Journal Issue: Children with Disabilities Volume 22 Number 1 Spring 2012
Risk Factors for Disabilities in Children
Many harmful exposures, from toxic exposures to marketing practices to social inequities, have been recognized as contributing to the rise in child disability.
Poverty is one of the most significant risk factors for disabilities and is especially troubling because one-fifth of all children in the United States were living in poverty in 2010.26 Linking disability with poverty is hardly new, but the relationship is just as powerful with chronic conditions as with infectious disease.27 Poverty affects health on several levels: directly, through the psychological stress and social stigmatization that accompany living in poverty, and indirectly, through increased exposure to a wide range of environmental stressors such as pollution, crime, and lack of access to healthful food.28 People living in poor neighborhoods, especially racial or ethnic minorities, also face disproportionately high exposures to toxic and hazardous wastes, air pollution, contaminated water, and unsafe housing.29
Even without the deprivations of poverty, people may still suffer from being on the lower rungs of the social ladder. Michael Marmot described the phenomenon of a "social gradient," a direct, linear relationship between health and position in the social hierarchy, while examining members of the British civil service.30 These effects have been found elsewhere, including among children; moreover, the gradient appears to grow sharper (that is, the health of rich and poor diverges further) as children age, and "the adverse health effects of lower income accumulate over children's lives."31
In addition to the harmful effects of poverty, it has been argued that the overall level of inequality in a society also affects health. Richard Wilkinson and Kate Pickett have shown that countries with greater social inequities experience poorer health than more egalitarian countries on almost all available measures, including life expectancy, infant mortality and child health, obesity, and mental health; the United States, with its wide gaps between rich and poor, fares worse than most other developed countries, a difference that persists even when only wealthy individuals are considered.32 In other words, poor Americans fare much worse than wealthy Americans, but even wealthy Americans fare worse than wealthy (and even middle-class) residents of many other countries.33
Eliminating poverty would likely dramatically improve the overall health of the nation's population, but the changes in the structure of society required to significantly reduce poverty appear to be beyond the typical range of public policies. Indeed, efforts in the United States to address poverty on a national scale have stalled or lost ground in recent decades. Another approach to mitigating the negative health effects of poverty would ask how being poor leads to worse health (toxic exposures, psychological stress, lack of medical care) and then develop interventions that address those specific risks.
Airborne and Other Environmental Pollutants
Just as the deplorable conditions of Victorian-era slums led to insights into the causes and control of infectious disease, environmental disasters and epidemics over the past century have linked exposures to industrial pollutants and environmental chemicals with overt toxicity. In Queensland, Australia, an epidemic of childhood lead poisoning in the early 1900s was traced to lead in house paint, establishing the link that still haunts residents of older housing in many countries around the world.34 In December 1952, a dense fog of sulfurous particles from burning coal enveloped London for five days, leading to an estimated 12,000 deaths, mostly from respiratory or cardiovascular disease; children and older adults were especially vulnerable to the sulfur-laden coal smoke.35 This disaster—and a similar one in Donora, Pennsylvania, in 1957—began to focus people's attention on the harmful effects of air pollution, ultimately spurring the development of environmental regulations regarding levels of particulate matter. In the 1950s and 1960s, cases of severe congenital defects in the Japanese town of Minamata Bay were traced to mercury emissions from a local plastics factory.36
Scientists also have taken advantage of other "natural experiments" to test associations between health and air pollution. In the late 1980s, for example, C. Arden Pope and his colleagues showed that the closing of a Utah steel mill led to lower levels of airborne particles and lower mortality and hospitalizations.37 In 1996 the summer Olympic Games in Atlanta reduced traffic there, which led to lower air pollution and fewer hospitalizations.38 More recently, the introduction of E-ZPass, an electronic highway toll collection method, reduced traffic congestion and lowered the incidence of preterm birth and low birth weight by an estimated 6 to 9 percent among babies living within two kilometers of toll plazas along three major roadways in New Jersey and Pennsylvania.39
Airborne pollutants are known to contribute to other debilitating illnesses in both children and adults, including asthma. The most common childhood chronic condition in the United States, asthma affected an estimated 9.7 percent of American children in 2009.40 The disease, which is characterized by airway inflammation, difficulty breathing, and reduced respiratory function, takes a heavy physical and psychological toll on those affected. Its prevalence has risen steadily in most Western countries since the 1980s, although it seems to have leveled off in the past decade.41 The reasons for this pattern are not entirely clear, but airborne particles smaller than 2.5 microns (also called PM 2.5 or fine particles) have been associated with impaired lung function and asthma exacerbations.42 Exposure to prenatal smoking and secondhand smoke is also associated with impaired lung development, reduced lung function, and asthma, and other studies have linked airborne pollutants to preterm birth and lower birth weight as well as to chronic cough and bronchitis.43
These harmful effects of air pollution on respiratory function are well established. More recent studies are now finding links between exposure to air pollutants and reduced cognitive development. Black carbon (an airborne product of combustion from fossil fuels and other sources) has been associated with lower verbal and nonverbal intelligence and poorer memory performance in a Boston-based birth cohort of children aged eight to eleven.44 Frederica Perera and others, using polycyclic aromatic hydrocarbons (PAHs) as a biomarker, found that children with higher exposures to combustion products had diminished cognitive abilities.45 These links between airborne toxins and cognitive performance are less established, but they fit a larger pattern of toxic exposures interfering with brain development in young children.
The use of exposure biomarkers, which measure the amount or internal dose of a pollutant in the body, has allowed scientists to directly quantify the effects of exposures encountered by the general population.46 The increasing use of biomarkers is showing that industrial pollutants and environmental chemicals are not only harmful at the higher levels of exposure but at lower concentrations as well. For example, lead has long been associated with poorer intellectual development in children, but more recently exceedingly low blood lead levels (fewer than five micrograms a deciliter) have been linked with lower IQ scores. Even more troubling, the observed decrements in intellectual abilities are proportionately greater at the lowest blood lead levels, indicating that there is no "safe" level of exposure.47 Similarly, pregnant women are at risk of giving birth prematurely not only if they are smokers but if they are exposed to secondhand tobacco smoke.48 Scientists looking for "safe" levels of fine particles in air pollution found a steady relationship with adult mortality down to the lowest detectable levels.49 Thus, for some of the most established pollutants, increasing evidence of toxicity is appearing even at the lowest levels of exposure. Moreover, while it was once thought that only workers and urban dwellers were exposed to these industrial pollutants, it is now realized that these contaminants are ubiquitous: virtually no one is unexposed.50
The Rise of Autism: More Questions than Answers
The incidence of autism, one of the most disabling conditions of childhood, has increased dramatically in recent years, although it remains rare in comparison to conditions such as ADHD. An exhaustive study of California's birth and medical-service records reported an increase in the rate of autism diagnosis before the age of five from 6.2 per 10,000 births in 1990 to 42.5 in 2001. While some of this rise was explained by changes in diagnostic practices and an increased awareness of autism, these factors alone did not account for the dramatic increase in autism.51
Very little is known about risk factors for autism or autistic behaviors. While autism is believed to have a genetic component, such a rapid increase in prevalence points to an increase in one or more environmental risk factors. The little evidence available suggests the risk increases for mothers who live near a freeway during the third trimester of pregnancy and decreases for mothers who take prenatal vitamins in the period around conception.52 Other suspected causes of autism, such as mercury in childhood vaccines, have not been supported by the evidence.53 Autism may be a "test case" for the ubiquity and variety of man-made chemicals, many of which have never been tested for their health effects in humans, especially children.54 While any links between environmental chemicals and autism are speculative, it would not be surprising if a chemical (or combination of chemicals acting synergistically) were contributing to this heightened autism prevalence. It is worth asking whether a revision of the regulatory framework for environmental chemicals might begin to control the autism epidemic, even before the responsible toxicant(s) is identified.
Linking Environmental Toxicants to Psychopathology
Researchers are increasingly finding links between exposures to environmental toxicants and neurobehavioral disorders, one of the most rapidly rising categories of disabilities in children; one such disorder is ADHD, which affects almost one in ten children.55 Using a nationally representative sample, for example, Tanya Froehlich and her colleagues estimated that children with blood lead concentrations in the highest tertile—above 1.3 micrograms per deciliter (?g/dl)—were two and a half times as likely as children with the lowest blood lead concentrations (less than 0.8 ?g/dl) to meet criteria for ADHD.56 This finding is particularly disturbing because blood lead levels above 1.3 micrograms per deciliter are far below the current "level of concern" of 10 ?g/dl.
Similarly, children who were prenatally exposed to tobacco were nearly two and a half times more likely to meet criteria for ADHD than children whose mother did not smoke during pregnancy. Furthermore, lead and tobacco exposures interacted synergistically; children in the highest lead category who were also prenatally exposed to tobacco smoke were eight times as likely to meet diagnostic criteria for ADHD as children with neither exposure. Several other lines of evidence link lead exposure with neurobehavioral disorders. Neuroimaging studies, for example, have associated lead exposure with reduction in gray matter volume in the prefrontal cortex, a key area of the brain necessary for executive functions, impulse control, and decision making.57 Another study cites declining blood lead levels as the primary reason for the decline in homicides and other criminal behaviors over the past thirty years.58
Although the evidence is less definitive, other chemicals, such as organophosphate pesticides, mercury, and polychlorinated biphenyls (PCBs), have also been linked to the development of ADHD.59 While the use of biomarkers has allowed scientists to connect environmental exposures to disabilities in children, the long latency between exposure and disability makes it difficult to establish these links with certainty. Still, these studies raise serious questions about the need to revise the existing regulatory framework—which essentially allows children to be exposed to suspected toxicants or chemicals until there is definitive proof of their toxicity.
The Emergence of Endocrine Disruptors
One emerging area of concern is a class of chemicals known as "endocrine disruptors" because of their ability to mimic natural hormones.60 Evidence from several recent studies has linked prenatal exposure to phthalates and bisphenol A (BPA)—ubiquitous, estrogenic-mimicking chemicals found in plastics—with endocrine-sensitive outcomes such as decreased anogenital distance (a condition linked to infertility), decreased "masculine" play in boys, and externalizing behavioral problems in girls; this link suggests that endocrine disruptors can alter neurological development.61 While most evidence on the effects of endocrine disruptors concerns sex hormones or the thyroid, some endocrine disruptors (known as "obesogens") may mimic other hormones, including those involved in the development of obesity. The role of obesogens in the obesity epidemic is still speculative, but a chemical called tributyltin has been identified as a possible obesogen in some animal studies.62 In addition, one national cross-sectional study found associations between body mass index—a measure of obesity—and phthalates in adolescent girls.63
The Rise of Obesity and Diabetes
Americans have become steadily heavier over the past thirty years. In a nationally representative sample taken in 2007–08, almost 17 percent of children and adolescents aged two to nineteen were classified as obese, up from 5 percent in 1971–74 and 10 percent in 1988–94.64 Obese children are more likely to become obese adults, who are at heightened risk for type II diabetes, cardiovascular disease, and some cancers.65 Diabetes is also on the rise in young people, where it can have especially serious health consequences (compared with a later onset).66 Being obese can also have profound psychosocial effects on children; one study found that obese children fared as badly or worse on several measures of psychological functioning and stress as children who had cancer.67
For conditions such as obesity and diabetes, the dialogue surrounding prevention typically focuses on individual "lifestyle choices."68 It is easy to blame a person for eating too much, getting too little exercise, or smoking cigarettes. But lifestyle choices depend to a large extent on social context, a point that is too often unacknowledged. For children, whose preferences are still developing and who are open to a wide range of influences, it is easy to see how their "choices" may be manipulated by outside factors.
Marketing and advertising are staples of modern life, affecting how each of us views and interacts with the world. This is especially true for children. Children see an average of fifteen television commercials for food every day (in addition to ads on billboards, online, and elsewhere), the vast majority of which feature foods high in sugar, fat, or sodium.69 Food and beverage companies spend upward of $10 billion annually marketing to children, and several experimental and cross-sectional studies support the thesis that advertising alters children's taste preferences as well as the amount they eat.70 In one study, children given identical food in either a plain bag or a McDonald's bag rated the food in the branded bag as better tasting; the effect was stronger in children who had more TV sets in their home and who ate at McDonald's more often.71 In another study, children who watched cartoons interspersed with food ads ate more than children who watched cartoons with other kinds of commercials.72 The increase in consumption was greater for overweight children than for those of normal weight, and greater still in obese children, suggesting that some individuals may be more susceptible than others to these influences.73
Skeptics may dismiss the notion of advertising as "mind control," but repeated exposure at a very young age can have a profound effect on a child's later actions, even into adulthood. Children are thought to be capable of some "defense" against persuasion by marketing by age eight, at which point most children are able to recognize advertisements and evaluate their claims accordingly. But there is little evidence that children above age eight are any more resistant to the effects of advertising than younger children.74 Ads do not simply make factual claims about their product; they are designed to create emotional associations, often at an unconscious level, and to bypass the "rational" parts of the brain.75 Nor is the effect of advertising limited to food and obesity. Repeated studies have linked tobacco marketing to teenagers' decision to start smoking, and several cross-sectional and longitudinal studies have linked exposure to alcohol marketing to adolescents' being more likely to start drinking and to drink more frequently.76
The built environment, the physical design of the areas around children's homes, can play a powerful role in determining children's "lifestyle choices." Many children live in neighborhoods with few (if any) sidewalks, bike lanes, parks, and green spaces that encourage exercise. Urban (or suburban) sprawl has created dependence on cars by placing destinations farther apart, while parents' concerns about crime may further reduce the amount of time children spend outside. Conversely, neighborhoods designed to be "walkable" encourage exercise and physical activity.
At the same time, over the past several decades schools faced with budget cuts have been dropping physical education programs to save money, while installing soda machines to raise badly needed sponsorship funds.77 Recently, many schools have improved children's nutrition by regulating the offerings in vending machines and providing more nutritional items in school cafeterias, but such actions have largely taken place on a school-by-school or district-by-district basis.78 Several lines of evidence link features of the built environment with obesity or overweight in children and adults.79 There is less agreement about the most effective interventions, largely because changing the physical structures of neighborhoods and cities is difficult and costly. But the evidence does suggest that tackling the obesity epidemic will require attention to the built environment as well as to individual behavioral change.
Consumption of healthful or unhealthful foods is typically discussed in terms of lifestyle choices. However, eating a healthful diet is highly dependent on having markets nearby that sell affordable fresh fruits and vegetables, and such places may be scarce or nonexistent in poor neighborhoods, while cheap, highly processed fast food is plentiful—even if, as some have argued, home-cooked food is actually less expensive (in terms of raw ingredients) than the fast-food equivalent.80