molecular mechanisms have yet to be fully elucidated. The aim of the present review was to provide a brief overview of what is currently known regarding the molecular mechanisms underlying cardiac developmental toxicity in offspring induced by gestational exposure to PM(2.5).