The text below is adapted from Steven Gilbert's A Small Dose of Toxicology.
Children are at greater risk from exposure to toxic chemicals because of their small size: relative to their size, children eat, drink, and breathe more than adults. Also, children, especially the very young, are more susceptible to toxic chemicals because their organs are still rapidly developing, and dividing cells are more easily harmed than mature cells. For example, the brain is not fully developed until the late teens, and grows especially rapidly during the first seven years of life. Also, during the first year of life, the metabolism of agents by the liver is reduced. This is why the half-life of caffeine, for example, can be measured in days for the newborn while it is hours for the adult.
Children also exhibit behaviors that increase their exposure to toxic agents in their environment: they play on the floor or ground, they put their hands in their mouth, and they are curious about their surroundings. Combined with their low body weight, proportionately higher intake of food, water, and air, and their developmental stage, these behavioral factors contribute to elevated risks.
For a long time it was thought that the placenta offered the developing fetus significant protection from hazardous agents. We know now that the majority of agents readily cross the placenta and expose the developing fetus to whatever the mother has been exposed to. For compounds that readily distribute throughout body water, the fluid surrounding the infant (amniotic fluid) will have the same level of the compounds as the mother's blood. Fetal exposure to methylmercury can actually be higher than that of the mother because the developing infant acts as a storage site for maternal mercury.
Lead in Children's Toys, Candy, and Jewelry (2006)
Lead in children's products was highlighted by several serious incidents of lead poisoning, including one death, from ingestion of jewelry containing lead (MMWR 2004, 2006). Many of the jewelry pieces contained over 50% lead, and hundreds of thousands of items were recalled. A report from Los Angeles County estimated that 34% of the children with elevated blood lead levels were exposed to lead-containing products brought into the home, such as folk and traditional medications, candy, ceramic dinnerware, and metallic toys and jewelry. More recently, lead was discovered in vinyl lunch boxes, where it was used to stabilize the PVC (vinyl) plastic. Lead exceeding the CPSC standard (0.06% by weight, or 600 ppm) was also found in paint on imported children's toys. Many consider this to be an excessive amount and have advocated state and federal regulations to lower the amount of lead allowed in paint and to require the testing of children's toys for lead. Despite our knowledge about the effects of lead exposure on children's health, we continue to needlessly expose those who are most vulnerable.
Alcohol Use During Pregnancy
Despite alcohol's long history of use, the adverse effects of maternal alcohol consumption on the developing fetus wasn't described until 1968, by French researchers at the University of Nantes. In 1972, the cluster of effects was further described and named Fetal Alcohol Syndrome (FAS) by researchers at the University of Washington in Seattle, USA. FAS is characterized by physical and facial abnormalities (Figure 4.2), slow growth, central nervous system dysfunction, and other disabilities. The related brain damage can be severe, leaving the child with serious learning and functional disabilities that have lifelong impacts. Another form of alcohol-related effects is Fetal Alcohol Effect (FAE), where children are born with learning or memory disabilities, but without the characteristic physical abnormalities. The disabilities associated with fetal alcohol exposure are now described as Fetal Alcohol Spectrum Disorder (FASD), which recognizes the range of effects alcohol has on development. In addition, alcohol consumption during pregnancy causes an increase in stillbirths and spontaneous abortions. It is extremely important to recognize that alcohol consumption during pregnancy results in the largest number of preventable mental disabilities in the world.
The mildly estrogenic compound Bisphenol-A (BPA) was first created in 1891 by Aleksandr Dianin, a Russian, who named it "Dianin's Compound." In 1938, the much more potent synthetic estrogen diethylstilbestrol (DES) was synthesized by Leon Golberg, a graduate student at the University of Oxford in England. In 1941, the FDA approved DES's use for menopausal symptoms and in 1947, its use to prevent miscarriages. However, in 1953, the first study was published indicating that DES was not effective in preventing miscarriages. Manufacturers continued to market DES to pregnant women until 1971, when the first study was published linking DES to vaginal cancer in female children of women taking DES. Between 1941 and 1971, millions of women and their children were exposed to DES.
Meanwhile, in the 1940s and 1950s, the chemical industry discovered that BPA was an excellent hardener for epoxy resins and the plastic polycarbonate. It is now used in a wide range of products, from plastics to linings of food cans, with an estimated use per year of 6 billion pounds. The CDC has found that over 90% of Americans have BPA in their urine, with the highest exposure occurring in infants and children. Overt toxicity from exposure to BPA occurs at only very high doses, but more subtle effects on the endocrine system occur at very low doses. Though animal studies and limited human studies have found endocrine-related health effects, government agencies have been reluctant to ban or restrict the use of BPA. Recently, local governments such as Washington State have moved to ban BPA from plastic baby bottles in an effort to reduce exposure to the most vulnerable.
Taking Lead Home (1998)
In 1998 a California mother requested a blood lead level determination for her 18-month-old child (MMWR, 2001). The result was a blood lead level (BLL) of 26 μg/dL, which was well above the Center for Disease Control's (CDC) 10 μg/dL recommended criterion for clinical case management. It was subsequently found that the father had a BLL of 46 μg/dL; the Occupational Safety and Health Administration (OSHA) requires that workers with BLLs greater than 40 μg/dL receive additional medical examinations. Further testing found that his 4-month-old daughter had a BLL of 24 μg/dL. This worker was employed in a company that refinished antique furniture, some of which was covered with lead-based paint. Subsequent testing of co-workers found that two refinishers had BLLs of 29 and 54 μg/dL and four carpenters had BLLs of 46, 46, 47, and 56 μg/dL. A child in another family had a BLL of 16 μg/dL. What will be the long-term effects on the intellectual abilities of these children?
By far the largest use of arsenic is in treating wood to prevent decay or insect damage. Several compounds are used, but the vast majority of wood is treated with a pesticide called chromated copper arsenate (CCA), first used in the 1940s. CCA is a water-based mixture of inorganic salts of chromium, copper, and arsenic that is forced into the wood under pressure. Wood treated with CCA is still found in decks, playground equipment, outdoor furniture, fences, construction lumber, utility poles, piers, and pilings. The amount of arsenic in treated wood can be quite large. A standard eight-foot length of treated 2" x 4" lumber contains as much as 15 grams of arsenic. To put this in perspective the lethal dose of arsenic in humans is 70 to 200 mg or about 1 mg/kg. Since December 31, 2003, CCA was no longer used in wood for most residential settings, including decks and play sets. There are a number of arsenic-free wood preservatives on the market that are registered for use in treated wood for residential use.
The health risks of exposure to arsenic-treated lumber have been debated for years, although it is well known that inhaling sawdust from construction with treated lumber can be quite dangerous. Ideally the arsenic-based wood preservative is "fixed" to the wood, but research has shown that arsenic leaches from the wood with rainfall and that arsenic can be rubbed off from the surface by hand contact. Arsenic contamination of soil under decks often exceeds hazardous waste cleanup standards. Children who play on decks or other treated surfaces pick up arsenic on their hands and later ingest some of the arsenic when they put their hands in their mouth or pick up food. Health professionals, the wood preserving industry, and public interest groups have hotly debated the hazards of these exposures. In 2002, producers of arsenic-treated wood reached an agreement with EPA to phase out the residential uses of arsenic treated lumber, including decks, play equipment, fences, etc. CCA will still be available for commercial uses such as utility poles. The alternative wood treatment most used to replace CCA is a copper-based preservative called ammoniacal copper quaternary, or ACQ. ACQ has a much lower toxicity to humans than CCA.
US EPA Fast Facts on Children's Environmental Health: Data on asthma , lead, cancer, developmental disabilities
The articles included below are all open-access.
Sherry G. Selevan, Carole A. Kimmel and Pauline Mendola, “Identifying Critical Windows of Exposure for Children’s Health,” Environmental Health Perspectives 108, Suppl. 3 (2000): 451-455.
Lynn R. Goldman and Sudha Koduru, “Chemicals in the Environment and Developmental Toxicity to Children: A Public Health and Policy Perspective,” Environmental Health Perspectives 108, no. 3 (2000): 443-448.
B. Weiss and P. J. Landrigan. 2000. "The developing brain and the environment: an introduction". Environmental Health Perspectives 108 Suppl. 3:373-4
Landrigan, Phillip et al. (2002). "Environmental Pollutants and Disease in American Children: Estimates of Morbidity, Mortality, and Costs for Lead Poisioning, Asthma, Cancer, and Developmental Disabilities". Environmental Health Perspectives, 110 (7): 771-778
Braun, J et. al. (2006). Exposures to Environmental Toxicants and Attention Deficit Hyperactivity Disorder in U.S. children. Environmental Health Perspectives, 114(12):1904-1909
Ma, Xiaomei, Patricia A. Buffler, Robert B. Gunier, Gary Dahl, Martyn T. Smith, Kyndaron Reinier, and Peggy Reynolds. "Critical Windows of Exposure to Household Pesticides and Risk of Childhood Leukemia." Environmental Health Perspectives 110.9 (2002): 955-60.
Flower, Kori B., Jane A. Hoppin, Charles F. Lynch, Aaron Blair, Charles Knott, David L. Shore, and Dale P. Sandler. "Cancer Risk and Parental Pesticide Application in Children of Agricultural Health Study Participants." Environmental Health Perspectives 112.5 (2004): 631-35.
Chensheng Lu, Kathryn Toepel, Rene Irish, Richard A. Fenske, Dana B. Barr, Roberto Bravo. "Organic Diets Significantly Lower Children’s Dietary Exposure to Organophosphorus Pesticides". Environ Health Perspect. (2006) February; 114(2): 260–263.
Commission for Environmental Cooperation. Toxic Chemicals and Children’s Health in North America: A Call for Efforts to Determine the Sources, Levels of Exposure, and Risks that Industrial Chemicals Pose to Children’s Health.
Schettler, T, Stein, J, Reich F, Valenti M. 2000. In Harm’s Way: Toxic Threats to Child Development. Greater Boston Physicians for Social Responsibility.