Research: Children's Health

Newborns' Exposure To Toxins Could Be Behind Sharp Rises In Asthma, Allergies And Lupus

Exposure of developing fetuses and newborns to low levels of environmental toxins such as lead, mercury and dioxin, as well as nicotine and ethanol, could be behind the recent sharp rises in asthma, allergies and autoimmune disorders like lupus, according to a Cornell University researcher.

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. "Right now, we underestimate health risks that are occurring due to early exposure."

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. Th1 cells are involved in countering cancer and they attack pathogens, from viruses to intracellular bacteria, that get inside cells. 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. Throughout pregnancy, both the fetus and mother have inhibited Th1 responses to prevent a fetal-maternal mutual immune attack that would lead to miscarriage. 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.

"Exposure to certain drugs and chemicals in the last trimester can really mess things up," said Dietert. There is some evidence that low doses of lead, mercury, ethanol or drugs like dexamethasone (a common steroid) can permanently keep an immune system in a late gestational Th2-promoting stage that is out of balance for responses later in life. Yet, the same low doses of these agents do not impair an adult immune system, Dietert said.

"I think this goes a long way toward explaining the epidemic rises in allergies and autoimmune disorders," said Dietert. 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.

In his talk, Dietert pointed out the types of errors that can occur by relying on adult-safety data only. For example, far lower doses of toxins induce chemical changes in a fetus's immune system compared with an adult's, and exposure to these toxins during the perinatal period produces a broader number of effects than in adults.

Dietert outlined seven windows during development when exposure to low levels of toxins can have long-term impacts and are not modeled in the adult. For example, lead can interfere with immune-dependent reproductive development; dioxin or nicotine around birth can prevent the crucial maturation steps of certain immune cells, called dendritic cells; and ethanol can impair the ability of immune cells called macrophages to mature in response to lung surfactant proteins that are produced just before birth.

The American Chemistry Council, the U.S. Department of Agriculture and the National Institute of Environmental Health Sciences funded the study.

Second-Hand Smoke Linked To Health Risks In Children And Women

On Sept. 29, the California Air Resources Board (ARB -- released a report linking environmental tobacco smoke (ETS) to a variety of health effects ranging from asthma, Sudden Infant Death Syndrome (SIDS) and increased incidences of breast cancer in non-smoking pre-menopausal women.

"These findings again heighten the need to minimize the public's exposure to tobacco smoke," said ARB executive officer, Catherine Witherspoon. "This information should be considered before anyone lights up another cigarette, especially around infants and children."

The joint ARB and the Office of Environmental Health Hazard Assessment (OEHHA) report cites new evidence that links secondhand tobacco smoke to a wide variety of adverse health effects, including increased incidences of cancer, heart disease and respiratory ailments, as well as the increased incidences of breast cancer in non-smoking pre-menopausal women. In addition to the breast cancer finding, other significant findings of the report include the correlation of exposure to secondhand smoke to premature and low birth-weight babies, SIDS, bronchitis, pneumonia, the induction and exacerbation of asthma, and to middle ear infections in children. In adults, ETS has been identified as a cause of lung and nasal sinus cancer, eye and nasal irritation and now asthma.

"Secondhand smoke is more than just an annoyance. The scientific record is increasingly clear that smokers are putting their families and friends at risk if they regularly smoke in their presence," said Dr. Joan Denton, director of OEHHA.

Secondhand smoke is a complex mixture of compounds formed by the burning of tobacco products and from exhaled smoke. ARB officials said that ETS has been found to be a critical source of exposure to other toxic air contaminants such as benzene, 1,3 butadiene, and arsenic. In California each year, tobacco smoke is responsible for the release of 40 tons of nicotine, 365 tons of respirable particulate matter (RSP), and 1907 tons of carbon monoxide.

As required by state law, the Scientific Review Panel on Toxic Air Contaminants (SRP) has reviewed the report's data, its scientific procedures and methods used to support the data, and its conclusions and assessments. The SRP approved the report, recommends that the ARB list ETS as a toxic air contaminant (TAC), and also recommends that OEHHA add it to its list of TACs that may disproportionately impact children.

The process of identifying ETS as a TAC was initiated in 2001 when ARB staff began an evaluation of the potential for human exposure to ETS, while OEHHA staff began an evaluation of its health effects. The results of these evaluations were included in a report that was released for public comment in 2003. Upon modifications due to public comments, the report was submitted to the SRP for review. The SRP then examined the report's process and findings, and made several recommendations for corrections until the final report being released today was approved. With SRP approval, the report forms the technical basis for regulatory action. If ETS is formally listed as a TAC, the ARB is required by law to determine if there is a need to further control outdoor exposures.

In 1997, the ARB approved an earlier ETS report and forwarded it to the California Department of Health, where the state's anti-smoking unit is located.

This article originally appeared in the 10/01/2005 issue of Environmental Protection.

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