Children’s health is determined by the interaction of a multitude of influences, reflecting complex processes. We divide these influences into biological, behavioral, and environmental (physical and social) even though our model of children’s health views their effects as highly intertwined and difficult to isolate. This chapter provides a summary of published literature and a framework for understanding those influences.
Biological influences as discussed in this chapter include genetic expressions, prenatal influences, as well as biological constraints and possibilities created by perinatal and postnatal events plus prior states of health. Behavioral influences include the child’s emotions, beliefs, attitudes, behaviors, and cognitive abilities that affect health outcomes. Environmental influences are wide-ranging and include infectious agents, toxins such as lead and air pollution, and social factors such as loving interactions with caregivers, socioeconomic resources in the family and community, and peer relationships, segregation, racism, culture, the availability and quality of services, and policies that directly or indirectly affect these other interactive influences (see Box 3-1).
Organization of Influences on Children’s Health. Children’s biology Children’s behavior
The role and effect of biological, behavioral, and environmental influences change as children grow. For example, a pharmacological agent like thalidomide is highly toxic within a narrow window during pregnancy but not afterward, an attachment to a caring adult is especially critical during infancy, and peer influences appear to grow steadily from toddlerhood through adolescence. Even within a childhood stage, health influences can act in very different ways because of the differing cultural interpretations that families attach to them.
While biology, behavior, and environmental categories are useful for organizing our discussion, it is important to understand that healthy development is not the product of single, isolated influences or even types of influences. Warm and nurturing parenting is an important family influence, but prematurity or visual impairment can make an infant unresponsive to a mother’s initial nurturing. Mothers may react with apathy or disinterest, which produces even more withdrawal on the part of the infant (Lozoff, 1989). While simplified schematics or models help to organize understanding of the influences on children’s health both during childhood and beyond, life is not as simple as these models suggest.
One caveat should be kept in mind in reading through the following review of evidence. Few of the cited studies drew their evidence from randomized experiments. And few if any of the nonexperimental studies included all relevant variables in their data and analyses. Thus, the findings reported in these studies are likely to suffer from exclusion of potentially important categories of influences, so that the associations that are reported as being important may be due to their associations with a more important or equally important characteristic, or due to interactions with other types of factors so that their effect may be manifested primarily or only in certain population groups. A related problem is that few of the cited studies include data that represent the whole population of children. Thus, the findings that are reported as significant may be significant only in the population studied or similar populations. Nonetheless, the committee found the evidence to be sufficiently compelling to warrant inclusion when there was a plausible, well-supported connection between the influence and health.
Moreover, inferences about the relative importance of the variety of influences are heavily dependent on the nature of the theoretical models that underlie statistical analysis. If more proximal influences are mixed with more distal ones, they may appear to have stronger effects, even in situations in which more distal factors are operating on a multiplicity of proximal influences and therefore have cumulatively greater effect overall. Thus, future research should adapt more appropriate pathway techniques to help to sort out the patterns by which the influences interact to produce different states of health.
Finally, the relative lengths of the following sections are not meant to signify the relative importance of the influences. For some, the prevalence is less well known than for others. From the viewpoint of influences on population or sub-population health, the relative frequency of the different influences is at least as critical as the degree of the risk that they pose to individuals. Additional research is needed to refine understanding of the relative contribution of each of the influences and the relevance of each across a variety of social and cultural groups.
A child’s biology determines how physiological processes unfold and how organ systems adapt to outside influences. Biological response patterns, including responses to stress, novel situations, and primary relationships, can directly and indirectly influence other biological, cognitive (learning), and behavioral processes. The term “biological embedding” has been used to describe how the external environment influences and shapes the biological environment (including the central nervous system), which in turn changes the way the individual interacts with the external environment (Hertzman, 1999).
DNA provides the blueprint for life. The units of heredity, or genes, are specific sequences of DNA that code for proteins that affect the particular physiology and anatomy of an individual. All cells contain the full array of genes but, depending on the cell type, some are expressed while others are not; for example, certain genes coding for proteins in the retina are expressed in the cells of the eye, but not in the pancreas cells.
Disruptions in genes can be caused by events before, during, or after conception and may produce disorders immediately or later in life. A parent can pass on a defective or abnormal gene or set of genes, a malfunction can occur during combination of maternal and paternal DNA, or exposure to an outside substance or condition can occur after conception that alters the genes in the fetus. Physical and social environments (e.g., family, community, school, culture) interact with and influence these biological processes.
Influences of Genes on Responses to Different Environments
Classically, genes have been considered to be the “instructions” for building proteins, although it is clear now that they have other functions as well. A gene may affect health as a result of the interaction of its protein product with another aspect of a child’s biology. The combinations of these interactions may result in an enhanced, worsened, or inconsequential change in health status. For example, sometimes an alteration in the gene (i.e., mutation) is identified due to the presence of a particular disease state, or it can be deduced that an individual with the mutation has a high probability of developing a particular disease. Understanding the biological pathway of the disease and its interactions with other biological processes facilitates treatment options by modifying the causal path. In the case of Huntington’s disease, for example, the disorder appears to be in part mediated by glutamate excitotoxicity; giving patients a substance that blocks this effect (glutamate receptor antagonists) interrupts this pathway and may retard the manifestation of the disease (Ferrante et al., 2002). The influence of genes on health always exists in an environmental context; in the next sections we describe how genes affect behavior and the physical and social environments.
Genes and Behavior. That genes affect behavior has been amply demonstrated in honeybees (Ben-Shahar et al., 2002) and higher animals (Ruby et al., 2002; Chester et al., 2003; Hendricks et al., 2003). Examples in humans are being rapidly discovered, including genes that influence the relationship between exposure to trauma and susceptibility to posttraumatic stress disorder (Stein et al., 2002), genetic polymorphisms that protect against alcoholism (Wall, Carr, and Ehlers, 2003), mutations that result in sleep disorders (Wijnen et al., 2002), and several genes that are associated with simple phobias (Gelernter et al., 2003).
Genes and the Physical Environment. The physical environment includes ubiquitous agents (e.g., ultraviolet light, amino acids and sugars in the diet, noise, speech) and somewhat less universally encountered ones (e.g., loud music, medications, pollutants). Some genes result in poor outcomes following common environmental exposures (e.g., phenylketonuria with phenylalanine, galactosemia with galactose, xeroderma pigmentosa with ultraviolet light exposures). Individuals with these genotypes are likely to be affected by the disease because they have a high chance of being exposed to the physical environmental agent. In some cases, the physical environment can be modified to improve outcomes (e.g., a phenylalanine-free or galactose-free diet may improve IQ, no sunlight or ultraviolet exposure may reduce skin cancers). There are also gene alterations resulting from uncommon physical environmental exposures that affect health. Examples include a higher risk of lung cancer in individuals lacking glutathione S-transferase mu who smoke (Perera et al., 2002) and noise-induced hearing loss in some individuals exposed to high levels of noise—the gene or genes in this case are just being discovered (Kozel et al., 2002). These genes are known as susceptibility genes. An example of a positive susceptibility gene to a physical environmental agent may be that for perfect pitch. It appears that individuals with exposure to music and a family history of perfect pitch are more likely to acquire perfect pitch (Alfred, 2000).
Genes and the Social Environment. The identification of genes that confer susceptibility to adverse or beneficial responses following exposure to diverse social environments has only just begun. In one study, abused children with a genotype conferring high levels of neurotransmitter-metabolizing enzyme monoamine oxidase A expression were less likely to develop antisocial problems in adulthood (Caspi et al., 2002). The risk of developing alcohol abuse or dependence also appears to have both a genetic susceptibility and a family influence (Macciardi et al., 1999; McGue et al., 2001), as does the risk for relapse and poor outcomes with schizophrenia (Campbell, 2001).
Characteristics of Gene-Environment Interactions
The expression of certain genetic characteristics depends on the environment in which they occur. Thus, gene expressions that lead to a disease in one context may not lead to a disease, or may result in a different disease, in another context (Holtzman, 2002). Inheriting a single copy of the hemoglobin S gene makes an individual resistant to malaria (Aidoo et al., 2002). However, inheriting two such genes gives the individual sickle cell anemia, a severe disease. Outside of malaria-endemic areas, sickle cell trait, the inheritance of one copy of hemoglobin S, has no known adaptive benefit and may be maladaptive. A single cystic fibrosis gene has been postulated to be protective against diarrheal diseases such as cholera, conferring a survival advantage to individuals who carry one copy of the gene (Rodman and Zamudio, 1991). However, individuals with two such genes have cystic fibrosis, a severe disorder with altered pulmonary and gastrointestinal function. Other examples of genes with positive influence also exist in given environments. The gene or genes that confer protection from cancer (Gonzalez et al., 2002; Reszka and Wasowicz, 2002) have been described.
Genes may confer susceptibility only during a specific span of time, referred to as a critical period. For example, 20 percent of children are extremely sensitive to thalidomide during a critical 15-day period from day 20 to day 35 of gestation, although the gene or genes responsible for this enhanced sensitivity have not yet been identified (Finnell et al., 2002). Presumably there are narrow windows of rapid development throughout childhood, including puberty, but critical windows of sensitivity to disruption have not been adequately described (Selevan et al., 2000). The complex interrelationships between genetics and environmental stimuli are not clearly defined and are an active area of current research.
Understanding of the genome has rapidly expanded the study of the ways in which genes interact with diverse influences (e.g., physical and social environments) to affect health. Expression of genes (the amount of the protein encoded for by the gene) has a profound influence on the health of the individual. Gene expression is determined by many factors, such as promoters, regulators, mutagens/carcinogens/teratogens, X-inactivation, message stability, rate of protein degradation, prior exposures, all of which are affected by the environment. Interactions between genes and the environment influence different physiological pathways and adaptation (Holtzman, 2001) and may lead to adaptive or maladaptive phenotypes. An interesting example is the hygiene theory of childhood asthma, which postulates that children living in hygienic, low-pathogen environments develop an imbalance between two types of immune cell classes (TH1 and TH2). Children with an imbalance of TH1 and TH2 are more likely to develop allergies and asthma when confronted with allergens. When children live in low-hygiene, high-pathogen environments, they develop a strong system of immune regulators (a balance between TH1 and TH2 cells), and they are less likely to develop allergies or asthma (Yazdanbakhsh et al., 2002). Children living on farms or in homes with at least two cats or dogs in the first year of life have been shown to have significantly lower rates of allergic sensitization tested at 6–7 years (Ownby et al., 2002).
Healthy development depends on gene expression being responsive to changes in the environment. For example, the radical change in the environment at birth is responsible for changing the expression of genes to enable the baby to make the transition from intrauterine to extrauterine life. These include the production of proteins that close the ductus arteriosus (Kajino et al., 2001), alter lung liquid absorption (Matalon and O’Brodovich, 1999), produce barrier function in the skin (Harpin and Rutter, 1983), produce immunoglobulins, and alter gene expression in brain development. Thus, to be healthy, newborns must make profound changes in gene expression as they transition from intrauterine to extrauterine environments.
Converging findings from genetics and molecular biology demonstrate that a host of internal and external signals can stimulate or inhibit gene expression, including subtle factors such as the light-dark cycle (Hegarty, Jonassent, and Bittman, 1990) and tactile stimulation (Mack and Mack, 1992). This pattern of contingency is now recognized as part of the normal process of development in embryology and developmental biology, and there is a growing body of literature demonstrating how factors, including internal neural and hormonal events and external sensory events, activate or inhibit gene expression during individual development (see Davidson, 1986, 2001; Gilbert, 2000; Holliday, 1990).
Chemicals in the environment (air, water, dirt, dust, food) move into the body across such biological barriers as skin, lungs, and the gastrointestinal system. Exposure is considered to be contact of the agent with the biological barrier; following exposure, the agent crosses the barrier and is found inside the body (the internal dose). After uptake or absorption across the barrier, chemical agents (including drugs) are distributed throughout the body, metabolized, and eliminated (U.S. Environmental Protection Agency, 2003; Atkinson et al., 2001).
The rate of elimination varies substantially for different agents; some are eliminated in a matter of minutes; others may be found in the body for years following exposure. The amount of chemical/biochemical/vitamin/mineral stored or measured in the body is called the “body stores” or “body burden” of that agent. The committee has adopted the term “body burden” in this report. Body burdens of a chemical or drug represent the amount of cumulative exposure and, in some instances, can be transferred to another individual (e.g., from a mother to the fetus or infant through the placenta or in breast milk).
Body burdens can improve or harm health, based on their biological characteristics and presence during certain periods of development. Maternal body burdens of either lead or polychlorinated biphenyls (PCBs) impair the cognitive function of offspring if present during critical periods during fetal development (Gomaa et al., 2002; Lai et al., 2002). A body burden of lead in the bones of young children has been associated with poor social behavior (Needleman et al., 2002; Wald et al., 2001), poor cognitive performance or development (Lanphear et al., 2003; Rogan and Ware, 2003), and impaired pubertal progression (Selevan et al., 2003). The relative impact of body burdens varies with developmental stage. Relatively lower body burdens of organic mercury will reduce cognitive development in young children more than at older ages (U.S. Environmental Protection Agency, 2000c; National Research Council, 2000).
Some body burdens can have positive impacts on healthy development. For example, maternal body burdens of folate during the early first trimester of pregnancy significantly reduce the risk of a baby with a neural tube defect (Wald et al., 2001). Adolescents with higher levels of folate also have a significantly decreased risk of juvenile hypertension (Kahleova et al., 2002), and adults with high folate stores appear to be at substantially lower risk of cardiovascular disease (Wald, Law, and Morris, 2002). Some body stores that are beneficial at lower levels can become harmful at higher levels: a baby’s appropriate body burdens of iron will improve cognitive outcome, but an inappropriately high body burden of iron potentiates oxidative stress (Rao and Georgieff, 2001) or can cause iron overload disease. Low maternal or fetal levels of vitamin A are associated with developmental disease, as are high levels.
The impact of some body burdens vary across time and, to be understood, must be assessed at different times. For example, a maternal body burden of PCBs causes exposure to both the fetus and to the newborn via breast milk. Body burdens at one time may also impact measures of health in later time frames. A child who has received treatment for Hodgkin’s lymphoma, increasing the genotoxic body burden, is at risk for secondary cancers (Hack et al., 2002).
While not without controversy (Huxley et al., 2002), there is a growing literature on the potential role of “perinatal programming,” referring to the processes in which specific influences during critical or sensitive periods of development can have lifetime consequences by altering metabolic pathways and other physiological systems. This appears to be a special case of the more general phenomenon of how environmental influences can be embedded in biology during critical and sensitive periods of development.
In humans, the relationship between fetal growth, postnatal growth, and the risk of such diseases as hypertension, coronary heart disease, and non-insulin-dependent diabetes have been frequently studied (Bertram and Hanson, 2002; Barker, 1998). Both human epidemiological and animal experimental studies support the hypothesis that relative undernutrition in the fetus results in significant and relatively permanent changes in important physiological systems (Nathanielsz, 1999). Perinatal programming indicates that sensitive or critical periods of development may have lifelong effects and influence the development of chronic diseases later in life (Ingelfinger, 2003). However, it does not discount the potential effect of the external environment (Seckl, 1998; Ingelfinger and Woods, 2002; Falkner, 2002; Roseboom et al., 2001) in modifying the effects.
Fetal undernutrition is believed to induce persistent changes in several metabolic pathways, but the exact mechanisms are only now being pieced together through a range of animal experiments and human measurement studies (Seckl, 1998; Barker, 1998). Because it is likely that events occurring at other times modify prior influences, there is a growing interest in understanding the predisease pathways and biological changes that occur prior to the recognition of a vast array of clinical outcomes. Currently many of these predisease markers are either below current limits of detection or produce changes that are not currently measured on a routine basis (Lucas et al., 1999; Keller et al., 2003; Ingelfinger, 2003).
Examples of such programming during particular sensitive or critical periods of development are coming to light. For example, low numbers of nephrons are associated with hypertension, and it has been shown that individuals whose mothers experienced severe protein-calorie malnutrition during the third trimester, when nephron development takes place, are most at risk of hypertension (Roseboom et al., 2001; Keller et al., 2003). Outcomes associated with programming early in life may also promote health. For example, rats receiving high levels of licking and grooming as pups are less fearful compared with rats that received low levels of licking and grooming (Francis et al., 2002). The mechanism for this change in behavioral programming appears to be the influence of maternal licking on gene expression during a critical period of development and subsequent changes in the development of synaptic receptor sites for specific neurotransmitters (Francis et al., 1999).
Similar environmental influences on the development of behavioral pathways have been described in rhesus monkeys (Champoux et al., 2002), and studies of premature human infants show substantially greater increases in body weight after introduction of massage therapy (Field, 2002). In contrast, disruption of maternal bonding during infancy has been shown to have profound negative effects on later relationships (National Research Council and Institute of Medicine, 2000).
As used in this report, behavior refers to a child’s emotions, beliefs, cognitions, and attitudes, as well as his or her overt behaviors. Some behaviors are planned and deliberate; others are reflexive, impulsive, and contingent on environmental circumstances. A child’s emotions, beliefs, and attitudes affect health, principally through the way they modify a child’s explicit and overt behaviors, such as his or her health and life-style choices. These in turn alter the child’s eventual health outcomes. Examples include social and interactional behaviors (e.g., compliance with parental requests, peer interactions), health preventive behaviors (e.g., avoiding smoking, driving with a seat belt, choosing good friends), or illness-management-related behaviors (e.g., behavioral adherence with a treatment regimen or health care appointments).
Health-related behaviors may be health promoting (those that increase the likelihood of future health, such as regular balanced diet and exercise) or health impairing (those that adversely cause actual morbidity or mortality, such as smoking, drinking, or reckless driving). A body of recent research suggests how these behaviors develop and describes the role of family, peers, and social environment, including media, in shaping this developmental process (Tinsley, 2003). While behaviors like smoking, drinking, and exercise are known to affect later health, it is not clear how these behaviors develop in childhood (McGinnis and Foege, 1999).
Often these health behaviors are considered proxies for health, even though they may not necessarily constitute health per se. Some health policies attempt to change youth behaviors that are thought to affect health. An example is the requirement for regular school attendance, which may both reflect current health and exert effects on a given child’s likelihood of future health.
Behavioral influences on children’s health are often reciprocal, both influencing and influenced by parents, peers, and others. For example, parenting style, family traditions, and peer influences affect not only fairly simple youth behaviors, such as compliance with behavioral requests or participation in health prevention programs (Patterson and Fisher, 2002), but also more complex behaviors, such as participation with disease management regimens. This section focuses on the internal psychological factors that underpin children’s behavior, with implications for subsequent health outcomes.
Emotions, Attitudes, and Beliefs
In addition to the influence of explicit behaviors on health, a child’s internal emotional, attitude motivation, or belief states may exert effects on health. For example, research on both adults and children has shown direct relationships between internal attitudinal and personality factors and health outcomes, perhaps through mechanisms that link internal emotions, attitudes, and beliefs with stress reactions and immune responses (Berry and Worthington, 2001; Herbert and Cohen, 1993; Kiecolt-Glaser, 1999, Lawler et al., 2000). Thus, external events perceived as stressful by a child may function as triggers for an asthma or inflammatory bowel disease flare, over and above any biological exposure or adherence to therapy (Rietveld and Prins, 1998; Santos et al., 2001). Presumably such effects are conveyed through a child’s emotional arousal states, which in turn result in physiological changes, such as increased pulse and elevated blood pressure, glycemic, and immune responses. This research has solid empirical support in both the adult human and animal research fields (McEwen, 1998; Seeman et al., 1997), but it is less firmly established for children.
The hallmark of childhood is the constant exposure to new developmental challenges. As children acquire new physical and cognitive skills and experiences, their behaviors change. They explore, practice, and experiment and as a result they change and are changed. The resulting behaviors are both manifestations of their health and have significant implications for it. At each new exposure, the child may respond in a variety of ways that in turn unleash a variety of reactions in his or her caregiver and in others around him.
From birth, infants recognize, prefer, and are soothed preferentially by their mother’s voice (Mehler et al., 1978; DeCasper and Fifer, 1980). They suckle more in response to it (Mehler et al., 1978), and mothers in turn are gratified by their ability to sooth their children (Klaus et al., 1972). Thus the beginnings of attachment are initiated. As an infant continues his or her explorations and trials, which themselves influence health, they produce reactions from caretakers that in turn further affect the infant’s behavior and health. One of the first developmental challenges faced by an infant is adaptation to extrauterine life. Low-birthweight infants experience more difficult transitions and are more likely to be fussy during social interactions and less likely to smile and vocalize (Beckwith and Rodning, 1992; Barnard and Kelly, 1990). These infant reactions in turn impose stresses on the parent, which may affect the child’s health through impaired attachment. If the parent responds in a fashion that induces further stress in the infant, the increased stress in turn may affect the infant’s ability to secrete adequate amounts of growth hormone (Skuse et al., 1996), potentially leading to growth impairment or failure to thrive.
Attempts to make this transition are met with a variety of parental and cultural responses, all of which influence infants in ways that facilitate or impede their development. Nearly a quarter of infants respond to new stimuli in a negative fashion (Kagan et al., 1998); their early infancy imposes a series of challenges that are especially daunting and many are found to still be socially wary and exhibit evidence of physiological stress at age 6 years (Kagan et al., 1987).
Emotional development and the establishment of social relationships are among the greatest challenges of infancy and early childhood. Emotions are fundamental for human attachments, social interactions, and self-satisfaction. Therefore, the extent to which infants evoke sympathetic and empathetic emotions in others and eventually develop these emotional expressions themselves greatly influences their subsequent health. Children who do not attain these skills are more likely to encounter rejection from caretakers and peers (Dodge et al., 2003; Schultz et al., 2000). The complex interplay of genetics, parenting, and societal reactions illustrates just how precarious the early years are and how central infant behavior is for subsequent health (Rutter, 1998).
Attitudes, Beliefs, and Circumstances
The effects of individual, family, and community attitudes and beliefs on health behavior have been well described. A substantial body of research has been conducted on issues related to adherence to treatment regimens, both among parents of younger children and among adolescents (McQuaid et al., 2003; Volovitz et al., 2000; Davis et al., 2001). This work focused initially on asthma and diabetes and more recently on substance use and HIV/AIDS treatment (Manne, 1998). Current research is informed by several related theoretical models of behavior, all of which take into account youths’ attitudes, beliefs, and subjective perceptions about the risks of negative outcomes, as well as the perceived benefits and difficulties of treatment (Hochbaum, 1956; Ajzen, 1991; Rogers, 1983; Bandura, 1994).
In accordance with these models, data suggest that both parents’ and youths’ attitudes are moderately predictive of subsequent health care behaviors, whether in the context of seizures (Kyngas, 2001; Kyngas et al., 2000), asthma (Kyngas, 1999), diabetes (Wysocki et al., 2000; Ott et al., 2000), or sexual risk avoidance (Stanton et al., 1996; St. Lawrence et al., 1995; Jemmott and Jemmott, 1994).
These conceptual considerations lead directly to specific interventions, such as motivational enhancement strategies to encourage youths’ substance abuse treatment compliance (Carroll et al., 2001), engaging them in sexual risk prevention activities (Stanton et al., 1996; St. Lawrence et al., 1995), and using collaborative goal-setting strategies in enhancing adolescent diabetes self-care (Delamater et al., 2001). In addition, these theories help explain why and how child compliance may be positively (or adversely) affected by peer and family support (LaGreca and Bearman, 2002; LaGreca et al., 2002; Liss et al., 1998), as well as the support available through a good relationship between the youth and his or her health care team (DiMatteo, 2000; Kyngas et al., 2000). The effect of and the need for support may vary as a function of age (Steinberg, 1999).
Research has documented the impact of chronic illness on child and adolescent adjustment (DiMatteo, 2000; Kyngas et al., 2000). Not infrequently, depression, anxiety, low self-esteem, or other adjustment difficulties may ensue as a result of the underlying illness, increasing risk for treatment nonadherence (Wise et al., 2001; Murphy et al., 2001; Davis et al., 2001) or worsening the outcome of the primary illness (Kuttner et al., 1990; Hauser et al., 1990). Available evidence suggests that good communication skills and the development of positive relationships with the clinical team may offset the effects of negative emotions on health care adherence (Buston, 2002; García and Weisz, 2002; Shaw, 2001).
Emotion, Cognition, and External Influences
The importance of cognitive ability and understanding inappropriate health-related behaviors must also be considered. Children’s ability to understand safety rules and health behaviors increases with age (Morrongiello et al., 2001). Over time they acquire the capacity to conceptualize and understand the longer term consequences of their behaviors on their health (Thomas et al., 1997). Conversely, children with developmental disabilities or impaired language ability often show increased difficulties in adhering to necessary behaviors, including health-maintaining ones (Stansbury and Zimmerman, 1999).
While attitudinal, motivational, cognitive, and emotional factors may all exert direct effects on health-related behaviors, the role of environmental factors in these behaviors should not be underestimated. For example, under some circumstances, behavioral factors may contribute less to youths’ actual health care behaviors than making available a more easily used medication, such as a long-acting form of medication in the case of birth control (Stevens-Simon et al., 2001; Omar et al., 2002) or providing more stable living situations in the case of adolescents’ likelihood of adhering to an HIV/AIDS drug regimen (Conanan et al., 2003). In addition, children’s behaviors may directly affect parents’ ability to adhere to a treatment regimen (Searle et al., 2000), just as parental response styles may affect the likelihood of a child’s complying with specific requests (Patterson and Fisher, 2002).
Cultural construction of health and disease may also affect compliance with certain treatments by both parents and children. For example, in many cultures, so-called teething diarrhea is considered to be a normal part of growth and development and thus health-seeking behavior or adherence to treatment regimens for the “illness” would be unlikely (Stanton et al., 1992).
In sum, all these psychological factors, whether a child’s perceptions of peer norms, self-efficacy beliefs, attitudes about health and health care, or level of motivation to pursue specific health care behaviors, contribute to health-related choices and behaviors. With increasing age, children’s behaviors, such as substance use, academic performance, violence, suicide, and auto accidents, constitute a major influence on future health. According to findings from the Global Burden of Disease study, these behavioral aspects of health are likely to exert even greater prominence in coming decades, as behavioral and life-style-related health conditions (e.g., auto accident injuries, consequences of smoking, depression) increase in their relative effect on children’s health and illness (Murray and Lopez, 1996).
Complicating this point, however, is the fact that certain behaviors and emotions can serve both as health influences and outcomes. Determining when a behavior is an influence rather than a health outcome can be difficult, because children’s current behaviors can affect both future behaviors and subsequent health outcomes. Regardless of the classification and especially due to the inability to distinguish behaviors as health influences or outcomes, data on children’s health behavior are an important component of a system that seeks to track child health and health behaviors.
The physical environment affects children’s health by exposing them to a wide variety of external conditions. These include chemical, biological, and physical influences that exert their impact by being taken into the body (e.g., lead, methyl mercury, persistent organic pollutants) or interacting with body surfaces (e.g., ultraviolet light, physical abuse, particulate matter in air pollution) or the senses (e.g., noise, odors). The built environment affects the ways in which children are differentially exposed to some of these influences. Exposure is the sum of all exposure factors over the course of time, including the home, school, child care, and play areas. Exposures during the prenatal period can also affect children’s health.
Although exposures of the ovum or the sperm prior to conception may have profound health effects on a child, including development of an abnormal fetus,1 in this section we focus on prenatal influences. In most cases, exposures of the fetus are from maternal exposure. Exposures of the mother during pregnancy can come from many sources; common sources include maternal occupation, substance use, diet and water consumption, and paraoccupation (occupational chemicals or other hazards brought home by other family members). The strongest workplace exposure associations are lead, mercury, organic solvents, ethylene oxide, and ionizing radiation and poor reproductive outcome, including birth defects (Agency for Toxic Substance and Disease Registry, 1993; Schardein, 2000).
Use of tobacco, alcohol, and illicit drugs also have harmful effects. Tobacco use during pregnancy is a major cause of fetal and newborn morbidity and mortality (small for gestational age, persistent pulmonary hypertension, sudden infant death syndrome, poorer intellectual functioning) (Nicholl, 1989; Golding, 1997; Day et al., 1992; Kline, 1987; U.S. Environmental Protection Agency, 1992; Bearer et al., 1997). Heavy drinking during pregnancy is the cause of fetal alcohol syndrome (FAS), the leading known cause of mental retardation (Abel and Sokol, 1987; Sokol, Delaney-Black, and Nordstrom, 2003). Conservative estimates place the incidence of FAS at 0.33/1,000 live births (Abel and Sokol, 1991). More common effects include alcohol-related birth defects, alcohol-related neuro-developmental defects, and subtle effects on a variety of behavioral, educational, and psychological tests resulting from low to moderate levels of drinking during pregnancy (Institute of Medicine, 1996). While the effects of maternal prenatal use of cocaine, opiates, and methamphetamines on infant cognitive development and behavior remain controversial (owing to confounding environmental factors) (Bays, 1990; Tronick and Beeghly, 1999), the effects on maternal-infant interactions are more established (Breiter et al., 1997; Singer, 2000).
There are multiple short critical periods during the development of a fetus when a short, acute exposure may cause a problem. For this reason, exposures need to be tracked as highs and lows on a daily basis rather than as monthly averages. For example, water quality is regulated by monthly averages. However, a daily peak may exceed a threshold of concern and still be within the regulatory limit.
A recent review concluded that neural tube defects and small-for-gestational-age births are moderately associated with contaminated drinking water (i.e., trihalomethanes) (Bove et al., 2001). Oral clefts, cardiac defects, and complete nasal obstruction (choanal atresia) were found in studies evaluating trichloroethylene-contaminated drinking water (Bove et al., 2001). Food may also contain environmental teratogens. A well-known example is the epidemic of cerebral palsy that followed maternal consumption of fish contaminated with organic mercury in Minimata Bay, Japan (Harada, 1978).
Characterization of exposures over time depends on developmental stage and the mechanism by which the agent produces its effect (EPA exposure guidelines, 2003). Multiple types of exposure may interact to produce their effect by the same mechanism, as for example the exposure to multiple insecticides that interfere with cholinesterases (National Research Council, 1993). Children have unique susceptibilities to chemical exposures (see Box 3-2).
Children’s Unique Susceptibility to Chemical Exposures. Children are more susceptible than adults to chemical exposures, and their exposure varies, depending on their physical location, breathing zones, oxygen consumption, types and amount of (more...)
Six outdoor air pollutants are regulated by the Clean Air Act: ozone, respirable particulate matter, lead, sulfur dioxide, carbon monoxide (CO), and nitrogen oxides. The effects of repeated or long-term exposure to outdoor air pollutants on the developing lungs of children are not well understood. Indoor air pollution, which is generally not regulated (one notable exception being laws prohibiting indoor smoking in public spaces), results primarily from (1) the products of combustion, such as CO, nitrogen dioxide, particulates, and sulfur dioxides; (2) volatile organic compounds, such as formaldehyde, benzene, and trichloroethylene; (3) the products of tobacco smoking (approximately 3,800 chemicals); and (4) molds.
Health effects from these diverse indoor air pollutants include respiratory irritation with cough and wheezing, exacerbation of asthma, allergic responses, cancer, and central nervous system effects (headache, nausea) (American Academy of Pediatrics, 2003). Exposure to asbestos, leading to lung cancer, is also a concern due to the prevalence of asbestos in schools and some homes (U.S. Environmental Protection Agency, 1987; American Academy of Pediatrics, 1987).
Some water pollutants are biological agents, some are chemical agents, and some are radionuclides (physical agents). Biological agents generally come from fecal contamination and include such bacteria as salmonella and E. coli, such viruses as hepatitis A and rotavirus, and such parasites as Cryptosporidium parvum. Chemicals in water include such metals as lead, mercury, and arsenic, such natural toxins as Pfiesteria toxins, organic chemicals including pesticides, PCBs, trichloroethylene, and chlorination by-products, such inorganic ions as nitrates, and such radionuclides as radon. Systems affected by these contaminants include the central nervous system, the gastrointestinal system, and the hematological system. Many of these chemicals are also carcinogens. Children have been found to be at higher relative risk of gastrointestinal illness from contaminated water (Wade et al., 2003). In addition, children are both more highly exposed and more susceptible to the contaminants found in water. For example, lead in drinking water was found to be the cause of lead poisoning in several infants whose blood lead exceeded 10 mcg/dl (Baum and Shannon, 1997; Shannon and Graef, 1992).
Food contaminants can be broadly categorized as either pathogenic or toxic. Pathogenic agents include bacteria, viruses or parasites, bacterial toxins, aquatic organisms that elaborate toxins, and toxins that accumulate in the food chain, such as domoic acid. Toxic chemicals in food can be divided into three categories: (1) pesticides that have been deliberately applied to the food source; (2) colors, flavors, or preservatives deliberately added to food during processing; and (3) chemicals that inadvertently enter the food chain, such as PCBs, heavy metals, and persistent pesticides such as DDT. Particular effects of food contaminants on children include such behavior changes as hyperactivity (Carter et al., 1993) and developmental neurotoxicity from pesticide exposure in food (National Research Council, 1993).
Children also are a demographic subgroup prone to infectious diseases because of their exploratory behavior, lack of prior exposure to most infectious agents, and association with other children. Substantial advances in vaccines have reduced rates of many infectious diseases during the past decades. Nonetheless, infectious agents remain a major threat to children’s health, particularly with the increase in antibiotic resistance among various infectious organisms and the emergence of new infectious agents (i.e., new strains of flu).
Children are highly exposed and susceptible to some infections that are spread by droplets from coughing and sneezing. Respiratory syncytial virus, the leading cause of serious upper and lower respiratory tract infection in infants and children, accounts for 125,000 hospitalizations and 450 deaths annually in the United States, and it may predispose children to asthma later in life. Annual epidemics occur from November to April, and virtually all infants are infected by age 2 (Black, 2003). Cytomegalovirus infection is spread in child care centers through both urine and saliva containing live virus; rates for preschool-age children in the United States range from approximately 5 to 30 percent (Centers for Disease Control and Prevention, 1985). Children are also particularly susceptible to other infectious agents, such as rotavirus and Norwalk virus, salmonella, and E. coli O157:H7, which cause diarrhea and dehydration and sometimes severe complications.
Children are also more highly exposed to vector-borne (e.g., via ticks, fleas) or certain zoonotic (e.g., hosted by dogs, cats, horses) pathogens due to their increased time outdoors, play activities, and behaviors. Vector-borne pathogens include Lyme disease, highest among 5–9-year-olds (Centers for Disease Control and Prevention, 2002a), and Rocky Mountain spotted fever, most prevalent under age 10 (Centers for Disease Control and Prevention, 2000b). Some arboviruses, which are transmitted by different species of mosquitoes, preferentially infect the young (e.g., La Crosse encephalitis carried by a woodland mosquito; Centers for Disease Control and Prevention, 1990a, 1998a). Cat scratch disease, carried by cats, has an estimated annual incidence of 22,000 cases, with the highest age-specific incidence in children less than age 10. Up to 25 percent of these cases result in severe systemic illness (Centers for Disease Control and Prevention, 2002a).
Few studies have estimated children’s exposure to noise or the effect of noise on children’s health, but there is suggestive evidence of its effect. Children appear to be routinely exposed to more noise than the recommended upper limit proposed by the U.S. Environmental Protection Agency in 1974 (De Joy, 1983; Roche et al., 1982). Noise-induced hearing loss in one or both ears among children ages 6 to 19 was found to be 12.5 percent (or 5.2 million children) (Niskar et al., 2001) and more frequent among high school students actively involved in farm work compared with peers not involved (Broste et al., 1989). In a sample of 1,218 children, 1 in 20 school-age children had minimal sensorineural hearing loss and 37 percent of the children with this hearing loss failed at least one grade (K–12) (Bess et al., 1998). Even mild hearing loss is associated with increased social and emotional dysfunction among school-age children.
Noise exposure in childhood is associated with a stress response (Tafalla and Evans, 1997—in male college students), headaches (Odegaard et al., 2003), sleep deprivation (Corser, 1996; Cureton-Lane and Fontaine, 1997), elevated blood pressure and heart rate (Matheson et al., 2003; Evans et al., 2001; Regecova and Kellerova, 1995), and poor performance including reading comprehension and long-term memory (Matheson et al., 2003; Stansfeld et al., 2000).
Exposure to ultraviolet B radiation from sunlight exposure and the use of tanning equipment during childhood can result in substantial morbidity and mortality later in life. Health risks from exposure vary with skin type and include sunburn, skin cancer (the most common malignant neoplasm in the U.S. adult population), phototoxicity and photoallergy, skin aging, and cataracts. Approximately 80 percent of lifetime sun exposure occurs before the age of 18. Episodic high exposures sufficient to cause sunburn, particularly during childhood and adolescence, increase the risk of melanoma (Saraiya et al., 2003).
Ionizing radiation comes from both natural and manmade sources. Natural sources include radon, cosmic radiation, and ingested radon and fallout. Manmade sources include medical X-rays and some consumer products. The consequences of exposure for children’s health include birth defects from prenatal exposures (microcephaly, mental retardation), neurological damage in younger children, and cancer (American Academy of Pediatrics, 1998).
Home, School, and Work Settings
The quality of their housing influences children’s health. Housing conditions can contribute to the incidence of asthma, injuries, and lead poisoning (Manuel, 1999). As children age, they spend more time in physical locations outside the home, such as child care, school, and workplace settings that expose them to new physical environments. Thus, parents’ choice of child care facility may affect both indoor and outdoor (e.g., playgrounds, backyards) exposures. For example, child care exposure to cigarette smoke may differ from exposure in children’s own homes (Wright et al., 1989).
School-age children spend 35 to 50 hours per week in and around school buildings. In some communities, schools have been built on relatively undesirable land, such as landfill sites like Love Canal. Schools are often located on old industrial sites or near highways, resulting in exposure to auto emissions and air pollution (Frumkin, 2003). Many school buildings are old and poorly maintained, leading to exposures to air pollutants, radon, asbestos, pesticides, and lead (Etzel and Balk, 1999). The U.S. General Accounting Office reported that 20 percent of primary and secondary schools had indoor air quality problems; more than half had environmental pollutant or building ventilation problems that could affect air quality (U.S. General Accounting Office, 1995). Radon above the EPA’s action level was found in 2.7 percent of schools surveyed during the 1990–1991 school year (U.S. Environmental Protection Agency, 1992). Asbestos, used extensively in schools until the 1970s, was still present in more than 8,500 schools in 1980, potentially exposing over 3 million students (U.S. Environmental Protection Agency, 1987).
Many adolescents have jobs that may expose them to occupational hazards (Pollack et al., 1990). Every year, at least 70 children die from work-related incidents (Centers for Disease Control and Prevention, 1996) and more than 65,000 are injured severely enough to seek care in emergency departments (Brooks et al., 1993). Under the Fair Labor Standards Act of 1938, which regulates work hours and safety, children younger than 18 are prohibited from working with hazardous chemicals in nonagricultural jobs. Prohibitions on chemical work in agriculture extend only to age 16, and work by children and adolescents on their own family farms is unregulated at the national level. During 1992–1995, 155 deaths were reported among agricultural workers age 19 and younger; 64 (41 percent) of these youths were working in their family’s business (Derstine, 1996). For each death, many more experience nonfatal injury (Rivara and Barber, 1985), usually from farm machinery or exposure to toxins.
Child Injury and the Provision of Safe Environments
Injuries are the leading cause of death among children between ages 1 and 19, accounting for more deaths than homicide, suicide, congenital anomalies, cancer, heart disease, respiratory illness, and HIV combined (Centers for Disease Control, 10 leading causes of death, 1997). Although the total number of unintentional injury deaths has declined by more than 40 percent during the past 20 years (CDC Injury Mortality Stats), the rates of childhood injury are much higher in the United States when compared with other developed countries. In 2001, unintentional injuries consttuted 70 percent of all injury deaths to children and adolescents (0 to 20 years) in the United States (National Center for Health Statistics, 2004).
The enormous impact of injury on children’s health is manifest by the fact that approximately 18 hospitalizations and 233 emergency department visits occur for every injury death (Grossman, 2000). As injury deaths continue to decline, nonfatal injuries continue to be important causes of child morbidity and disability and substantially reduce quality of life, especially among adolescents. However, it should be noted that data collection on nonfatal injuries is incomplete.
The elements of a safe and healthy physical environment differ according to a child’s developmental stage. The American Academy of Pediatrics has conducted extensive reviews of the literature to establish the evidence-based recommendations in The Injury Prevention Program, an age-appropriate prevention education program (www.aap.org/family.tipmain.org/) for physicians and families. Recommendations include counseling parents on use of infant car seats, never leaving infants and toddlers alone in pools or bathtubs, the use of safety equipment for in-line skating and skateboarding, and firearm safety.
STEP 2: DEVELOP ANNUAL REPORTS AND STANDARDIZED MEASURES BASED ON EXISTING DATA SETS
The goal-setting effort of Step 1 would highlight areas in which measurement of the quality of child and adolescent health and health care services is strong, as well as areas in which valid and reliable measures do not yet exist, areas that are difficult to measure, and populations that are difficult to reach. Step 2 focuses attention on the need to develop annual reports and standardized measures in the seven priority areas based on existing data sets, building on the multiple efforts of professional, public, and private-sector organizations.
While a large number of measures exist, efforts to monitor and improve the health and health care quality of children and adolescents are hampered by the absence of routine annual reports that focus on child and adolescent health and health care quality, as well as variations in both the measures themselves and the underlying data sources that support them. In the latter area, the committee has identified two issues of particular concern: (1) the absence of consistent measurement of disparities in health and health care quality to support the development of targeted interventions at the national and state levels, and (2) the retention of unnecessary or obsolete measures resulting from the adoption of standardized core measure sets over time, which can be addressed through a periodic review process.
Existing Opportunities to Include Children and Adolescents in Annual HHS Reports
The Secretary of HHS is already required to produce annual reports on health care quality and disparities (HHS, 2010a, 2010b), as well as annual reports on national prevention initiatives (HHS, 2011b; NPC, 2010). These reports provide valuable opportunities to include specific attention to children and adolescents and to draw attention to the ways in which their needs may different from those of older populations.
Standardized Measurement of Disparities in Health and Health Care
The changing demography of America’s youth increases the importance of recognizing and addressing pervasive disparities and inequities in child and adolescent health and health care. As with the measurement of health and health care quality, the measurement of disparities involves multiple dimensions and criteria. Though many studies measure disparities in terms of racial or ethnic differences, disparities also involve issues of gender, household income, educational status of the child or parent, insurance type, and medical practice setting (see Chapter 2).