Chemical Pollutants

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Chapter 700 Chemical Pollutants

As many as 80,000 synthetic chemicals have been developed worldwide since World War II, assuring that children everywhere face certainty of chemical exposure. Children are especially likely to be exposed to the nearly 3,000 high-production-volume (HPV) chemicals that are produced in amounts of 1 million pounds or more per year and are most widely dispersed in the environment. Biomonitoring data on blood and urine levels of over 200 synthetic chemicals obtained by the Centers for Disease Control and Prevention (CDC) in a sample of the U.S. population through the National Health and Nutrition Examination Survey (NHANES) document that American children are exposed to a broad array of synthetic chemicals. In some cases, children carry a greater body burden than adults. The 2006 World Health Organization (WHO) publication Preventing Disease through Healthy Environments: Towards an Estimate of the Environmental Burden of Disease estimates that approximately one third of deaths among children 0 to 1 yr of age can be attributed to environmental factors. Southeast Asia and the Western Pacific house half of the world’s children and are among the most rapidly industrializing regions of the globe, often with limited controls in place to reduce environmental exposures for children.

Children are uniquely vulnerable to chemical pollutants for several reasons:

1 Children have proportionally greater exposures to many environmental pollutants than adults. Because they drink more water, eat more food, and breathe more air per kg of body weight, children are more heavily exposed to pollutants in water, food, and air. Children’s hand-to-mouth behavior and their play close to the ground further magnify their exposures.

2 Children’s metabolic pathways, especially in the first months after birth, are immature. Although in some instances children are better able than adults to cope with environmental toxicants because they are unable to metabolize them to their active form, children are frequently less able to detoxify and excrete chemical pollutants.

3 Infants and children are growing and developing, and their developmental processes are uniquely sensitive to disruption by chemical pollutants. The disability resulting from exposures to chemicals during windows of early vulnerability can be severe and lifelong (Table 700-1).

Table 700-1 EFFECTS OF SELECTED CHEMICAL POLLUTANTS ON INFANTS AND CHILDREN

CHEMICAL POLLUTANT	EFFECT(S)
Diethylstilbestrol	Adenocarcinoma of the vagina after intrauterine exposure
Thalidomide	Phocomelia after intrauterine exposure
Trichloroethylene	Elevated risk of leukemia after intrauterine exposure
Alcohol	Fetal alcohol syndrome after intrauterine exposure
Lead	Neurobehavioral toxicity from low-dose exposure
Nitrosamine, vinyl chloride, ionizing radiation	Increased risk of cancer after intrauterine exposure
Organophosphate insecticides	Developmental neurotoxicity
Environmental tobacco smoke	Increased risk of sudden infant death syndrome and asthma

4 Because children have many future years of life, they have time for the development of multistage chronic diseases that may be triggered by early exposures.

A fundamental problem in environmental pediatrics is that only about 65% of HPV chemicals have been tested for their potential hazards to human health, and fewer than 30% have been assessed for their pediatric or developmental toxicity. In the USA chemicals are regulated under the 1976 Toxic Substances Control Act (TSCA), which assumes that chemicals cause no harm until proven dangerous and places the burden on government to demonstrate harmful health effects. This approach has been ineffective in protecting children against chemical toxicity. By contrast, the Registration, Evaluation, Authorization and restriction of Chemicals (REACH) legislation, passed by the European Union in 2006, requires chemicals to be proven safe before they come to market and places the burden on industry to document chemical safety. The Kids Safe Chemicals Act, which was introduced to the U.S. Congress in 2009 but failed to pass, takes an approach to chemical regulation similar to that of REACH. In 2009 the Environmental Protection Agency (EPA) for the first time required manufacturers of 67 pesticide chemicals to determine whether these chemicals have potential to disrupt the endocrine system. The United Nations Environment Programme (UNEP) is the agency within the United Nations that is responsible for international activities related to the sound management of chemicals. UNEP promotes chemical safety by providing information, policy advice, and technical guidance on toxic chemicals to developing and transitional countries. UNEP advocates for the establishment of international treaties to ban and control chemical substances. UNEP coordinates with other international organizations such as the Food and Agriculture Organization of the United Nations.

A large and growing body of evidence accumulated over the past four decades documents that chemical pollutants in the environment can cause disease and dysfunction in children. High-dose exposures can cause acute, clinically evident disease. Lower-dose exposures can cause subclinical injury—injury that is very real but detectable only through special testing—such as decreases in intelligence, shortening of attention span, and disruption of behavior. As is detailed in the following sections of this chapter, disease and dysfunction in children have now been definitively linked to heavy metals, pesticides, air pollutants, and plastics chemicals.

Chemical Pollutants of Major Concern

Air Pollutants

The outdoor air pollutants of greatest concern are photochemical oxidants (especially ozone), oxides of nitrogen (NO_x), fine particulates, sulfur oxides, and carbon monoxide. These pollutants result principally from the combustion of fossil fuels. Automotive emissions are the major source of air pollution worldwide, followed by fixed sources such as power plants.

Elevated values of air pollutants, especially fine particulates, ozone, and NO_x, are associated with respiratory problems in children, including decreased pulmonary expiratory flow, wheezing, and exacerbations of asthma. Fine particulate air pollution, even at low levels, is associated with slight increases in cardiopulmonary mortality and with an increased death rate from sudden infant death syndrome (SIDS) (Chapter 367). Evidence from a prospective cohort study of air pollution and lung development in California demonstrates reduced lung growth from ages 10-18 yr, which leads to clinically significant decreases in lung function that persist into adulthood. It is notable that these effects were seen at air toxic levels below the National Ambient Air Quality Standards (NAAQS) set by the Clean Air Act, highlighting the fact that government regulatory standards are not thresholds below which toxic exposures are harmless.

Indoor air also can be an important source of respiratory irritation, because many children spend 80-90% of their time indoors. Indoor air pollution has become especially important in the USA since the energy crises of the 1970s, which led to the construction of tighter, more energy-efficient homes. Second-hand cigarette smoke is an especially hazardous constituent of indoor air and a powerful asthma trigger. Allergens in indoor air can contribute to respiratory problems and include cockroach, mite, mold, and cat and dog allergens. Some indoor molds produce chemical toxins called mycotoxins. Environmental tobacco smoke is another major contributor to exacerbations of childhood asthma.

Through 2010, there have been at least 17 crude oil spills worldwide of more than 30 million U.S. gallons of oil since the first recorded spill in 1917; 10 have occurred since 1980, the largest in 2010. Although specific composition and concentrations vary, crude oil contains many toxic chemicals that are of concern to human health, including heavy metals (e.g., zinc, cadmium, and lead) (Chapters 701 and 702), volatile organic compounds (including benzene, toluene, ethyl benzene, and styrene), and semivolatile organics (such as polycyclic aromatic compounds). Chemical dispersants—mixtures of detergents and organic solvents—are often used to break up spilled oil and may also have potential adverse effects on health. Toxic effects may occur from exposure from contact with the skin, eyes, respiratory tract, or diet (e.g., drinking of contaminated water or eating of contaminated seafood). Common reported symptoms from direct exposure to crude oil include eye redness and burning, rashes, sore throat, respiratory difficulty, and acute neurologic symptoms such as headache and nausea. Children with asthma may be particularly vulnerable to respiratory toxicity. The amount and duration of exposure along with individual genetic variability influence the degree of symptoms.

It is important to note that most information on health effects comes from studies of exposed adult workers; there are few studies of health effects, acute or long-term, in children. Several of the compounds found in oil spills are classified as possible or potential carcinogens, endocrine disruptors, and neurotoxins. Studies of workers exposed to spilled oil have noted elevated blood concentrations of heavy metals like lead and cadmium, evidence of genotoxic effects, and endocrine disruption (as manifested by prolactin and cortisol changes). Children and teens are at risk for exposure in a variety of settings, including recreational activities like swimming and boating as well as clean-up efforts. Children should not be allowed to play in or around areas where the water or beach contains oil or sludge. In light of teenagers’ propensity to not adhere as well as adults to workplace safety regulations, teens should not be directly involved in spill clean-up efforts.

Lead

Lead exposure occurs worldwide (Chapter 702). Exposure is especially common in countries that still permit leaded gasoline. In the USA, pediatric blood lead levels have declined by more than 90% in the past 20 yr, principally as a result of removal of lead from gasoline. Nevertheless, the CDC estimates that more than 310,000 children 1 through 5 yr of age still have blood lead levels of 10 µg/dL and higher. The prevalence is especially high among poor minority children in inner cities and is far higher in many developing and transitional countries. Blood lead levels as low as 5 µg/dL have been associated with a variety of neurocognitive deficits, including decreased intelligence, shortened attention span, and increased risk for asocial behavior. Although the extent of injury is directly proportional to the lead dose, the relative impact of lead on intelligence appears to be greater at blood levels below 10 µg/dL. Lead-based paint and the lead dust it produces as it ages are the major source of exposure in the USA. Because intact lead-painted surfaces invariably break down to produce lead dust, efforts to further reduce the number of children poisoned by lead in the USA must focus on the identification and permanent removal of all lead-based paint, intact or not, from residences. Leaded gasoline, industrial pollutants, and cottage industries remain major sources of lead pollution in many developing countries.

Mercury

Children may be exposed to either inorganic or organic mercury (Chapter 701). Inorganic mercury produces dermatitis, gingivitis, stomatitis, tremor, and acrodynia. Organic or methyl mercury is fat-soluble, readily penetrates the central nervous system (CNS), and is neurotoxic. Exposure to organic mercury occurs principally through consumption of fish that have accumulated mercury deposited in lakes and oceans as atmospheric fallout from combustion of coal; coal normally contains small quantities of mercury. Even low-dose exposure to organic mercury has been shown to be hazardous to the developing fetal brain, and pregnant women are therefore advised to curtail consumption of mercury-containing fish such as tuna and swordfish. Although adverse neurologic effects have not been related to exposure from the preservative thimerosal, which contains ethyl mercury, thimerosal has been removed from routine childhood vaccines and maternal Rh vaccine (RhoGam, Ortho Clinical-Diagnostics Inc. USA, Rochester, NY) as a precautionary measure.

Asbestos

Between 1947 and 1973, asbestos was sprayed as insulation on classroom walls and ceilings in about 10,000 schools in the USA. Subsequent deterioration of this asbestos has released inhalable asbestos fibers into the air and thus poses a risk to children. Asbestos is a human carcinogen, and the two principal cancers caused by asbestos are lung cancer and mesothelioma. U.S. federal law requires that all schools be inspected periodically for asbestos and that the results be made public. Removal is required only when asbestos is visibly deteriorating or is within the reach of children. In most cases, placement of barriers (drywall walls or drop ceilings) provides appropriate protection.

Environmental Tobacco Smoke

Smoking during pregnancy poses a hazard to the fetus (Chapter 90). Infants born to women who smoke are, on the average, 10% smaller than infants born to nonsmoking women. Infants of parents who smoke have a higher risk of sudden infant death syndrome. Nicotine from tobacco smoke appears to be a developmental neurotoxin.

Passive smoking also is a hazard to children. In the USA, 43% of children younger than 12 yr live in a home with at least one smoker. Children exposed to environmental tobacco smoke have increased lower respiratory illness, more middle-ear effusions, and more viral respiratory illnesses than unexposed children.

Pesticides

Pesticides are a diverse group of chemicals used to control insects, weeds, fungi, and rodents. Approximately 600 pesticides are registered with the EPA.

Diet is a major route of children’s exposure to pesticides, because they are exposed to residues of multiple pesticides on fruit and vegetables. Children also may be exposed in homes or schools, on lawns, and in gardens. They may be exposed to pesticide drift from agricultural areas that have been sprayed. Children employed in agriculture or living in migrant farm camps are at risk of exposure to many pesticides.

Pesticides can cause a range of chronic toxic effects: polyneuropathy and CNS dysfunction (organophosphates); hormonal disruption and reproductive impairment (DDT, kepone, dibromochloropropane); cancer (aldrin, dieldrin, chlorphenoxy herbicides [2,4,5-T]); and pulmonary fibrosis (paraquat). Children’s exposure to pesticides can be reduced by minimizing applications to lawns, gardens, schools, and playgrounds; by adapting techniques of integrated pest management; and by reducing pesticide applications to food crops.

Children can be acutely overexposed to pesticides (Chapter 58). The organophosphates and carbamates both engender neurotoxicity through inhibition of acetylcholinesterase and cause the largest number of acute poisoning cases. Symptoms include meiosis (although not in all cases), excess salivation, abdominal cramping, vomiting, diarrhea, and muscle fasciculation. In severe cases, the child may experience loss of consciousness, cardiac arrhythmias, and death by respiratory arrest. The war gas sarin is an organophosphate. See Chapter 58 for treatment of poisoning from drugs, chemicals, and plants.