Introduction

As children mature, they become progressively more independent of parental care and supervision. Each developmental stage means new opportunities for exposures to hazardous substances in play settings, in schools, and in adolescents' occupational environments.

Young Child (2 to 6 years old)

With the newly acquired ability to run, climb, ride tricycles, and perform other mobile and exploratory activities, the young child's environment expands, as does the risk of exposure.

Many of a young child's toxic exposures may occur from ingestion. If the child's diet is deficient in iron or calcium, the small intestine avidly absorbs lead. Pica is still a consideration - children aged 6 years and younger are at high risk for soil pica [ATSDR 2001a]. One study used aluminum, silicon, and titanium tracers to examine soil ingestion in 59 children 1-3 years old who played outdoors. Soil intake ranged from a minimal estimate of 108 milligrams (mg)/day to a maximum of 1,834 mg/day of soil - more than any other age group [Binder et al. 1987]. Children's blood lead concentrations are correlated with their intake of lead-containing dust from hand-to-mouth activities and oral exploration. This may result in appreciable absorption of lead from indoor sources and from outdoor lead-contaminated soil [Paustenbach D et al. 1997]. Arsenic contamination of residential soil was found to correlate with urine and tissue levels of arsenic in children living near copper smelting facilities [Hwang et al. 1997].

School-aged Children (6 to 12 years old)

School-aged children spend increasingly greater amounts of time in outdoor, school, and after-school environments. They may be exposed to outdoor air pollution, including

• widespread air pollutants,
• ozone, particulates, and
• nitrogen and sulfur oxides.

These result primarily from fossil fuel combustion. Although these pollutants concentrate in urban and industrial areas, they are windborne and distribute widely. Local pockets of intense exposure may result from toxic air and soil pollutants emanating from hazardous waste sites, leaking underground storage tanks, or local industry. One example of a localized toxic exposure adverse effect was seen in children exposed to high doses of lead released into the air from a lead smelter in Idaho. When tested 15 to 20 years later, these children showed reduced neurobehavioral and peripheral nerve function [ATSDR 1997b].

A clinician taking an exposure history of a school-aged child and his or her parents should ask about school and after-school environments. Children may ingest or inhale dirt or dust contaminated with arsenic, mercury, or other environmental toxicants during play or other normal activities. Questions could include exposures to indoor and outdoor air pollutants and contaminated drinking water and soil.

In addition, some school age children engage in activity such as

• lawn care,
• yard work, and
• trash pickup.

These and other work situations may put them at risk for exposures to hazardous substances such as pesticides used to treat lawns.

Adolescents (12 to 18 years old)

But nothing more than just adolescent behavior may result in toxic exposures. Risk-taking behaviors of adolescents may include exploring off-limit industrial waste sites or abandoned buildings. For example, in one reported case, teenagers took elemental mercury from an old industrial facility and played with and spilled the elemental mercury in homes and cars [Nadakavukaren 2000]. Teens may also climb utility towers or experiment with psychoactive substances (inhalant abuse, for example). Cigarette smoking and other tobacco use often begins during adolescence. For more information about adolescent tobacco use see CDC Office of Smoking and Health at http://www.cdc.gov/tobacco

Compared with younger children, adolescents are more likely to engage in hobbies and school activities involving exposure to

• solvents,
• caustics, or
• other dangerous chemicals.

Many adolescents may encounter workplace hazards through after-school employment. Working adolescents tend to move in and out of the labor market, changing jobs and work schedules in response to employer needs or their own life circumstances [Committee on the Health and Safety Implications of Child Labor 1998]. In the United States, adolescents work predominately in retail and service sectors. These are frequently at entry-level jobs in

• exterior painting of homes,
• fast-food restaurants,
• gas stations and automotive repair shops,
• nursing homes,
• parks and recreation, and
• retail stores.

Such work may expose adolescents to commercial cleaners, paint thinners, solvents, and corrosives by inhalation or splashes to the skin or eyes. The National Institute of Occupational Safety and Health (NIOSH) estimated that, on average, 67 workers under age 18 died from work-related injuries each year during 1992-2000 [NIOSH 2003]. In 1998, an estimated 77,000 required treatment in hospital emergency departments [NIOSH 2003].

For more information about adolescent workplace toxic exposures, see Woolf et al. [2001]. Workers younger than 18 years of age are protected under the federal Fair Labor Standards Act (FLSA), which limits the number of hours and types of hazardous work young workers can do [NIOSH 2003]. For more information, see the complete NIOSH tables at http://www.cdc.gov/niosh/docs/2003-128/

State laws also protect adolescent workers. Vocational/technical training is sometimes exempt from these laws because it is assumed that this work is done in a supervised, educational setting. That this is not always the case, see [Woolf et al. 2001; Knight et al. 2000].

Looking internationally, the International Labour Office (ILO) reported that an estimated 352 million children age 5-17 worked in economic activity in 2000 [ILO 2002]. About 185 million children under 15 were doing actual "child labor," and 171 million children (age 5-17) worked in hazardous conditions.

Metabolic Vulnerability of Adolescents

Metabolic processes change during adolescence. Changes in cytochrome P450 expression [Nebert and Gonzalez 1987] result in a decrease in the metabolism rate of some xenobiotics dependent on the cytochrome CYP (P450) - for example, the concentration of theophylline increases in blood [Gitterman and Bearer 2001]. The metabolic rate of some xenobiotics is reduced in response to the increased secretion of growth hormone, steroids, or both that occur during the adolescent years [Gitterman and Bearer 2001]. The implications of these changes on the metabolism of environmental contaminants are areas of intense research. By the end of puberty, the metabolism of some xenobiotics achieves adult levels.

Puberty results in the rapid growth, division, and differentiation of many cells; these changes may result in vulnerabilities. Profound scientific and public interest in endocrine disruptors - that is, chemicals with hormonal properties that mimic the actions of naturally occurring hormones - reflects concerns about the effect of chemicals on the developing reproductive system. Even lung development in later childhood and adolescence may be disrupted by chronic exposure to air pollutants, including

• acid vapors,
• elemental carbon,
• nitrogen dioxide, and
• particulate matter [Gauderman et al. 2004].

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