BACKGROUND: Particulate matter (PM), a major component of ambient air pollution, accounts for a substantial burden of diseases and fatality worldwide. Maternal exposure to PM during pregnancy is particularly harmful to children's health since this is a phase of rapid human growth and development. METHOD: In this review, we synthesize the scientific evidence on adverse health outcomes in children following prenatal exposure to the smallest toxic components, fine (PM RESULTS: Maternal exposure to fine and ultrafine PM directly and indirectly yields numerous adverse birth outcomes and impacts on children's respiratory systems, immune status, brain development, and cardiometabolic health. The biological mechanisms underlying adverse effects include direct placental translocation of ultrafine particles, placental and systemic maternal oxidative stress and inflammation elicited by both fine and ultrafine PM, epigenetic changes, and potential endocrine effects that influence long-term health. CONCLUSION Policies to reduce maternal exposure and health consequences in children should be a high priority. PM
Adult ; Air Pollutants/adverse effects* ; Air Pollution/prevention & control* ; Animals ; Cardiovascular Diseases/chemically induced* ; Child Health ; Child, Preschool ; Disease Models, Animal ; Endocrine System Diseases/chemically induced* ; Epigenomics ; Female ; Humans ; Immune System Diseases/chemically induced* ; Infant ; Infant, Newborn ; Male ; Maternal Exposure/adverse effects* ; Nervous System Diseases/chemically induced* ; Oxidative Stress ; Particle Size ; Particulate Matter/adverse effects* ; Placenta ; Pregnancy ; Pregnancy Outcome/epidemiology* ; Prenatal Exposure Delayed Effects/epidemiology* ; Respiratory Tract Diseases/chemically induced* ; Young Adult

Animals ; Caffeine/adverse effects* ; Central Nervous System Stimulants/adverse effects* ; Dose-Response Relationship, Drug ; Female ; Fetal Growth Retardation/chemically induced* ; Immune System Diseases/chemically induced* ; Male ; Organ Size/drug effects* ; Pregnancy ; Pregnancy Complications/immunology* ; Rats ; Spleen/growth & development*

OBJECTIVETo evaluate the role of adiponectin in regulating tumor necrosis factor alpha (TNF alpha) production and preventing fulminant autoimmunological damage of hepatocytes following concanavalin A (Con A) injection into mice.

METHODSThree days after recombinant plasmids pAA-neo-mAd were injected into the mice via the tail veins, Con A was injected into the mice. Mice transfected with empty pAA-neo vector served as controls. The serum levels of alanine aminotransferase (ALT), TNF alpha and adiponectin were detected, and histological examination of livers was carried out at different time points after the Con A injection. All results were subjected to statistical analyses.

RESULTSHistological examinations showed that the damage in livers of mice with high serum adiponectin levels was milder than that of the controls. The serum levels of ALT and TNF alpha were both lower than those of the controls (P less than 0.01, respectively). Statistical analyses showed the serum levels of ALT was negatively related to the levels of adiponectin in the sera (r=-0.5034).

CONCLUSIONAdiponectin is effective in protecting hepatocytes from Con A-induced immunological injury. The mechanism of this protective effect may be caused by inhibiting the synthesis and/or release of TNF alpha.

Adiponectin ; blood ; pharmacology ; Alanine Transaminase ; blood ; Animals ; Concanavalin A ; adverse effects ; Female ; Immune System Diseases ; chemically induced ; pathology ; prevention & control ; Liver ; drug effects ; pathology ; Liver Diseases ; pathology ; prevention & control ; Mice ; Mice, Inbred BALB C ; Tumor Necrosis Factor-alpha ; blood