Study Shows How Secondhand Smoke Injures Babies' Lungs
UC Davis researchers today described in unprecedented biochemical and
anatomical detail how cigarette smoke damages the lungs of unborn and newborn
children.
The findings illustrate with increased urgency the dangers that smokers'
families and friends face, said UC Davis Professor Kent Pinkerton, and should
give family doctors helpful new insight into the precise hidden physical
changes occurring in their young
patients' lungs.
"Smoke exposure causes significant damage and lasting consequences in
newborns," Pinkerton said. "This research has a message for every
parent: Do not smoke or breathe secondhand smoke while you are pregnant. Do not
let your children breathe secondhand smoke after they are born."
Pinkerton added that the results from this study are further proof that
secondhand smoke's effects on children are not minor, temporary or reversible.
"This is the missed message about secondhand smoke and children," he
said. "Parents need to understand that these effects will not go away. If
children do not grow healthy lungs when they are supposed to, they will likely
never recover. The process is not forgiving and the children are not going to
be able to make up this loss later in life."
The 2006 Surgeon General's Report on secondhand smoke estimates that more than
126 million residents of the United States age 3 or older are exposed to secondhand smoke. Among
children younger than 18 years of age, an estimated 22 percent are exposed to
secondhand smoke in their home; estimates range from 11.7 percent in Utah to 34.2 percent in Kentucky.
To get the word out to parents about the dangers of secondhand smoke, two
states (Arkansas and Louisiana) have made it illegal to smoke in a car with young
passengers. In California, a similar bill, AB 379, is currently under
consideration in the state Legislature.
The new UC Davis research is reported in today's issue of the American Journal
of Respiratory and Critical Care Medicine. The lead author is Cai-Yun Zhong, a former UC Davis
graduate student now working at ArQule Biomedical
Institute in Boston; the co-authors are Ya Mei Zhou, also a former UC Davis graduate student and now
investigating breast cancer signaling pathways at Buck Research Institute in
Novato, Calif.; Jesse Joad, a UC Davis pediatrician
who studies children's lung development and cares for sick children in the UC
Davis Health System; and Pinkerton, a UC Davis professor of pediatric medicine
and director of the UC Davis Center for Health and the Environment.
The Pinkerton research group is one of the few groups in the nation capable of
studying the effects of environmental contaminants on unborn and newborn
animals. Their 15 years of studies on mice and rats have yielded greater
understanding of how air pollution affects human lungs and health through
experiments that attempt to reproduce true exposure conditions to environmental
air pollutants.
The new study was done with rhesus macaque monkeys, in order to obtain the best
possible understanding of what happens in people. Pregnant macaques were
exposed to smoke levels equal to those that a pregnant woman would breathe if
someone in her home or workplace smoked. Newborn macaques were exposed to
secondhand smoke levels similar to those a human baby would breathe if it was
cared for by a moderate-to-heavy smoker.
What the researchers found is that environmental tobacco smoke wreaks havoc in
babies at a critical time in the development of lungs -- when millions of tiny
cells called alveoli (pronounced al-VEE-o-lye) are being formed.
Alveoli are the place where oxygen passes from the lungs into the bloodstream.
Human infants are born with only about one-fifth of the 300 million alveoli
they will need as adults. They construct almost all those 300 million alveoli
between birth and age 8.
Pinkerton's group had previously shown that rats exposed to secondhand smoke
while in the womb and after birth developed hyper-reactive, or
"ticklish," airways, which typically occurs in children and adults
with asthma. The airways in those rodents remained hyper-reactive even when the
secondhand smoke exposure stopped. Thus, this early exposure to environmental
tobacco smoke created a long-lasting and perhaps permanent asthma-like
condition.
In the new study, the researchers analyzed step-by-step how the alveolar cells'
inner workings reacted to cigarette smoke. They found the normal orderly
process of cell housecleaning had gone haywire.
In healthy people, cells live and die on a schedule. Programmed cell death,
called apoptosis (a-pop-TOE-sis), is regulated by genes that increase or
decrease various chemical reactions in the cell.
But in this study, when baby monkeys were exposed to cigarette smoke before and
after birth, apoptosis went awry. Critical cellular controls regulating cell
death turned off. Alveolar cells died twice as fast as they should have.
"If you are killing cells at a higher rate during a critical developmental
stage, when they are supposed to be proliferating in order to create new
alveoli, the lungs may never be able to recover," Pinkerton said.
Funding for the study, "Environmental Tobacco Smoke Suppresses Nuclear
Factor Kappa B Signaling to Increase Apoptosis in Infant Monkey Lungs,"
was included in a five-year, $1.5 million research
grant from the National Institute of Environmental Health Sciences
and $450,000 from taxes on sales of tobacco products in California.
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