Children's Health Policy Review

Children's Health Policy Review

Monday, March 3, 2003

The federal government has published proposed, revised cancer risk assessment guidelines that contain significant conclusions and changes in the way the EPA will assess the risk from cancer-causing chemicals in the environment.

For the first time ever, the federal government has formally acknowledged that children are more vulnerable to the effects of carcinogens than adults. In fact, chemicals that cause cancer via genetic mutations were up to 65 times more potent when exposures occur during childhood instead of adulthood. The average carcinogen that damaged DNA in the government's analysis was found to be 10 times more potent during childhood than in adulthood. In half of the cases, these carcinogens showed more than a tenfold increase in potency when exposure occurred in early life. By incorporating these factors, the new risk assessment methods show that children accumulate up to 50 percent of their lifetime cancer risk by their second birthday (Figure 1).

For cancers with long latency periods (cancers that occur later in life) this increased potency during early childhood equates to about a doubling of lifetime cancer risk. For childhood cancers, with short latency periods, these findings point to far greater risks than had previously been assumed by federal risk assessments prescribed by public health statutes, and raise important new questions about the relationship between fetal and infant exposure to chemicals, and ongoing increases in incidence rates for a number of childhood cancers (Table 1).

Table 1. Children's vulnerability to carcinogens may contribute to increasing rates of many childhood and adolescent cancers. [17]

Childhood cancers on the rise

All cancers combined

Leukemia, cancer of the blood cells

Non-Hodgkins lymphoma, cancer of lymphatic cells in the immune system

Certain brain or central nervous system (CNS) tumors

Liver tumors

Soft tissue tumors, cancers that develop from muscle, connective tissue, fat, or blood vessels

Tumors that develop from the ovary, testes, egg or sperm (germ cells), or placental cells (trophoblast)

Epithelial tumors (including thyroid tumors), which develop from epithelial cells that make up the outer layers of the skin or internal body cavities and form the lining of many organs such as the thyroid

Certain types of bone cancer

Eye tumors

Sympathetic nervous system (SNS) tumors. The SNS is a subdivision of the nervous system that includes certain nerves originating from the neck and back in addition to the center of the adrenal gland (the adrenal medulla)

View detailed version of Table 1

These new guidelines underscore both the urgent need, and the clear benefits, that would derive from dramatically reducing early life exposures to cancer-causing chemicals in food, air, water, and common consumer products. Historically, the federal government has assumed that children and adults face the same level of risk to the harmful effects of carcinogens. To protect children from these significantly increased risks, all federal agencies must adopt risk assessment methods that account for this increased vulnerability to carcinogens early in life.

Children at higher risk to carcinogens. Through its review of 23 peer-reviewed studies of cancer incidence from the past 50 years, EPA has determined that infants up to age two are, on average, ten times more vulnerable to carcinogenic chemicals than adults, and for some cancer-causing agents are up to 65 times more vulnerable. The Agency also found that children from age two to 15 are three times more vulnerable to carcinogens than adults.

These potency factors reflect the enhanced capacity of carcinogens to harm children, but do not incorporate excess risks driven by children’s higher exposures relative to adults on a body weight basis, which further intensify cancer risk in early life. Under its new guidelines EPA will require risk assessors to incorporate both of these factors — enhanced potency and higher relative exposures for children — in calculations to set safety standards.

Scientists have long understood that children face unique risks for the harmful effects of chemicals, but the federal government has been slow to incorporate this science in its regulatory safeguards. In the 1996 Food Quality Protection Act, Congress passed protections for children from the effects of pesticides, for health effects other than cancer. Despite their limited application, the EPA has used these provisions to prove that a number of common pesticides used in the home and on food pose a high risk to children, including the top home pesticide Dursban, leveraging bans and shifting markets to safer chemicals.

With the publication of its new cancer risk assessment guidelines, the EPA has extended these protections for children’s health to cancer-causing chemicals that damage DNA, for all routes of exposure. The guidelines will improve EPA’s ability to protect children’s health.

Table 2. Children are routinely exposed to mutagenic carcinogens.

Carcinogens that damage DNA

Source of exposure


Arsenic pesticides in wooden playsets and decks
Drinking water (contaminants from mining and power plants)

Mutagen X and Brominated organics

Drinking water (water chlorination byproduct)


Indoor air (offgases from building materials)
Paper, dyes, paper coatings


Gasoline fumes, glue, paint, furniture wax, detergent


Food and drinking water (contaminants from gasoline and coal-fired power plants)

Why are children more vulnerable to carcinogens? In a National Academy of Sciences’ assessment of children’s vulnerability to pesticides, the Academy describes four factors that may contribute to children’s unique vulnerability to the harmful effects of chemicals:

  • Children’s exposures are greater pound-for-pound than those of adults.
  • Children are less able than adults to detoxify and excrete chemicals.
  • Children’s developing organ systems are more vulnerable to damage from chemical exposures.
  • Children have more years of future life in which to develop disease triggered by early exposure.

EPA’s new potency estimates probably reflect some of these factors, including metabolic differences and longer latency periods, but do not incorporate differences in exposure between adults and children. Children’s higher exposures to chemicals, pound for pound, act to further increase the effects of carcinogens during childhood.

Many cancers are thought to arise from a single mutant precursor cell, which then divides and multiplies. Children are believed to be more vulnerable to carcinogens in part because their cells are rapidly dividing, promoting faster growth of cancerous tissue.

Children also differ from adults in their ability to break down, inactivate or detoxify some chemicals due to differences in the maturity of their metabolic system, and age-related, genetically-driven status of their metabolic pathways. Because of these differences, cancer-causing chemicals can linger in a child’s body for longer periods of time before being excreted, increasing the probability of damage.

In early fetal life the protective capillary barrier that surrounds the brain and filters out blood pollutants is immature, allowing the brain to be exposed to higher doses of toxic chemicals carried in blood. The immune system of a fetus and child is immature, impairing its ability to eradicate cancer cells. Rapid cell growth characterizing childhood may accentuate the effect of genetic polymorphisms (or genetic differences) associated with increased chemical sensitivity. [1] Any one of these differences may put children at greater risk for particular kinds of cancer; together, they impart up to a 65-fold increase in sensitivity to carcinogens

For children, higher exposures to chemicals, pound for pound, intensify cancer risks in early life. In addition to being more vulnerable to the effects of carcinogens, children are also exposed to higher doses of carcinogens, pound for pound, than adults. On a body weight basis, children breathe three times as much air as adults, and ingest three times as much dust and soil as adults because they put their hands in their mouths frequently. They drink up to seven times as much water as adults, and eat more than three times the amount of fats in food that adults eat [2, 3] (Figure 2). All of these routes expose children to cancer-causing contaminants. The combined effect of children’s increased vulnerability and their higher exposures to carcinogens relative to adults is an accumulation of up to 50 percent of lifetime cancer risk in the first two years of life (Figure 1).

Sources of carcinogens in children’s bodies. The federal government’s National Toxicology Program considers 228 chemicals as either known human carcinogens, or “reasonably anticipated” to cause cancer in humans [4]. The State of California considers 475 chemicals to be carcinogenic [5]. The University of Maryland lists 853 mutagenic chemicals and other agents in safety data for laboratory personnel, in what it calls only a “partial” accounting [6]. No one is systematically tracking the use of any of these chemicals in consumer products, or the resulting human exposures to these chemicals, in spite of the chemicals’ known or potential human health hazards.

In a recent study of chemicals in the human blood and urine, EWG found an average of 53 carcinogens in nine people tested [7]. These chemicals ranged from common solvents in consumer products to pesticides banned 25 years ago that continue to contaminate the food supply. Scientists have never assessed the additive effects of the complex suite of carcinogens in each human body that stems from a myriad of exposure sources.

For children, common sources of exposure to carcinogens include ingredients in consumer products, and contaminants in food, water, and air. Where federal safety standards exist for these media, they do not account for the enhanced potency of carcinogens to children.

EPA is currently conducting a cancer risk assessment focused on children’s exposure to arsenic on pesticide-infused outdoor lumber commonly used for playsets and decks [8]. Their final assessment should incorporate the guideline provisions that would result in a more accurate representation of the increased cancer risk during childhood.

Last week the Consumer Product Safety Commission (CPSC) issued a decision to allow the continued use of PVC in children’s toys, even though PVC leaches animal carcinogens [9]. The Commission failed to consider data on the enhanced vulnerability of children to the effects of carcinogens in its assessment, but will likely not reopen its decision without a formal petition. The same chemicals plasticizers, known as phthalates, are commonly used in cosmetics, and may put a developing male fetus at increased risk for testicular cancer when he is exposed in the womb through his mother’s use of personal care products [10].

In their newly-released report on children’s health indicators, EPA estimates that 98 percent of children live in counties in which cancer risk from diesel particulate pollution emitted from trucks and buses exceeds the 1-in-10,000 cancer risk benchmark, using State of California risk factors. These risks are an underestimate: the Agency believes their computer-generated exposure concentrations underestimate actual levels, and their risk estimates do not account for the increased potency of carcinogens during childhood [11].

EWG has conducted research on a number of cancer-causing chemicals in water and consumer products for which in utero or early life exposures drive health risks, and for which EPA’s new cancer guidelines indicate cancer risks are higher than previously believed. These include atrazine, a pesticide that contaminates the tap water of more than seven million people in the Midwest and that is linked in animal and worker studies to reproductive cancers [12]; and a banned mutagenic pesticide called DBCP that contaminates the tap water of more than one million Californians [13]. Both of these chemicals pose a particularly elevated risk to bottle-fed infants, drinking formula reconstituted from tap water, who face higher relative exposures pound for pound than any other segment of the population.

Mutagens commonly found in drinking water include common byproducts of water chlorination, including brominated organics, and a chemical known as “MX,” or Mutagen X, one of the most powerful mutagens ever tested. MX directly damages cellular DNA material, causes multiple internal cancers in rats, occurs in public drinking water supplies, and is unregulated. As much as 50 percent of the mutagenicity associated with chlorinated tap water is attributed to MX [14].

New drinking water standards for some mutagenic water chlorination byproducts went into effect last year, and were based on a cost-benefit analysis that assumed up to 2,000 cases of bladder cancer annually induced by these chemicals. The actual number of bladder cancers may be approaching 4,000, considering EPA’s new findings on children’s risk to carcinogens. EPA will need to reevaluate drinking water standards for these and other mutagenic chemicals found in drinking water in light of the early in life exposure issues.

EPA’s new guidelines currently apply to chemicals that cause cancer through direct damage to DNA (mutation). Some carcinogens are believed to cause cancer by other mechanisms (phthalates and atrazine, for example), and are not yet covered under the new guidelines. Interestingly, the Agency uses supporting data from non-mutagenic carcinogens in its conclusions that mutagenic carcinogens are more potent in early life exposures. The EPA also found that several non-mutagens were more carcinogenic when exposure occurred in early life. EWG is hopeful that the final guidelines from EPA will extent to all carcinogens regardless of the mechanism by which they act, as supported by the science.

Regardless, many chemicals linked to mutagenic activity are commonly used in consumer products and can contribute to children’s exposures to carcinogens. Among these are the pesticides diuron and ethylene oxide; formaldehyde, a common ingredient in dyes, paper, and paper coatings; the paint solvent fumaric acid; and ethylene glycol, used as a solvent in wood stains and varnishes.

Certain childhood cancers continue to increase in incidence. The incidence of childhood cancer has increased since the 1970s. In the past ten years, rates of increase in overall cancer incidence for children has leveled off, but a number of specific types of cancer continue to increase in incidence. Cancer was the fourth leading cause of death for children and adolescents between the ages of 0 and 19 behind injury, homicide, and suicide [18]. For newborn boys and girls, the chance of developing cancer by the age of 20 is 1 in 300 and 1 in 333, respectively [18].

EPA’s new guidelines do not necessarily imply that children are expected to develop cancer more frequently than adults. Exposures in utero or during childhood can lead to cancer years later. But certain kinds of childhood cancers continue to increase in incidence, at rates not explained by better detection. Chemical exposures may be driving some of these increases.

For adolescents (ages 15 to 19), the annual incidence of cancer increased from 183 per million between 1975 and 1979 to 203.8 per million between 1990 and 1995. The largest contributor to this increase was testicular and ovarian germ cell tumors [15]. The most common cancers of young children (from birth to age 14, but especially from birth to age four) are nervous system tumors and leukemias. In adolescents, the most common types of cancers are lymphomas, carcinomas and germ cell and other gonadal tumors [11].

Tumors that have increased in incidence in children and adolescents (from birth to age 14, and/or from birth to age 19) since either 1975 or 1987, through 1999, include: leukemia (lymphoid leukemia, acute lymphoblastic leukemia, and acute non-lymphocytic leukemia), non-Hodgkin’s lymphoma, liver tumors, malignant bone tumors (osteosarcomas), soft-tissue sarcomas (tumors that arise from connective tissue such as muscle or bone), germ-cell tumors (tumors that develop from testicular or ovarian cells), and malignant epithelial tumors [11, 15, 16, 17].

One of the most deadly types of childhood CNS tumors, primary neuroectodermal tumors, has increased over two percent every year between 1987 and 1999, and the incidence of this tumor type is now about 200 percent higher than in 1975 [17]. Sympathetic nervous system tumors have been increasing in girls since 1987 at an estimated average of four percent per year [17]. In boys ages up to age 14, the incidence of germ cell tumors that spread to the head or spine have increased in incidence an average of nine percent every year since in 1987 [11, 16, 17].

A number of kinds of chemical exposures have been linked to childhood cancer, including exposures to pesticides, solvents, and exhaust fumes. For example, parental exposure to pesticides or pesticide use in the home has been linked to brain cancer, leukemia and non-Hodgkin’s lymphoma in children. Other childhood cancers linked to pesticide exposure are Wilms’ tumor and Ewings’ sarcoma. Childhood leukemia is associated with living near a heavy traffic area or parental exposure to solvents or exhaust gas, and ionizing radiation has been linked to brain cancer and leukemia [11]. Leukemia is the most common type of childhood cancer. Children who live in developed countries are at higher risk than children who live in developing countries for the most common type of childhood leukemia, acute lymphoblastic leukemia (ALL) [17]. Another type of cancer, hepatoblastoma, has been increasing at an average rate of over four percent a year since 1987. Liver tumors are rare in children, but incidence of hepatoblastoma is over 400 percent higher than in 1975. Hepatoblastomas have been associated with parental exposure to metals, petroleum products, paint, and alcohol, among other things [18].

Ramifications and recommendations. EPA’s findings heighten the importance of focusing measures to prevent cancer on the first years of life. Their new guidelines have the potential for far-reaching application. For instance, the Agency’s ongoing risk assessment for cancer risks faced by children exposed to arsenic-treated wood used in decks and playsets will likely be affected. It remains to be seen if other Agencies will adopt the protocols set forward by EPA. Notably, the Consumer Product Safety Commission regulates common consumer products used by children that contain cancer-causing chemicals. Currently, chemicals can be incorporated in consumer products and sold on store shelves, even in products used by children, with no up-front cancer testing.

EWG’s recommendations include the following:

  • The federal government should prohibit the use of carcinogenic chemicals in products destined for use by children.
  • Manufacturers should conduct pre-market cancer studies of their chemicals, and find no evidence of carcinogenicity, before using the chemicals in children’s products.
  • EPA should incorporate the increased cancer potency factors recommended in the guidelines in its ongoing assessment of children’s cancer risk from arsenic-treated wood.
  • EPA should extend the recommendations in its guidelines to carcinogens that act through mechanisms other than direct mutagenicity, given that supporting studies used by the Agency in developing the guidelines included chemicals believed to cause cancer primarily through non-mutagenic pathways.
  • CPSC should reopen its recent decision to permit the continued use of PVC in children’s toys, given that PVC leaches animal carcinogens, and that the Commission failed to consider data on the enhanced vulnerability of children to the effects of carcinogens in its assessment.
  • EPA CPSC, and the Food and Drug Administration (FDA) should assess current federal safety standards for chemicals in air, food, water, and consumer products in light of EPA’s new guidelines that more fully account for cancer risk during childhood.


  1. Environmental Protection Agency (EPA). 2000. Summary of the workshop on information needs to address children's cancer risk. National Center for Environmental Assessment, Office of Research and Development. EPA/600/R-00/105, September 2000. Available online at
  2. Environmental Protection Agency (EPA). 1997. Exposures Factors Handbook: Volume I - General Factors. Office of Research and Development, National Center for Environmental Assessment EPA/600/P-95/002Fa. Available online at
  3. Environmental Protection Agency (EPA). 2002. Child-Specific Exposure Factors Handbook (Interim Report). Office of Research and Development, National Center for Environmental Assessment EPA-600-P-00-002B. Available online at
  4. National Toxicology Program (NTP). 2002. 10th Report on Carcinogens.
  5. Office of Environmental Health Hazard Assessment (OEHHA). 2002. Chemicals known to the State to cause cancer or reproductive toxicity. State of California Environmental Protection Agency. Available online at
  6. Sax, NaRL. 1989. Dangerous Properties of Industrial Materials, 7th Ed. A partial list of mutagens from this handbook is available online at /os/ch/mutagen.html.
  7. Environmental Working Group (EWG). 2003. BodyBurden: The Pollution in People. Available online at
  8. Environmental Working Group (EWG). 2002. All Hands on Deck. Available online at
  9. Consumer Product Safety Commission (CPSC). 2003. Denial Letter (dated February 26, 2003) of Petition HP99-1 [Requesting Ban on Use of Polyvinyl Chloride (PVC) in Products Intended for Children Five Years of Age and Under. Available online at
  10. Environmental Working Group (EWG). 2002. Phthalates in Cosmetics. Available online at
  11. Environmental Protection Agency (EPA). 2003. Childhood Cancer - America's children and the environment: Measures of contaminants, body burdens, and illnesses. Second Edition. Available online at
  12. Environmental Working Group (EWG). 1999. Into the Mouth of Babes.
  13. Environmental Working Group (EWG). 2002. Consider the Source. Available online at
  14. Booker, SM. 2000. NTP taps disinfection by-products for study. Environ Health Perspect 108(2): A64-6.
  15. Ries, LAG, Smith, MA, Gurney, JG, Linet, M, Tamra, T, Young, JL and Bunin, GR. 1999. Cancer incidence and survival among children and adolescents: United States SEER Program 1975-1995. National Cancer Institute. Bethesda, MD. Publication Number 99-4649. Available online at
  16. Ries, LAG, Eisner, MP, Kosary, CL, Hankey, BF, Miller, BA, Clegg, L and Edwards, BK. 2002. SEER Cancer Statistics Review 1973-1999: Childhood Cancer. National Cancer Institute. Bethesda, MD. Available online at
  17. Ries, LAG, Eisner, MP, Kosary, CL, Hankey, BF, Miller, BA, Clegg, L and Edwards, BK. 2002. SEER Cancer Statistics Review 1973-1999: Childhood Cancer by the International Classification of Childhood Cancer (ICCC). National Cancer Institute. Bethesda, MD. Available online at
  18. Ries, LAG, Smith, MA, Gurney, JG, Linet, M, Tamra, T, Yound JL, Bunin, GR. 1999. Cancer Incidence and Survival among Children and Adolescents: United States SEER Program 1975-1995, National Cancer Institute, SEER Program. NIH Publication Number 99-4649. Bethesda, MD. Available online at


Figure 1.

figure 2 - because children eat, drink and breathe more than adults relative to their size, their relative exposure to harmful pollutants is greater

Source: EWG compilation of risk factors and exposure factors from:
• Environmental Protection Agency (EPA). Supplemental Guidance for Assessing Cancer Susceptibility for Early-Life Exposure to Carcinogens. External Review Draft. Available online at
• Environmental Protection Agency (EPA). 1997. Exposures Factors Handbook: Volume I - General Factors. Office of Research and Development, National Center for Environmental Assessment EPA/600/P-95/002Fa. Available online at
• Environmental Protection Agency (EPA). 2002. Child-Specific Exposure Factors Handbook (Interim Report). Office of Research and Development, National Center for Environmental Assessment EPA-600-P-00-002B. Available online at

Figure 2.

figure 2 - because children eat, drink and breathe more than adults relative to their size, their relative exposure to harmful pollutants is greater

• Environmental Protection Agency (EPA). 1997. Exposures Factors Handbook: Volume I - General Factors. Office of Research and Development, National Center for Environmental Assessment EPA/600/P-95/002Fa. Available online at
• Environmental Protection Agency (EPA). 2002. Child-Specific Exposure Factors Handbook (Interim Report). Office of Research and Development, National Center for Environmental Assessment EPA-600-P-00-002B. Available online at