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Kent E. Pinkerton, Ph.D. A new study by University of California Davis researchers details how the lungs of infants are damaged by secondhand cigarette smoke. NIEHS grantee Kent Pinkerton and colleagues exposed pregnant rhesus macaque monkeys to the same amount of smoke a woman would be exposed to if someone in her home or workplace smoked. Likewise, newborn monkeys were exposed to secondhand smoke levels equivalent to what a human baby would be exposed to if one of its parents or caregivers was a moderate to heavy smoker. The research discovered that during pregnancy and the early postnatal period, critical times for lung development, secondhand smoke exposure caused premature death of alveolar cells due to apoptosis. Exposure to tobacco smoke was shown to suppress NF-κB activity and down-regulate NF-κB-dependent anti-apoptotic genes resulting in the increase of apoptotic death of alveolar cells in lung tissue. Exposure in children to second hand smoke is a hazardous and widespread public health problem even though smoking continues to decline in the U.S. Exposure during the perinatal period causes adverse effects on lung development and reduces lung function. The current research conducted in this laboratory sheds light on the precise cellular mechanisms disrupted by environmental tobacco smoke and may elucidate new pathways for treating lung function decrements. Presumably, killing cells at a higher rate during a critical developmental period when alveoli are supposed to be proliferating may have permanent effects on lung function. Pinkerton concludes that "smoke exposure causes significant damage and lasting consequences in newborns. The lungs may never be able to recover." Citation: Zhong CY, Zhou YM, Joad JP, Pinkerton KE. Environmental Tobacco Smoke Suppresses Nuclear Factor-{kappa}B Signaling to Increase Apoptosis in Infant Monkey Lungs. Am J Respir Crit Care Med. 2006 Aug 15;174(4):428-36. |
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