Originally published October 12 2005
Cornell researchers claim that early exposure to toxins could contribute to asthma
by Mike Adams, the Health Ranger, NaturalNews Editor
Rod Dietert, professor of immunotoxicology at Cornell, led a study that considered the role toxins like mercury and ethanol might be playing in the increasing number of asthma and lupus cases.
The real dangers from environmental toxins most likely occur early in life, said Rod Dietert, professor of immunotoxicology at Cornell's College of Veterinary Medicine, presenting a paper on the topic Oct. 4 at the 14th Immunotoxicology Summer School Conference in Lyon, France.
However, most laboratory studies look at the health effects of the toxins on adult animals.
"We are deluding ourselves to think that adult data are going to allow us to understand the risks of perinatal exposures," said Dietert, referring to the period close to the time of birth.
He advocates a more detailed two-generation screening in which information on toxins and their impact on immune systems is recorded not only for the adult mother but also for her offspring.
It had been previously thought that adult-exposure safety testing when coupled with superficial two-generational tests could predict the health risks for adults as well as fetuses and children.
But it is now clear that current safety testing lacks the ability to detect many early life immunotoxic changes, including those leading to allergy and autoimmunity -- an immune state in which antibodies are formed against a person's own body tissues.
One issue resulting from early exposure to environmental toxins and drugs involves two types of immune system helper cells: T helper 1 (Th1) and Th2.
Th2 cells promote release of some antibodies to counter such extracellular pathogens as bacteria and parasites.
However, Th2 cell responses can result in the overproduction of antibodies called IgE antibodies, which are implicated in producing allergic responses.
As soon as the baby is born, however, a healthy infant's immune system quickly increases Th1 capacity so that levels are roughly balanced with those of Th2.
When an infant's immune system remains biased toward Th2 responses because of toxin exposure and never matures its own Th1 capacity, the baby develops a higher risk, not only for asthma and allergies during childhood but also for autoimmune diseases and comprised antiviral and anticancer responses in later life.
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