Body Burden: The Pollution in Newborns: Babies are vulnerable to chemical harm
JULY 14, 2005
Parents know intuitively that babies in the womb are more vulnerable to the effects of industrial chemicals than adults. A pregnant woman may avoid using hair dye and nail polish, pumping gas, or painting the nursery, for example, to protect her baby. This intuition is backed by science that has unfolded primarily over the past two decades. In 1993 the National Academy of Sciences enumerated, in a Congressionally mandated study, the primary factors that contribute to children's unique vulnerability to the harmful effects of chemicals (NAS 1993):
A recent review by government scientists of the "critical windows" of vulnerability reveals an urgent need for public health policies that recognize childhood sensitivity (Selevan et al. 2000). Many of these windows of vulnerability are found in the early months of human pregnancies, when cells are multiplying and differentiating into specific tissues and organs. Exposures during these times can lead to permanent damage. But a child's vulnerability continues long beyond early pregnancy: the central nervous system, immune, reproductive and endocrine systems, for example, continue to mature even after birth (NAS 1993, Makri et al. 2004). As a whole, these windows facilitate more pronounced risks and effects for chemical exposures in childhood than adulthood. For example, a mother's exposure to dioxins, mercury, or certain pesticides during pregnancy could measurably harm her baby, while affecting her own health perhaps not at all.
In a decades-long mercury poisoning disaster in Minamata, Japan that began in the 1950s, some babies born to women who ate mercury-polluted seafood died within days of birth, while their mothers were free of symptoms. Autopsies revealed that in adults, mercury induced lesions that were concentrated in a few areas of the brain. In the fetus, however, mercury spawned lesions over nearly the entire brain cortex.
In the decades following Minamata, scientists have developed a much fuller understanding of children's vulnerability to chemicals, discovering links between a host of health problems — including asthma, childhood cancer, and brain damage — and such common contaminants as solvents, pesticides, PCBs, and lead (Trasande and Landrigan, 2004). A recent National Academy of Sciences study suggests that environmental factors contribute to at least 28 percent of childhood developmental disabilities (NAS 2000a).
The latest research investigates not only relationships between disease and exposures, but the root causes of chemically-induced disease with in uteroorigins. This research pinpoints traits of a fetus that contribute to vulnerability: low levels of some chemical-binding proteins in the blood, immature excretion pathways, and an immature blood brain barrier, for instance, which combine to increase the transfer of chemicals from the blood to the aptly named "target organs" that may ultimately bear the harm.
The risks to a baby derive not only from his or her physical makeup, but also from the very behaviors and events that prepare the baby for life outside the womb. Beginning in the fifth month of pregnancy, babies regularly swallow and breathe, building muscles essential for survival after birth. Through these actions, the lungs and the gut are filled, again and again, with the same amniotic fluid that collects the baby's urine. Pollutants like plasticizers and pesticides excreted in urine accumulate in this fluid and are cycled right back into the baby's body through the mouth and nose. And in the third trimester the mother's body dissolves stored, maternal fat, shunting it to the baby through the blood, but with this fat the child also receives the persistent pollutants clinging to it, like PCB's, flame retardants, and dioxins. Faced with such diverse exposures and armed with a body ill-equipped to rid itself of chemicals, it is small wonder that a developing baby so often proves vulnerable to chemical exposures (Makri et al. 2004).
Some studies are beginning to measure the sensitivity of a child relative to an adult for suffering impacts from chemical exposures. For instance, studies of mutagens called polyaromatic hydrocarbons (PAHs) — target chemicals examined in this study and waste products from burning gasoline and garbage — found that even though levels of PAHs are thought to be lower in the fetus than the mother (Srivastava et al. 1986), the fetus bears more cancer-inducing DNA damage from the exposures (Whyatt et al. 2001).
But health and environmental officials have been slow to act on the wealth of studies on childhood vulnerability produced in the past 20 years. After nearly a decade of review, the Environmental Protection Agency updated its cancer risk guidelines in 2003 to explicitly acknowledge the importance of childhood exposures. The agency concluded, after a review of 23 studies of early life exposures to cancer-causing chemicals, that carcinogens average 10 times the potency for babies than adults, and that some chemicals are up to 65 times more powerful (EPA 2005a).
EPA's new policy, though, targets only cancer. It leaves EPA with no formal policy regarding childrens' vulnerability to chemicals that damage the immune system, the brain, or the hormone system, kidney, liver, lungs, thyroid or a host of other potential targets, even though plenty of evidence says that children face higher risks for harm.
JULY 14, 2005
Parents know intuitively that babies in the womb are more vulnerable to the effects of industrial chemicals than adults. A pregnant woman may avoid using hair dye and nail polish, pumping gas, or painting the nursery, for example, to protect her baby. This intuition is backed by science that has unfolded primarily over the past two decades. In 1993 the National Academy of Sciences enumerated, in a Congressionally mandated study, the primary factors that contribute to children's unique vulnerability to the harmful effects of chemicals (NAS 1993):
- A developing child's chemical exposures are greater pound-for-pound than those of adults.
- An immature, porous blood-brain barrier allows greater chemical exposures to the developing brain.
- Children have lower levels of some chemical-binding proteins, allowing more of a chemical to reach "target organs."
- A baby's organs and systems are rapidly developing, and thus are often more vulnerable to damage from chemical exposure.
- Systems that detoxify and excrete industrial chemicals are not fully developed.
- The longer future life span of a child compared to an adult allows more time for adverse effects to arise.
A recent review by government scientists of the "critical windows" of vulnerability reveals an urgent need for public health policies that recognize childhood sensitivity (Selevan et al. 2000). Many of these windows of vulnerability are found in the early months of human pregnancies, when cells are multiplying and differentiating into specific tissues and organs. Exposures during these times can lead to permanent damage. But a child's vulnerability continues long beyond early pregnancy: the central nervous system, immune, reproductive and endocrine systems, for example, continue to mature even after birth (NAS 1993, Makri et al. 2004). As a whole, these windows facilitate more pronounced risks and effects for chemical exposures in childhood than adulthood. For example, a mother's exposure to dioxins, mercury, or certain pesticides during pregnancy could measurably harm her baby, while affecting her own health perhaps not at all.
In a decades-long mercury poisoning disaster in Minamata, Japan that began in the 1950s, some babies born to women who ate mercury-polluted seafood died within days of birth, while their mothers were free of symptoms. Autopsies revealed that in adults, mercury induced lesions that were concentrated in a few areas of the brain. In the fetus, however, mercury spawned lesions over nearly the entire brain cortex.
In the decades following Minamata, scientists have developed a much fuller understanding of children's vulnerability to chemicals, discovering links between a host of health problems — including asthma, childhood cancer, and brain damage — and such common contaminants as solvents, pesticides, PCBs, and lead (Trasande and Landrigan, 2004). A recent National Academy of Sciences study suggests that environmental factors contribute to at least 28 percent of childhood developmental disabilities (NAS 2000a).
The latest research investigates not only relationships between disease and exposures, but the root causes of chemically-induced disease with in uteroorigins. This research pinpoints traits of a fetus that contribute to vulnerability: low levels of some chemical-binding proteins in the blood, immature excretion pathways, and an immature blood brain barrier, for instance, which combine to increase the transfer of chemicals from the blood to the aptly named "target organs" that may ultimately bear the harm.
The risks to a baby derive not only from his or her physical makeup, but also from the very behaviors and events that prepare the baby for life outside the womb. Beginning in the fifth month of pregnancy, babies regularly swallow and breathe, building muscles essential for survival after birth. Through these actions, the lungs and the gut are filled, again and again, with the same amniotic fluid that collects the baby's urine. Pollutants like plasticizers and pesticides excreted in urine accumulate in this fluid and are cycled right back into the baby's body through the mouth and nose. And in the third trimester the mother's body dissolves stored, maternal fat, shunting it to the baby through the blood, but with this fat the child also receives the persistent pollutants clinging to it, like PCB's, flame retardants, and dioxins. Faced with such diverse exposures and armed with a body ill-equipped to rid itself of chemicals, it is small wonder that a developing baby so often proves vulnerable to chemical exposures (Makri et al. 2004).
Some studies are beginning to measure the sensitivity of a child relative to an adult for suffering impacts from chemical exposures. For instance, studies of mutagens called polyaromatic hydrocarbons (PAHs) — target chemicals examined in this study and waste products from burning gasoline and garbage — found that even though levels of PAHs are thought to be lower in the fetus than the mother (Srivastava et al. 1986), the fetus bears more cancer-inducing DNA damage from the exposures (Whyatt et al. 2001).
But health and environmental officials have been slow to act on the wealth of studies on childhood vulnerability produced in the past 20 years. After nearly a decade of review, the Environmental Protection Agency updated its cancer risk guidelines in 2003 to explicitly acknowledge the importance of childhood exposures. The agency concluded, after a review of 23 studies of early life exposures to cancer-causing chemicals, that carcinogens average 10 times the potency for babies than adults, and that some chemicals are up to 65 times more powerful (EPA 2005a).
EPA's new policy, though, targets only cancer. It leaves EPA with no formal policy regarding childrens' vulnerability to chemicals that damage the immune system, the brain, or the hormone system, kidney, liver, lungs, thyroid or a host of other potential targets, even though plenty of evidence says that children face higher risks for harm.
