Chapter 17. Environmental Pediatrics

It is only in the last 50 years that diseases linked to environmental contamination have been recognized in pediatrics. Most environmental exposures now understood to be harmful to children were initially identified as a result of acute epidemics of illness affecting groups of people. For example, polluted outdoor air was not well understood to be unhealthy until the London Smog of 1952.1 An estimated 4000 people died from exposures to the very heavy air pollution; deaths were unusually high among the very young and the elderly. This led to the development of the first laws to regulate air pollution. Mercury was not understood to be harmful until an epidemic of cerebral palsy occurred among infants living near Minamata Bay, Japan, in the 1950s (Minamata disease).2 Between 1959 and 1972 in Iraq, seed grain treated with a mercury fungicide was accidentally eaten by humans instead of being planted in the fields, and thousands of Iraqi people developed mercury poisoning.3,4

The harmful effects of polychlorinated biphenyls came to light in 1968 when an epidemic of acne occurred among people in Japan; the disease was traced to the use of cooking oil inadvertently mixed with polychlorinated biphenyls (PCBs). About 2000 Japanese people exposed to the oil were diagnosed with Yusho (oil disease).5-7 Dioxin’s health effects were not well known until 1975 when a chemical plant explosion in Seveso, Italy, released large amounts of dioxin, and children in the area near the explosion developed chloracne, especially on areas of the body unprotected by clothing.8-10 Drinking water contamination became well recognized in 1986 when a cluster of childhood leukemia was uncovered in Woburn, Massachusetts, and was epidemiologically linked to drinking water supplied from 2 municipal wells contaminated with seepage of the animal carcinogens trichloroethylene, tetrachloroethylene, and chloroform from area chemical disposal pits that had been in use for several decades.11 Natural toxins began being recognized as potentially important indoor contaminants when, in 1994, a cluster of cases of acute pulmonary hemorrhage among infants was linked to inhalation exposures to natural toxins produced by molds that grow in chronically water-damaged environments.12

One of the most important themes that emerged from these acute epidemics of environmental diseases was that, unlike some other specialty areas of pediatrics, in environmental pediatrics, treatment of the individual patient is not sufficient; it is critical to identify and eliminate the sources of exposure so that disease does not recur in the known patients and so that additional cases do not occur.

Most signs and symptoms of illnesses linked to environmental contaminants are nonspecific and may occur only in association with fairly high-level exposures. The signs and symptoms of high-level, acute poisoning are relatively well-characterized for most chemicals. In contrast, the effects of low-level, chronic, and mixed exposures are poorly studied, particularly in infants and children. Establishing the environmental cause of a given illness is further complicated by the similarity of pollutant effects to those of other diseases. For example, a respiratory illness from an environmental pollutant may closely resemble an allergy or a respiratory infection. Diagnosis of an environmental disease requires a high index of suspicion and a thorough environmental history. While clinicians cannot assess the causal association between pollutant exposures and health effects, they should consider environmental causes of disease when children’s illnesses do not follow usual expected patterns.

A comprehensive intake of a new patient and ongoing anticipatory guidance should include an assessment of possible environmental risks to the child in the home environment. This includes discussion of the source of drinking water, potential access or exposure to toxins in the home environment or parental workplace and assuring that appropriate environmental monitoring is performed in the home, including fire and carbon monoxide detectors. Anticipatory guidance differs by the age of the child because environmental risks differ by age. When the baby is 2 months old, the clinician should ask about nitrate in drinking water, smoking, and water damage and mold growth in the home. At 6 months, clinicians should ask about lead in the home. When the child reaches school age, the pediatrician should ask questions about radon, mercury, carbon monoxide, ultraviolet light, and pesticides. Families should be advised to prevent excessive exposure to contaminants and their possible adverse effects. Commonly encountered environmental toxins and pollutants are described individually in this chapter. Discussions of specific toxins and management of exposures are also found in Chapter 120.

Carbon monoxide (CO) is an odorless gas produced by incomplete combustion of carbon-containing material. Common sources of exposure include house fires, automobile exhaust, and improperly ventilated water heaters, stoves, furnaces, fireplaces, and space heaters. Inhalation of CO is the leading cause of poisoning death in the United States. The diagnosis of carbon monoxide poisoning is readily suspected in the patient found unconscious in a house fire or running automobile. However, the diagnosis is difficult when the patient presents with nonspecific symptoms after an unrecognized exposure. Mild to moderate exposures present with malaise, nausea, vomiting, dyspnea, headache, dizziness, and confusion. Such patients are often misdiagnosed with influenza or gastroenteritis. Severe poisoning is characterized by syncope, seizures, coma, cardiorespiratory depression, and death. Diagnosis and treatment of carbon monoxide exposure is discussed in detail in Chapter 120.

The major sources of lead exposure among children in the United States is ingestion of lead-containing paint chips or lead-contaminated dust or dirt by hand-to-mouth activity. Although lead-based paint was banned in 1978 for use in homes, as many as three quarters of dwellings built before 1980 have lead-containing paint on their interior surfaces. Lead paint on interior and exterior window components becomes abraded into dust by repetitive opening and closing of the window. Lead poisoning also may result from use of certain herbal remedies, traditional cosmetics, imported spices, and ceramic cooking utensils. Lead poisoning has been caused by drinking water contaminated from lead pipes used in some older municipalities, and solder in home plumbing. Inhalation of lead-containing air may occur in children living in the vicinity of lead smelting and automobile battery plants and from clothing brought into the home by family members working in lead-related industries. Fishing weights, stained glass or ceramics may also lead to exposure. Gasoline containing tetraethyl lead, used to prevent engine “knocking,” was extensively used in the United States until the early 1980s and contributed to an increased concentration of lead in the soil.15

Lead serves no physiologic function. Ingested material containing lead is solubilized by gastric hydrochloric acid and then absorbed primarily in the upper gastrointestinal tract. Although adults absorb about 10% of ingested lead, children absorb as much as 50%. Absorption may be increased further by deficiencies of iron and other trace metals, malnutrition, and increased fat in the diet. About 70% to 90% of absorbed lead is deposited in the bones and about 5% is present in the red blood cells and their precursors in the bone marrow. Lead is very slowly excreted from the body, primarily in the urine, and its biological half-life has been estimated to be more than 15 years. The toxic effects of lead are primarily related to its binding to sulfhydryl ligands, leading to inhibition of a large number of enzymes. Lead toxicity is a function of the level of lead in the blood and tissues as well as the duration of exposure. In the red blood cell precursors, lead interferes with several steps in the heme synthetic pathway, which leads to an increased level of heme precursors, free erythrocyte protoporphyrin, and zinc protoporphyrin, in the mature red blood cells. At higher levels, lead reduces iron utilization, resulting in anemia.

In the immature, developing brain, even moderate elevations of lead are associated with neurobehavioral abnormalities and decreased intelligence quotients, which appear to be permanent. Lead can cause neuronal demyelinization, decreased numbers of neurons, decreased neuronal growth, interference with neuronal transmission, and sensorineural hearing loss that may result in significant delays in the acquisition of language and difficulty in auditory processing. At very high levels, lead can cause encephalopathy and cerebral edema, resulting in death or severe neurologic damage in survivors. Peripheral neuropathy and nephropathy that occur in lead-poisoned adults are unusual in children.

The magnitude of body lead is indicated by the blood lead level (BLL), and laboratory assessment is based primarily on blood levels determined by atomic absorption analysis. Recommendations regarding screening for lead exposure are reviewed in Chapter 12. Blood lead concentrations can be measured in capillary blood, but abnormal findings should be confirmed using venous blood because finger-stick capillary blood can be contaminated by trace amounts of lead-containing dust on the skin.

In 1991, the Centers for Disease Control and Prevention defined 10 μg/dL as the BLL that should prompt public health actions. This level does not, however, define a threshold for the harmful effects of lead. The physical and mental development of children can be affected at BLLs of less than 10 μg/dL.16,17

Symptoms that may be associated with lead poisoning are relatively nonspecific and include gastrointestinal complaints such as anorexia, constipation, abdominal pain, and vomiting. Signs and symptoms suggestive of central nervous system involvement include irritability, lethargy, changes in sleep pattern, and alterations in behavior and coordination. Seizures, hypertension, coma, and signs of increased cranial pressure are indicative of lead encephalopathy, which is usually associated with blood levels higher than 70 μg/dL.

In all exposed children, a health department inspection should be conducted to ascertain possible sources of lead in the home. Until this is possible, the child should be relocated to a known lead-free environment. If home therapy is being considered, a health department inspection should be done prior to starting treatment. A randomized controlled trial indicated that chelation therapy for children with BLLs between 25 and 45 μg/dL did not have a beneficial effect on chronic neuropsychological abnormalities; therefore, chelation therapy is usually reserved for children with a BLL higher than 45 μg/dL.18 However, medical evaluation, repeated testing, nutritional intervention to increase iron and calcium intake and decrease fat consumption, treatment of iron deficiency anemia, and investigation of the source of lead exposure are indicated. In the absence of clinical symptoms suggesting encephalopathy, children with lead levels of 45 to 69 μg/dL further management includes bowel decontamination if an abdominal radiograph shows possible lead particulate matter in the gastrointestinal tract, and chelation therapy. Chelation therapy can be started with 2,3-dimercaptosuccinic acid (succimer; DMSA) at 30 mg/kg per day for 5 days, followed by 20 mg/kg per day for 14 days. An alternate regimen is to use CaNa2EDTA as inpatient therapy at 25 mg/kg per day for 5 days. If there are unacceptable reactions to DMSA and CaNa2EDTA treatment with penicillamine can be considered at doses of 20 to 30 mg/kg per day for a duration of 4 to 12 weeks. The toxicity of penicillamine relegates it to use as a third line agent. In all of these children, follow-up neurodevelopmental monitoring should also be assured.

In children with a lead level over 70 μg/dL or symptoms suggesting encephalopathy require inpatient chelation therapy with parenteral agents. If encephalopathy is present intensive care treatment including intracranial pressure monitoring, and therapy for intracranial hypertension is mandatory, in addition to chelation therapy. Therapy is initiated with intramuscular dimercaprol (BAL) at 25 mg/kg per day divided into six doses. A second dose of BAL is given 4 hours after the initial dose, followed immediately by intravenous CaNa2edta AT 50 mg/kg per day as a single dose infused during several hours or as a continuous infusion. Adequate hydration must be ensured to maintain renal excretion. Therapy is continued for at least 72 hours, or until encephalopathy resolves. The American Academy of Pediatrics treatment guidelines for lead exposure are available at: http://aappolicy.aappublications.org/cgi/reprint/pediatrics;96/1/155.pdf. Another helpful resource is available at: A useful summary of the approach treatment of lead exposure is provided at http://www.cdc.gov/nceh/lead/casemanagement/caseManage_chap3.htm.

Mercury has been used for more than 3000 years in medicine and industry. Mercury occurs in three forms: the metallic element (quicksilver or elemental mercury), inorganic salts (mercurous or mercuric salts), and organic compounds (methylmercury, ethylmercury, and phenylmercury). Solubility, reactivity, biological effects, and toxicity vary among these forms.

Elemental mercury has been used in thermometers, sphygmomanometers, and thermostat switches. Dental amalgams contain mercury, silver, and other metals. Fluorescent light bulbs (usually 2–4 ft tubes) and disk (“button”) batteries also contain mercury. Elemental mercury also is used in some folk remedies.19,20

Elemental mercury is a liquid at room temperature and readily volatilizes to a colorless and odorless vapor. When inhaled, it easily passes through pulmonary alveolar membranes and distributes into red blood cells and the central nervous system. Less than 0.1% is absorbed after ingestion, and only minimal absorption occurs through the skin.5

Inhalation of high concentrations of mercury vapor can cause a fatal acute necrotizing bronchitis and pneumonitis.21 Fatalities have resulted from heating elemental mercury in inadequately ventilated areas.22

Children may present with rash, vomiting, muscle pain, and tachycardia. Clinicians may miss the diagnosis unless they ask the child about mercury exposures.

Long-term exposure to mercury vapor primarily affects the central nervous system. Early signs include insomnia, forgetfulness, loss of appetite, and mild tremor. These symptoms may be misdiagnosed as a psychiatric illness. Continued exposure results in progressive tremor and erethism, characterized by red palms, emotional lability, and memory impairment. Salivation, excessive sweating, and hemoconcentration may follow.

Although dental amalgams are a source of mercury exposure and are associated with slightly higher urinary mercury excretion,23 amalgams should not be replaced merely to reduce mercury exposure. Increased mercury vapor concentrations can be measured in exhaled air from persons with dental amalgams, but the biological significance is uncertain. Also unclear is the significance of the slight increase in urinary mercury excretion detected after dental amalgams are placed.

Inorganic Mercury

Acrodynia, or childhood mercury poisoning, was frequently reported in the 1940s among infants exposed to calomel teething powders containing mercurous chloride.24,25 Acrodynia has developed in infants exposed to phenylmercury used as a fungicidal diaper rinse26 and in children exposed to phenylmercuric acetate from interior latex paint.27

Inorganic mercury exposure is measured by urinary mercury determination, preferably using a 24-hour urine collection. Results greater than 10 to 20 μg/L are evidence of excessive exposure, and neurologic signs may be present at values greater than 100 μg/L. However, the urinary mercury concentration does not necessarily correlate with chronicity or severity of toxic effects, especially if the mercury exposure has been intermittent or variable in intensity. Whole blood mercury can be measured acutely, but values tend to return to normal (< 0.5–1.0 μg/dL) within 1 to 2 days after the exposure to metallic mercury vapor ends. In a representative sample of the US population, the geometric mean blood mercury levels were 0.3 μg/L for children 1 to 5 years old and 1.2 μg/L for women 16 to 49 years old.

Mercury accumulates in blood and in central nervous system and renal tissues and is very slowly eliminated. Chelating agents have been used to enhance mercury elimination, but whether chelation reduces toxic effects or speeds recovery in persons who have been poisoned is unclear. Succimer, an oral chelating agent for the treatment of childhood lead poisoning, increases urinary mercury excretion, but its efficacy is uncertain, and it must be considered experimental therapy for mercury poisoning. Mercury poisoning should be treated in consultation with a physician experienced in managing children with mercury poisoning.

Organic Mercury

Unlike inorganic mercury, organic mercury compounds are lipid soluble and essentially 100% absorbed after ingestion. Ethylmercury is found in thimerosal, an antiseptic and preservative for vaccines and other drug therapies. Thimerosal contains 49.6% mercury by weight. Before fall 1999, there was 12.5 to 25 μg of mercury in each dose of most diphtheria and tetanus toxoids, hepatitis B, acellular pertussis, Haemophilus influenzae type B, influenza, meningococcal, pneumococcal, and rabies vaccines. In 1999, recognizing the potential for excessive exposure, the American Academy of Pediatrics, along with the American Academy of Family Physicians, the Advisory Committee on Immunization Practices, and the US Public Health Service, issued a joint recommendation that thimerosal be removed from vaccines as quickly as possible.28,29 Currently, all routinely recommended vaccines manufactured for administration to infants in the United States are available in thimerosal-free formulation.

Organic mercury toxicity affects the central nervous system. Signs progress from paresthesias to ataxia, followed by generalized weakness, visual and hearing impairment, tremor and muscle spasticity, and then coma and death. Organic mercury also is teratogenic, causing disruption of the normal patterns of neuronal migration and nerve cell histology in the developing brain. In the Minamata Bay disaster and the Iraq epidemic, mothers who were asymptomatic or showed mild toxic effects gave birth to severely affected infants. The infants seemed normal at birth, but psychomotor retardation, blindness, deafness, and seizures developed over time.30

A reference dose is a dosage of a chemical that has been determined to be safe on the basis of available toxicity information, which is used to provide a basis for establishing safety standards and guidelines. The National Academy of Sciences, after reviewing methylmercury toxicity, determined that the reference dose for mercury, based on the development of neurobehavioral toxicity, should be established at 0.1 μg/kg/d.31

Ethylmercury has been less well studied than methylmercury. Very high exposures to thimerosal-containing products have resulted in toxicity.31-37

The effects of low-dose exposure are not known. There has been recent concern that organic mercury exposure from thimerosal-containing vaccines and other sources has played a role in the increased incidence of autism. The National Academy of Sciences reviewed this issue and determined that there is insufficient scientific evidence for a causal relationship.38

Organic mercury compounds concentrate in red blood cells, so whole blood may be used to diagnose excessive exposure. Blood mercury levels rarely exceed more than 1.5 μg/dL in the unexposed population, and a blood concentration of 5 μg/dL or greater is considered the threshold for symptoms of toxicity. Methylmercury also distributes into growing hair, thus providing a noninvasive means to estimate body burden and blood concentration over time. In the general population, the mercury level in hair is usually 1 ppm or less.39-42 There is no chelation agent approved by the US Food and Drug Administration (FDA) that is effective for methylmercury poisoning, although succimer has been used for the treatment of severe organic mercury poisoning.

Children who have had mercury poisoning should undergo periodic follow-up neurologic examinations by a pediatrician.

Guidelines for maximum exposure to mercury have been established by the Environmental Protection Agency at 0.1 μg/kg/d, by the FDA at 0.4 μg/kg/d, and by the Agency for Toxic Substances and Disease Registry at 0.3 μg/kg/d. The FDA and most states advise that pregnant women, young children, and women of childbearing age should not eat fish with mercury levels greater than 0.5 ppm. Most state health agencies advise limiting intake of freshwater fish having greater than 0.2 ppm of mercury, and the FDA advises that people at higher risk eat no more than 12 oz of fish a week, on average. Other states simply recommend that women and children not eat any large predator fish that tend to concentrate mercury.43 The levels of mercury in commercial fish and shellfish are reported at: http://www.fda.gov/Food/FoodSafety/Product-SpecificInformation/Seafood/FoodbornePathogensContaminants/Methylmercury/ucm115644.htm. In the United States, state specific recommendations for consumption of sport fish are available on the Environmental Protection Agency Web site: http://www.epa.gov/OST/fish/. The level of mercury in canned tuna differs by the type of tuna. Albacore tuna contains about 3 times more mercury than light tuna.44

Although the levels of mercury in commercial fish are regulated by the FDA, the federal government does not regulate the levels of mercury in fish caught for sport. Because of the potential for mercury contamination, many states have issued advisories recommending that the public limit or avoid consumption of certain fish caught for sport from specific bodies of water. In some areas of the United States, certain freshwater species (eg, walleye, pike, muskie, and bass) have levels of mercury that would result in substantial mercury intakes from a meal of fish. Most state health agencies advise limiting intake of freshwater sport fish having mercury concentrations of more than 0.2 to 1 ppm. Current state fish consumption advisories can be found on the Environmental Protection Agency Web site (http://www.epa.gov/OST/fish/).

High nitrate levels in water can have adverse health effects. Nitrate and other nutrients have been linked to blue-green algal blooms, which can produce toxic bacteria.45,46 Methemoglobinemia in infants may be caused by ingestion of water contaminated with nitrate, that is converted to nitrite by intestinal bacteria, which then oxidizes fetal hemoglobin to methemoglobin. Infants younger than 4 months of age who are fed formula reconstituted with nitrate-containing well water are at the greatest risk.

Evaluation and treatment of methemoglobinemia is discussed in Chapter 120. It is critical to identify and eliminate the exposure source prior to discharge. Reconstitution of formula with well-water is generally not recommended and, if used, well-water should be tested for safety.

N-nitroso compounds are some of the strongest known carcinogens and induce cancer in a variety of organs in more than 40 animal species, including higher primates. Exposures to nitrate in drinking water may be associated with increased risks of non-Hodgkin lymphoma, gastric cancer, bladder cancer, hyperthyroidism, and insulin dependent diabetes.47-53

Pesticides are widely available consumer products. Many aerosol products marketed for use in the home, sometimes called “over-the-counter bug bombs,” contain organophosphate and carbamate insecticides. Insecticides for garden and agricultural uses have a higher potential for toxicity because they are intrinsically more toxic and more concentrated. Acute organophosphate and carbamate toxicity diagnosis and management is discussed in Chapter 120.

Long-term effects of low-level exposures to pesticides have been documented. Organophosphate exposure has been linked to neurodevelopmental delays.54 Epidemiologic studies demonstrate associations between pesticide exposures and certain childhood cancers, including leukemia, all brain cancers, and non-Hodgkin lymphoma. A comprehensive review of studies showing an association between pesticides and childhood leukemia revealed higher risks among children whose parents were exposed to pesticides at work or who used pesticides in the home or garden. Several studies have linked home use of pesticides with childhood brain tumors. Using sprays or foggers to dispense flea or tick treatments, flea collars, home pesticide bombs, fumigation for termites, and pest strips were associated with having brain tumors. Studies in agricultural workers linked chronic exposures to chlorophenoxy herbicides with non-Hodgkin lymphoma. Pediatricians should ask questions about exposures to pesticides at home and suggest adoption of integrated pest management programs.

Polychlorinated biphenyls (PCBs) are clear, nonvolatile, hydrophobic oils that resist metabolism and persist in the environment. They were used primarily in the electrical industry as insulators until the late 1970s, when they were banned in the United States and northern Europe. There are still detectable levels of PCBs in human tissue and human milk. Polychlorinated dibenzofurans (PCDFs) are partially oxidated PCBs.

The source of exposure for most people to all of these compounds is contaminated food. Because the chemicals are not well metabolized or excreted, even very small daily doses accumulate to measurable amounts over years. The most concentrated source is sport fish from contaminated waters because the residues bioconcentrate, and fish usually is the food at the highest trophic level consumed by humans. Alaska Native people who consume the blubber of sea mammals and fishermen who eat their own catch from contaminated waters may have high exposures. The major dietary source for young children is human milk.

Chronic exposure to commonly encountered levels of PCBs is associated with lower developmental and intelligence test scores, including lower psychomotor scores, defects in short-term memory, and lowered intelligence quotients.55-60 Acute exposure has been documented twice in Asia, and affected children are found to have persistent behavioral abnormalities and cognitive impairment.61

Although many laboratories can measure PCBs, there are no agreed-on methods, quality assurance programs, or for diagnostic or therapeutic use. No regimen is known to lower body burden of these compounds.

Fish advisories for Lake Michigan recommend that individuals not eat more than one meal per month of salmon (with an average of 0.7 ppm PCBs), for a maximum of 12 meals per year. Women and children are advised to wait a month before eating another meal of Lake Michigan salmon to prevent PCBs from building up in the body.

PCB exposures can be reduced by cleaning (eg, fat removal) and cooking methods.

Types of radiation are shown in Figure 17-1. On average, the annual effective dose equivalent of ionizing radiation to a person in the United States is 0.006 Sv (0.6 rem), 37% of which is from radon, 13% from other natural sources, 24% from computerized tomography, 12% from nuclear medicine, 7% from interventional fluoroscopy, 5% from medical x-rays, and 2% from other man-made sources (see Fig. 17-2).

Radiation exposure may be instantaneous (atomic bomb), chronic (uranium miners), fractionated (radiotherapy), or partial-body. For a given dose, whole-body exposure is more harmful than partial-body exposure. Radioisotopes decay with time into stable elements and have physical half-lives of various lengths, from fractions of a second to millions of years. They also have biological half-lives related to the rate at which they are excreted from the body.

Acute effects of overexposure include acute radiation sickness (nausea, vomiting, diarrhea, declining white blood cell count, and thrombocytopenia), epilation (loss of hair), and death. Delayed effects largely are due to mutagenesis, teratogenesis, and carcinogenesis.

Ionizing radiation causes chromosome breaks in somatic cells (eg, lymphocytes and skin fibroblasts) that are detectable decades after exposure62 and presumably account for the increased rates of cancer observed after exposure in childhood or adulthood.

Intrauterine exposure to ionizing radiation may cause small head size alone or with severe mental retardation. Susceptibility to severe mental retardation is greatest at 8 to 15 weeks of gestational age, with some occurring during the 16th to 25th week. The lowest dose that caused severe mental retardation from atomic bomb exposure was 0.6 Sv, far above diagnostic exposures in medical radiology. The lowest dose that caused small head size without mental retardation was 0.10 to 0.19 Sv among conceptuses exposed at 4 to 17 weeks of gestational age.

Cancers after Radiation Exposure

An excess of thyroid cancer occurred in Japanese children exposed to the atomic bomb beginning at 11 years of age.63 An excess in breast cancer after childhood exposure to the atomic bomb was found when the cohort reached 30 years old.64 Thyroid ablation in 2 infants and thyroid neoplasia in the Marshall Islanders were due to fallout from nuclear weapons tests.

Accidental release of radiation from nuclear reactors can cause thyroid cancer. In 1986, a partial meltdown at a nuclear reactor in Chernobyl, Ukraine, occurred, and substantial amounts of radioactive isotopes were released into the atmosphere.65 Fallout occurred primarily in the Ukraine and Belarus, in neighboring countries, and, to a lesser extent, throughout the world. Twenty-five thousand people who lived 3 to 15 km from the plant were estimated to have received 350 to 550 mSv (35 to 55 rem) from external irradiation. This amount is 7 to 11 times the annual dose limit for radiation workers. Additional exposures occurred from the ingestion of radioisotopes (fallout) that contaminated food and water. Thyroid cancer developed in hundreds of children after a latent period of only 3 years.66

Radon

The US population is constantly exposed to radon, which accounts for 74% of background radiation (see Fig. 17-2). Radon gas comes from radioactive decay of radium, a product of uranium deposits in rocks and soil. Radon enters homes through cracks in the foundation, porous cinderblocks, and granite walls.14 Thus, radiation exposures in basements may be higher than those on the first-floor level.

When inhaled, radon decay products (also known as radon daughters or radon progeny) caused an increase in rates of lung cancer in uranium miners. Until recently, data were insufficient to detect an increased risk of lung cancer after lifelong residential radon exposure. A meta-analysis of 8 epidemiologic studies indicated a linear dose-response relationship with lung cancer detectable down to 4 pCi/L, the level at which home remediation is recommended. Although most of the dose of radon and radon decay products is delivered to the lungs, increasing the risk of lung cancer, some goes to the bone marrow. An ecological study in France showed an association between indoor radon concentration and acute myeloid leukemia in children under 10 years old.

The Environmental Protection Agency recommends that homes be tested for radon. Radon exposure can be reduced by increasing ventilation and by reducing the influx of radon in the home. Several methods of reducing exposure include sealing cracks in the foundation, creating negative pressure under the basement floor, and prohibiting the use of building materials containing excessive radium. When levels of radon higher than 4 pCi/L are found, repairs should be made to reduce the radon level.

Solar Radiation

Skin cancers may be induced by ultraviolet (UV) light. Because of the long latent period, skin cancers rarely occur in childhood except when there is markedly heightened sensitivity, as in xeroderma pigmentosum or in albinism. The incidence of melanoma has increased more rapidly than that of most cancers, and children who experience repeated sunburns are at risk.

In children, acute health effects associated with outdoor air pollution include increased respiratory symptoms, such as wheezing and cough, serious lower respiratory tract infections, and exacerbation of asthma.67 Increases in the number of hospital emergency department admissions have been observed when air pollution levels are elevated, which commonly occurs in major urban areas. Historically, episodes of very heavy air pollution (such as the London Smog of 1952) have been linked with increased death rates among adults and children. Most of the short-term respiratory effects of outdoor air pollution, such as symptoms of cough or shortness of breath, are thought to be reversible. The effects of repeated or long-term exposures to outdoor air pollution on the developing lungs of children are not as well understood.

Individual air pollutants typically exist as part of a complex mixture of multiple pollutants. Only a few air pollutants, however, are regularly monitored by the US government to assess outdoor (ambient) air quality. Those that are monitored regularly are respirable particulate matter, sulfur compounds, carbon monoxide, lead, nitrogen oxides, and ozone.

Particulate Matter

Particulate matter is a generic term for a variety of materials with many different characteristics. Both solid particles and liquid droplets are included, and the particle or droplet size can range from slightly above the molecular level (invisible to the naked eye) to large dust particles several hundred microns in diameter. Solid particulate matter, including soot and smoke, is generated by the incomplete combustion of organic matter. Particulate matter also can include dusts that come from the mechanical breakdown of solid matter (such as rocks, soil, and dust). Fine and ultrafine particulate matter is emitted by diesel engines, can be found in the smoke of forest fires, and is emitted by power plants in which the coarse particle fraction is filtered out.

Particle size is the major determinant of where the particles will be deposited in the respiratory system. Although particles larger than 10 µm in diameter are filtered out when air passes through the nose, smaller particles reach the lower airways. Children, however, frequently breathe through their mouths, thus bypassing the nasal filtration mechanism. Particles smaller than 2.5 μm can penetrate deeply into the lungs. The particles that reach the alveoli stay there permanently. The concentration of particulate matter smaller than 10 μm in air is called PM10. The concentration of particulate matter smaller than 2.5 μm in air is called PM2.5. The fine particles often contain the most toxic compounds.

Diesel automotive exhaust generates particles smaller than 1 μm that remain suspended in the atmosphere for longer periods of time and are more likely to be inhaled.

Several studies have noted an association between particulate air pollution and mortality among persons of all ages, as well as low birth weight and other outcomes such as intrauterine growth retardation and postneonatal infant death.

Sulfur Compounds

Sulfur-containing compounds include sulfur dioxide (SO2), sulfuric acid (H2SO4) aerosol, sulfate particles, and hydrogen sulfide (H2S). The primary source of sulfur dioxide is from burning coal; thus, major emitters of sulfur dioxide include coal-fired power plants, smelters, and pulp and paper mills. Sulfuric acid aerosol is formed in the atmosphere from the oxidation of sulfur dioxide in the presence of moisture. Facilities that either manufacture or use acids also can emit sulfuric acid aerosol. Hydrogen sulfide is emitted from a variety of industrial processes, including oil refining, wood pulp production, and waste water treatment, as well as from the operation of geothermal plants and landfills. Hydrogen sulfide, which has an odor similar to that of rotten eggs, can be detected at H2S levels that are far below those associated with physiological effects.

Carbon Monoxide and Lead

Large amounts of carbon monoxide may enter the outdoor air primarily through the incomplete combustion of motor vehicle fuels. Carbon monoxide poisoning is discussed in Chapter 120. Leaded gasoline was once an important source of lead exposure for children in the United States until it was discontinued. Lead exposure from this source continues to occur in emerging nations. Treatment of lead exposure is discussed earlier in this chapter. Newer automobiles produce far less carbon monoxide than do older vehicles. (See “Carbon Monoxide” above.)

Nitrogen Oxides

Although motor vehicle emissions contribute to outdoor levels of nitrogen oxides, emissions of nitrogen oxides from natural sources far outweigh those generated by human activity. Natural sources include intrusion of stratospheric nitrogen oxides, bacterial and volcanic action, and lightning. Most atmospheric nitrogen dioxide is emitted as nitric oxide, which is rapidly oxidized by ozone to nitrogen dioxide.

The levels of nitrogen oxides outdoors are generally lower than those found indoors. Infants living in homes with a nitrogen dioxide concentration exceeding 17.4 ppb had more days with wheeze, persistent cough, and shortness of breath than infants in homes with nitrogen dioxide concentrations lower than 5.1 ppb.68

Ozone

Ozone (O3) is a pervasive outdoor air pollutant. Outdoor ozone and other photochemical oxidants are secondary pollutants formed in the atmosphere from a chemical reaction between volatile organic compounds and nitrogen oxides in the presence of sunlight. The primary sources of these precursor compounds include motor vehicle exhaust, chemical factories, and refineries. Ozone is the principal component of urban summer smog. Levels of ozone are generally highest on hot summer days and increase to maximum levels in the late afternoon. It is common for air pollutants to occur together; for example, on days when ozone levels are high, outdoor air levels of fine particles and acid aerosols may also be high. Long-term exposure to ozone is linked to chronic respiratory symptoms and small deficits in pulmonary function tests. Chronic exposure to ozone pollution has been associated with de novo development of chronic lung disease, with mild pulmonary fibrosis, and with modest increases in small airway obstruction.

Long-term exposure to ozone is linked to chronic respiratory symptoms and small deficits in pulmonary function tests. Chronic exposure to ozone pollution has been associated with de novo development of chronic lung disease, with mild pulmonary fibrosis, and with modest increases in small airway obstruction. Ozone also may increase allergic response, possibly directing the immune response toward a Th2 pattern under certain conditions.69,70

Recent research has explored whether dietary antioxidant supplementation (400 IU vitamin E and 500 mg vitamin C) affects ozone-induced bronchial hyperresponsiveness in persons with asthma. In several, but not all, studies of adults, dietary supplementation was associated with higher lung function values during periods of ozone pollution. It is not yet known whether dietary antioxidant supplementation is helpful for children exposed to ozone.

Mycotoxins

Emerging evidence points to the importance of considering novel sources of indoor air pollution when an infant presents with recurrent respiratory illnesses. In immunocompetent children, indoor exposure to water damage and fungi has been clearly linked to asthma and allergic diseases. Some children who are exposed to fungi have persistent upper respiratory tract symptoms such as rhinitis, sinusitis, sneezing, and eye irritation, as well as lower respiratory tract symptoms such as coughing and wheezing. Less well recognized is disease linked to toxins from molds. Cases of acute pulmonary hemorrhage have occurred among infants living in homes with severe water damage and fungal growth.12 Clinicians should recognize and manage health effects related to mold exposure and moisture indoors.

More than 15,000 chemicals are produced at a rate of more than 10,000 pounds per year in the United States, and thousands of new chemicals are introduced into use each year. Few of these chemicals have been tested. Even among the 2800 chemicals used at more than a million pounds per year, more than half have not been tested for toxic effects on humans.71

Chemical contaminants in water are listed in Table 17-1. Children drink more water per kilogram of body weight than adults do, putting them at increased risk for health effects from contaminated water. Household water supplies can result in inhalation exposures as well. If volatile substances (eg, organic solvents) or gases (eg, radon gas) are present, these will enter the home during showering, bathing, and other activities. It has been estimated that 50% of the total exposure to volatile organics in drinking water is via this inhalation route.

Acute exposures to high levels of pollutants in water (and in foods) may result in acute gastrointestinal symptoms. There are numerous chemical exposures that can result in vomiting in children (see Table 17-2). Although less common than bacterial or viral causes of vomiting, they should be included in the differential diagnosis of children with very rapid onset of gastrointestinal symptoms after eating or drinking.

Nonorganic Chemicals in Water

Arsenic is ubiquitous in the environment. Human activities, such as smelting, coal burning, wood preservation, pesticide distribution, and other industrial processes produce at least 3 times more arsenic than natural processes. The toxicity of arsenic to humans depends on the form, with organic being less toxic than inorganic and pentavalent being less toxic than trivalent. Except in electronics, industrial uses of arsenicals are decreasing. Drinking water and food represent the major sources of arsenic for humans. Arsenic is a known human carcinogen that naturally occurs in drinking water in many parts of the United States.

Chromium in drinking water is regulated to protect against exposure to one of the valence states of chromium, chromium VI, which is a carcinogen.

Drinking water also represents a potential route of exposure to lead.

Combustion sources that release mercury into the air, such as coal-fired power plants used for generating electrical energy and municipal waste incinerators that burn garbage are sources of atmospheric mercury that are deposited into lakes and rivers by rain and snow. Risks of mercury ingestion are discussed earlier in this chapter. Mercury is converted by sediment bacteria in the water into methylmercury, which becomes concentrated in fish by biomagnification up the food chain. Mercury is a drinking water contaminant; however, the most important route of exposure is through consumption of methylmercury-contaminated fish.

Organic Chemicals in Water

Components of Gasoline

Gasoline has been stored in underground tanks that have over the years developed leakages, causing toxic chemicals to rapidly move into groundwater and eventually into drinking water supplies. The most toxic component of gasoline is benzene. It enters the water when gasoline is spilled or when gasoline tanks leak into the ground. Benzene is known to cause leukemia in humans, and aplastic anemia at high doses.

Nitrates and pesticides enter the water supply from urban and agricultural runoff of nitrogen fertilizers. Their effects are discussed earlier in this chapter. Pesticides may not be removed by conventional water treatment, and private wells may become contaminated with agricultural pesticides.

In 1986, an association was found between childhood leukemia and drinking water supplied from two municipal wells in Woburn, Massachusetts.17 The two wells were contaminated with trichloroethylene, tetrachloroethylene, and chloroform. Childhood leukemia rates in Woburn reported between 1964 and 1983 were twice the national rates.

In the 1970s, chlorination of waters having high natural organic content was found to cause the formation of chloroform and other chlorinated compounds called trihalomethanes. Residual levels of the disinfectants chlorine and chlorine dioxide are now found in some tap water. Epidemiologic studies show a correlation between trihalomethanes-containing drinking water and increases in the rates of rectal and bladder cancer.72

Natural Toxins

Natural toxins may produce either acute or chronic illnesses and a variety of clinical syndromes. Water from ponds and lakes may contain Cyanobacteria (blue-green algae), including Microcystis aeruginosa.

These bacteria produce cyanotoxins such as microcystins, some of which are hepatotoxic and neurotoxic compounds.

Water from the rivers flowing into the Chesapeake Bay on the Eastern shore of the United States has been contaminated with Pfiesteria piscicida and dinoflagellates that can produce neurotoxins.9 Chronic exposure to toxin-producing Pfiesteria dinoflagellates has been associated with learning and memory difficulties.