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Fetal Exposure To Toxins Could Be Behind Rise In Asthma

October 11, 2005
Cornell University
Most studies assessing health effects of environmental toxins like lead, mercury and dioxin as well as new drugs examine how these substances impact adult animals, while the real dangers may occur when developing immune systems of fetuses and newborns are exposed to toxins, according to Cornell University researcher Rod Dietert.

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The real dangers fromenvironmental toxins most likely occur early in life, said Rod Dietert,professor of immunotoxicology at Cornell's College of VeterinaryMedicine, presenting a paper on the topic Oct. 4 at the 14thImmunotoxicology Summer School Conference in Lyon, France. However,most laboratory studies look at the health effects of the toxins onadult animals.

"We are deluding ourselves to think that adultdata are going to allow us to understand the risks of perinatalexposures," said Dietert, referring to the period close to the time ofbirth. "Right now, we underestimate health risks that are occurring dueto early exposure."

He advocates a more detailed two-generationscreening in which information on toxins and their impact on immunesystems is recorded not only for the adult mother but also for heroffspring. It had been previously thought that adult-exposure safetytesting when coupled with superficial two-generational tests couldpredict the health risks for adults as well as fetuses and children.But it is now clear that current safety testing lacks the ability todetect many early life immunotoxic changes, including those leading toallergy and autoimmunity -- an immune state in which antibodies areformed against a person's own body tissues.

One issue resultingfrom early exposure to environmental toxins and drugs involves twotypes of immune system helper cells: T helper 1 (Th1) and Th2. Th1cells are involved in countering cancer and they attack pathogens, fromviruses to intracellular bacteria, that get inside cells. Th2 cellspromote release of some antibodies to counter such extracellularpathogens as bacteria and parasites. However, Th2 cell responses canresult in the overproduction of antibodies called IgE antibodies, whichare implicated in producing allergic responses. Throughout pregnancy,both the fetus and mother have inhibited Th1 responses to prevent afetal-maternal mutual immune attack that would lead to miscarriage. Assoon as the baby is born, however, a healthy infant's immune systemquickly increases Th1 capacity so that levels are roughly balanced withthose of Th2.

"Exposure to certain drugs and chemicals in thelast trimester can really mess things up," said Dietert. There is someevidence that low doses of lead, mercury, ethanol or drugs likedexamethasone (a common steroid) can permanently keep an immune systemin a late gestational Th2-promoting stage that is out of balance forresponses later in life. Yet, the same low doses of these agents do notimpair an adult immune system, Dietert said.

"I think this goes along way toward explaining the epidemic rises in allergies andautoimmune disorders," said Dietert. When an infant's immune systemremains biased toward Th2 responses because of toxin exposure and nevermatures its own Th1 capacity, the baby develops a higher risk, not onlyfor asthma and allergies during childhood but also for autoimmunediseases and comprised antiviral and anticancer responses in later life.

Inhis talk, Dietert pointed out the types of errors that can occur byrelying on adult-safety data only. For example, far lower doses oftoxins induce chemical changes in a fetus's immune system compared withan adult's, and exposure to these toxins during the perinatal periodproduces a broader number of effects than in adults.

Dietertoutlined seven windows during development when exposure to low levelsof toxins can have long-term impacts and are not modeled in the adult.For example, lead can interfere with immune-dependent reproductivedevelopment; dioxin or nicotine around birth can prevent the crucialmaturation steps of certain immune cells, called dendritic cells; andethanol can impair the ability of immune cells called macrophages tomature in response to lung surfactant proteins that are produced justbefore birth.

The American Chemistry Council, the U.S. Departmentof Agriculture and the National Institute of Environmental HealthSciences funded the study.

Story Source:

The above story is based on materials provided by Cornell University. Note: Materials may be edited for content and length.

Cite This Page:

Cornell University. "Fetal Exposure To Toxins Could Be Behind Rise In Asthma." ScienceDaily. ScienceDaily, 11 October 2005. <www.sciencedaily.com/releases/2005/10/051011063818.htm>.
Cornell University. (2005, October 11). Fetal Exposure To Toxins Could Be Behind Rise In Asthma. ScienceDaily. Retrieved April 21, 2015 from www.sciencedaily.com/releases/2005/10/051011063818.htm
Cornell University. "Fetal Exposure To Toxins Could Be Behind Rise In Asthma." ScienceDaily. www.sciencedaily.com/releases/2005/10/051011063818.htm (accessed April 21, 2015).

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