REPORTED HIGH PREVALENCE OF DEVELOPMENTAL DISABILITY
Twelve million American children (17%) are reported to suffer from one or more developmental disabilities. *1,2 Trends of these disorders over time are rising, although changes in reporting and diagnostic criteria are likely to explain some of the increase. For example, the numbers of children with learning disabilities, estimated to affect 5% to 10% of the public school population, 3,4 increased 191% between 1977 and 1994. The prevalence of attention deficit hyperactivity disorder (ADHD), previously estimated at 3% to 5% of school-aged children, has recently been reported to be as high as 12%. 5 Similarly, the prevalence of autism, previously reported as 0.5 to 1.0 case per thousand, is more recently reported as 2.0 cases per thousand. 6
The extent to which the unexpectedly high rates are attributable to improved recognition, reporting, altered diagnostic criteria, or true increases cannot be determined with available data. However, whether new or simply newly recognized, developmental disabilities are clearly an enormous burden to individuals, families, and society.
MULTIPLE ETIOLOGIES OF DEVELOPMENTAL DISABILITY INCLUDE PREVENTABLE TOXICOLOGIC CAUSES
An emerging body of evidence indicates that developmental disabilities result from complex interactions of genetic, toxicologic (chemical), and social factors. Among these various causes, toxicologic exposures deserve special scrutiny because they are readily preventable. There has been a recent explosion of research in developmental neurotoxicology, the science investigating the effects of early chemical exposures on the developing brain. This rather technical research, however, has been relatively inaccessible to the larger child development community and largely unknown to the wider public. In this brief article, we provide an introduction to some highlights of the developmental neurotoxicology literature. This growing body of research reveals substantial evidence that commonly encountered household and environmental chemicals contribute to the current burden of developmental disabilities. Such exposures are of particular concern for genetically susceptible individuals exposed during periods of developmental vulnerability. Promoting greater interdisciplinary understanding of this material is a matter of some urgency because most toxicologic exposures and the risks they confer are inherently preventable. The precise magnitude of the toxicologic component of disability has yet to be determined. Nonetheless, this substantial body of research—including laboratory animal, in vitro, and epidemiologic studies—underscores the need to eliminate developmental exposures to known and suspected developmental neurotoxicants wherever possible.
THEORETICAL FRAMEWORK FOR UNDERSTANDING TOXICOLOGIC INFLUENCES ON CHILD DEVELOPMENT
As one of several important early influences, toxicologic exposures interact with genetic and social factors to shape child development. Although developmental research typically focuses on only one of these domains at a time, it is increasingly recognized that complex interactions among these influences are most important. For example, several genes have been identified that influence susceptibility to environmental chemicals, including genes that affect lead absorption and metabolism (vitamin D receptor and delta aminolevulinic acid dehydratase genes 7) and genes that affect the metabolism of and vulnerability to organophosphate pesticides (genes coding for paroxonase and acetylcholinesterase 8–10). In effect, these genes modulate susceptibility to chemical exposures. New research designs, capable of addressing such interactions between genes and the environment (including both the chemical and social environment), are important for better understanding the causes of developmental disabilities.
LINKS BETWEEN CHEMICALS AND BRAIN DEVELOPMENT: WELL ESTABLISHED FOR A FEW COMMON CHEMICALS, UNSTUDIED IN MOST
Brain development begins early in fetal life and continues into adolescence. First, the general shape of the brain emerges. Throughout pregnancy, fetal brain cells proliferate, migrate to their appropriate locations, and differentiate into specialized cell types. Neurons form synapses, creating complex circuitry. Subsequently, neural circuits are refined and consolidated through programmed cell death (apoptosis), a process that continues into childhood and adolescence. This sequence of events is genetically programmed but mediated by a variety of neurotrophic biochemical compounds, including neurotransmitters. Interference with any stage of this process may alter subsequent stages and result in permanent impairments.
The developing brain is, therefore, uniquely susceptible to exposure to neurotoxic compounds. Extensive studies of a few well-known neurodevelopmental toxicants, including lead, mercury, alcohol, and nicotine, reveal multiple mechanisms by which these compounds disrupt normal brain development. These include alterations in levels of neurotransmitters or other neurotrophic compounds and impairment of cell division, migration, differentiation, synapse formation, and apoptosis.
For the purpose of this review, we focus on common household and environmental chemicals that impair development at levels of exposure experienced by significant portions of the general population. Our discussion is confined to a few examples of chemicals that have been extensively examined and found to be public health threats to neurodevelopment. In addition to these examples, however, a wealth of human and laboratory animal data documents the unique neurodevelopmental toxicity of alcohol, nicotine, and some drugs of abuse. These substances have been associated with a variety of neurodevelopmental problems including hyperactivity, attention deficits, learning disabilities, and IQ deficits. 11 More limited data raise concerns about the neurodevelopmental toxicity of additional commonly encountered chemicals, including some pesticides, metals, solvents, and others. With few exceptions, these chemicals of concern have not been adequately examined.
A historical perspective illustrates a fundamental theme in developmental neurotoxicology: The understanding of a given chemical advances slowly, and as it does, demonstrated toxicity tends to emerge at progressively lower levels of exposure. Although this review focuses on chemicals with a rich epidemiologic database, for most chemicals there are little or no human or laboratory neurodevelopmental toxicity data available. This is a matter of some concern because the fetus and child are already being exposed to untold numbers, quantities, and combinations of substances whose safety has not been established.
LEAD
Declining Threshold of Harm: From Encephalopathy to IQ Impairment
Lead is one of the first and perhaps best understood examples of a common chemical that harms brain development. This understanding has continued to advance over the period of a full century, during which time the recognized “toxic threshold” (the lowest exposure thought to be harmful) has relentlessly declined. Whereas very high lead exposures were recognized to cause encephalopathy, coma, and death in children as early as 1900, 12,13 residual effects in survivors of childhood lead poisoning went unrecognized for decades. The enduring effects of lead poisoning on child development became apparent only with the publication of longer follow-up observations in the 1940s, which noted persistent impairments in intellect, behavior, and sensory-motor function. 14 Subsequent studies began to suggest that lower levels of lead exposure might be associated with neurological damage as well. 15
A specific toxic threshold for lead was established for the first time in the 1960s. At that time a toxic blood lead level was set at 60 μg/dl, only modestly below the level at which encephalopathy occurs (80 μg/dl). 16 With improvements in study design over the next 30 years, research revealed effects of lead on IQ at progressively lower levels of exposure. 17 After repeated downward revisions, the toxic threshold for lead was most recently set at 10 μg/dl, the 1990 standard that still holds today. Subsequent meta-analyses have quantified the risk of low-level lead exposure estimating that an increase in blood lead from 10 to 20 μg/dl is associated with an average IQ loss of 2 to 3 points. 18,19
Significance of Small Effects: The Population Perspective
Although an IQ loss of a few points may have minimal significance for the average individual, it has profound implications when applied over large populations, 20 in effect, shifting the population distribution curve for IQ. When the population distribution curve for IQ, or any other neurobehavioral endpoint, is shifted by even a small amount there are dramatic effects at the high and low ends of the distribution, often referred to as the “tails.” As shown in a hypothetical example in Figure 1, a downward shift of a mere 5 points in the mean IQ results in a greater than 50% increase in the numbers of functionally mentally retarded individuals and a comparable decrease in the numbers of gifted individuals in the population. This small shift in average IQ therefore has enormous implications for society, translating, for example, into increased needs for special education and services, as well as a significantly diminished intellectual capacity within the population as a whole.
;)
Figure 1: Population effects of a small shift in average IQ. The upper chart shows the distribution of IQ scores in a hypothetical population where the average IQ is 100 and the standard deviation is 15. The gray area under the left “tail” of the curve represents the 2.3% of the population with an IQ <70, the score used to define mental retardation. In a population of 260 million, approximately 6 million people would fall below this line. The lower chart depicts an IQ distribution that results from lowering the average IQ by 5 points from 100 to 95. Now, 3.2% of the population, or 9.4 million people, have an IQ below 70. This represents more than a 50% increase in the numbers of mentally retarded. The numbers of gifted, defined as those with IQs greater than 130, have declined by more than 50% from 6 million to 2.4 million. Thus, a small shift in average IQ results in a greatly increased need for special education and services, as well as diminished intellectual capacity within the population as a whole.
96Emerging Links with Attention Deficits and Aggressive Behavior
Recent epidemiologic studies indicate that lead exposure is harmful even below the current 10 μg/dl standard. 21–25 Several studies suggest that there is no threshold below which lead exposure is without adverse effects, 26,27 and, importantly, that for a given increment in blood lead, the associated impact on IQ is greater below a blood level of 10 μg/dl than above. 28 Recent studies also suggest that, in addition to undermining IQ, low-level lead exposure is associated with impaired attention, hyperactivity, and antisocial and aggressive behavior. 27,29,30–33 Some of these effects have been observed at very low levels of exposure and may occur in the absence of detectable IQ effects. 30,34–36 The fact that adverse effects from lead exposure are apparently well below the toxic threshold of 10 μg/dl is no surprise considering that this currently recognized limit of “safe” exposure is nearly 13% of the blood lead concentration associated with encephalopathy and 8% of the lethal blood lead level. Indeed, it would be surprising if some neurological harm were not occurring a mere one order of magnitude below the lethal exposure level.
Widespread Exposures at Levels of Concern
The growing profile of developmental impacts from low-level lead exposure is of substantial concern considering that 4% of all American children 37 and as many as 36% of inner-city black children 38 exceed even the current increasingly obsolete toxic threshold of 10 μg/dl. The emerging nonlinear dose-response profile, which indicates greatest proportional impact occurs at blood levels currently considered normal, is also of concern because this suggests subtle lead-induced impairments are occurring throughout the general population. This is not unexpected because what is called a “normal” lead level today is actually two to three orders of magnitude higher than preindustrial background levels. For a substance such as lead, which appears to have toxic effects at any level of exposure, it is not surprising that adverse effects are apparent even within this “normal” range of exposure.
MERCURY/METHYLMERCURY
Declining Threshold of Harm: From Catastrophic Retardation to Subtle Learning Impairments
Like lead, mercury is a heavy metal that disrupts brain development. One of the common forms of mercury, methylmercury, is a low-level contaminant in many species of fish. Although direct exposure data are not widely available, indirect assessments (using dietary surveys and fish-mercury contamination data) suggest that environmental mercury, like lead, puts substantial numbers of children at risk. At high levels of developmental exposure, methylmercury causes severe disability such as mental retardation and cerebral palsy, whereas the more commonly encountered low levels of exposure can contribute to attention, memory, and language impairments. Unlike lead, however, the study of mercury effects on children is relatively young, having begun only approximately 50 years ago, and scientific consensus on low-dose toxicity has been achieved only in the last few years. 39,40
Mercury is usually released into the environment as a metal or an inorganic compound. Major human sources are coal-fired power plants and municipal and medical waste incinerators. Mercury released into the atmosphere often travels long distances before being deposited onto the earth’s surface. Bacteria present in sediments and water bodies convert mercury to methylmercury, which then bioaccumulates as it passes up the aquatic food chain. As a result of the growing burden of environmental mercury, fish consumed by pregnant women or women of reproductive age may pose a threat to the uniquely vulnerable fetal brain.
The effects of methylmercury on the developing brain were first recognized in the tragic poisoning epidemic in Minimata Bay, Japan, during the 1950s. In this episode, residents regularly consumed fish highly contaminated with methylmercury resulting from industrial discharges into the bay. Infants born to mothers who consumed the fish had a variety of neurological findings, including mental retardation, disturbances of gait, speech, sucking, swallowing, and reflexes, 41 whereas their mothers often showed no signs of mercury poisoning. Because methylmercury was not identified as the cause until very late in the course of the epidemic, mercury exposures were never quantified, and a toxic threshold for the effects seen at Minimata was never established.
The quantitative study of methylmercury neurotoxicity began with a second major poisoning epidemic in Iraq in 1972. In this tragic incident, infants were born with severe disabilities, including mental retardation, cerebral palsy, seizures, blindness, and deafness, after their mothers consumed bread contaminated with a methylmercury fungicide. As in Minimata, many mothers of affected infants suffered minimal if any symptoms themselves.
An apparent toxic threshold, implied in the first case reports of severely retarded infants, soon became obsolete. Within a few years it was evident that many children exposed prenatally to lower levels of mercury suffered delays in walking and talking despite apparently “normal” development in infancy. Subsequently, a variety of studies has established progressively lower thresholds for methylmercury effects by using increasingly sensitive methods of exposure and outcome assessment and improved statistical methods 42–44 (Fig. 2).
Figure 2: Mercury’s declining threshold of harm. The proven threshold of harm (░⃞) tends to decrease as knowledge is accumulated. This figure shows the trend for one neurotoxicant: mercury. Scientific understanding of mercury’s developmental neurotoxicity began with studies of the 1972 epidemic of mercury poisoning in Iraq. At that time, case reports of infants severely retarded at birth identified an apparent toxic threshold for mercury exposure of greater than 34 μg/kg/day.
97,98 (This appeared to be a “no observed effect level,” or NOEL, for severe retardation at birth.) Within a few years, however, it became apparent that many children exposed prenatally to lower levels of mercury were delayed in learning to walk and talk, despite apparently “normal” development in infancy.
99 Subsequently, a variety of studies on diverse populations have established progressively lower thresholds for mercury effects by using increasingly sensitive measures of neurological function and better statistical methods.
100–109 A recent large study has identified deficits in language, memory, and attention that occur at prenatal mercury exposures under 0.85 μg/kg/day. This level is less than 3% of the toxic threshold identified in the initial observations from the Iraqi epidemic. The presence of a “discernible insidious effect” on language, memory, and attention was noted, however, below even this low level
107 of 0.85 μg/kg/day, suggesting that the recognized threshold for neurological toxicity will continue declining as research methods improve. The black squares on the graph represent prenatal mercury exposures associated with adverse neurodevelopmental outcomes. The gray triangles (
) represent the World Health Organization (WHO), Environmental Protection Agency (EPA), and Agency for Toxic Substances and Disease Registry (ATSDR) recommended limits for human mercury exposure. The standard issued by the Food and Drug Administration (FDA), it should be noted, regulates the level of mercury in fish, rather than in people. As a result, a wide variety of exposures may occur within the FDA regulatory limit depending on how much and how often one eats fish and the mercury level of the fish consumed. The indicated exposure is that of a 60-kg woman eating at the high end of fish consumption (100 g/d, the 95–97th percentile) and eating fish that are contaminated at the FDA permitted limit. In this worst-case scenario, the woman is exposed to 1.65 μg/kg/d, or ∼16.5 times EPA’s recommended safe limit. Note: (1) Studies of the neurodevelopmental effects of mercury generally use hair or blood levels as markers of exposure, because these are more accurate indicators of exposure than dietary surveys. Health-based guidelines, however, are expressed as recommended limits of dietary exposure. For the purpose of comparing data between studies and for comparing effects levels with regulatory guidelines, exposures as indicated by hair and blood levels of mercury have been converted to approximate equivalent dietary exposures. The quantitative relationships between food intake, hair, and blood levels of mercury are described in the ATSDR Toxicologic Profile for Mercury.
110 (2) Study results that identified a range of exposures within which an effect was observed have been shown at the midpoint of that range. Because of differences in study methodology, the results are not strictly comparable between studies and shown here mainly to indicate general trends over time.
Most recently, a very large study in the Faroe Islands has identified deficits in language, memory, and attention 45 that occur at low levels of prenatal methylmercury exposure. These effects are associated with exposures that are less than 3% of the toxic threshold suggested by the earliest Iraqi observations. 46 However, even below the harmful exposure identified in the Faroe research, (0.85 μg/kg/d), a “discernible insidious effect” on language, memory, and attention was noted, 45 suggesting that the recognized threshold for neurological toxicity will continue declining as research methods continue to improve.
Widespread Exposures at Levels of Concern
Based on extrapolations from the Iraqi study, the EPA currently defines a safe upper limit for dietary mercury exposure at 0.1 μg/kg of body weight per day, a reference dose recently confirmed by the National Academy of Sciences. Exposures above this level pose increasing risks to fetal brain development. A woman of reproductive age exceeds this safe consumption limit by eating more than 1.5 ounces of swordfish or 7 ounces of tuna per week (based on average mercury concentrations of 1.0 and 0.2 μg mercury per gram of fish, respectively). A 20-kg child exceeds the safe consumption limit by eating a mere half-ounce of swordfish per week or 2.5 ounces of tuna per week. 47,48
Methylmercury exposure assessments suggest that 7% of U.S. women of reproductive age, as well as 20% of 3- to 6-year-old children, exceed the safe exposure limit. 49,50 An exposure assessment in New Jersey indicates that more than 20% of women of reproductive age exceed the limit, suggesting coastal populations may be at higher risk than suggested by the national average. 51 Exposure assessments specifically addressing risks to fish eaters suggest that on any given day, 50% of women of reproductive age who consume fish exceed the safe mercury exposure limit. 52 Based on a comprehensive review of relevant research, the National Academy of Sciences recently estimated that over 60,000 U.S. children are born each year at risk for learning and other disabilities due to prenatal methylmercury exposure.
POLYCHLORINATED BIPHENYLS
Background
Polychlorinated biphenyls (PCBs) are a large group of fat-soluble chemicals previously produced for industrial use as lubricants and insulators in electrical equipment. Although their production has been banned in most of the industrialized world for decades, their environmental persistence and bioaccumulation within the food chain have resulted in ubiquitous human exposures, particularly from the consumption of beef, dairy products, and fish that are relatively high in fat. 53
Declining Threshold of Harm: From Retardation to Pervasive Subtle Developmental Impairments
Like mercury and lead, the effects of PCBs on child development were not recognized until catastrophic epidemics drew attention to high-dose effects. These epidemics occurred in Japan and Taiwan in the early 1970s when thousands of people ingested rice oil accidentally contaminated with PCBs, as well as small amounts of other contaminants. As with other neurotoxicants, the developing fetus proved much more sensitive than the mother. Newborns who had been exposed had a variety of developmental effects, including reduced birth weight, hyperpigmentation, early tooth eruption, deformed nails, and gum hypertrophy. 54,55 In childhood, they also exhibited IQ impairment bordering on mental retardation, poor health, and increased behavior problems. 56–58
In contrast with the earliest studies of high-dose PCB poisonings, subsequent research focused on populations with background, or near-background exposures, including large prospective cohorts in Michigan, North Carolina, The Netherlands, and Germany. As exposure assessment has improved over the past several decades, persistent and pervasive adverse effects of prenatal exposure have emerged at these exposure levels commonly experienced by the general population (Fig. 3). In the newborn, the effects of prenatal PCB exposure include decreased birth weight, head circumference, and gestational age, as well as motor immaturity, poor lability, increased startle and decreased reflexes on the Brazelton Neonatal Behavioral Assessment Scale (BNBAS). 59,60 In early childhood, prenatal PCB exposure is associated with a variety of cognitive impairments (reduced memory and attention, decreased verbal ability, impaired information processing) and developmental delays (reduced psychomotor development), as well as adverse behavioral and emotional effects (decreased sustained activity, decreased high-level play, increased withdrawn and depressed behavior, increased activity level). 61–67 In preteen years, prenatal PCB exposure is associated with decreased word and reading comprehension, decreased full-scale and verbal IQ, and reduced memory and attention. 68,69
Figure 3: Polychlorinated biphenyls (PCBs): inadequate margins of safety (serum levels). Prenatal exposure to background levels of PCBs has been shown to adversely effect reflexes, memory, and neurological function as assessed by physical examination of infants and toddlers. Adverse effects on attention, memory, intelligence, and reading comprehension have been demonstrated in children followed-up to age 11 years.
69,111–129 Note: All health effects shown are associated with prenatal PCB exposure, except hyperactivity, which is associated with blood levels at 42 months of age.
Maternal PCB body burden also alters thyroid hormone status in mothers and infants. Higher maternal PCBs are associated with small but significant reductions in total thyroid hormone in both mothers and infants, as well as higher levels of thyroid stimulating hormone (TSH) in the infants. 70 Thyroid hormone is critical to brain development, and elevated maternal TSH levels during pregnancy, with or without reductions of thyroid hormone, are associated with reduced IQ in offspring years later. 71 These observations suggest that the adverse developmental effects of PCBs may be at least partly mediated through impacts on thyroid hormone. PCB exposures also modulate neurotransmitter levels, which may be another mechanism by which PCBs affect neurodevelopment.
Widespread Exposures at Levels of Concern
The pervasive effects of prenatal PCBs on development, behavior, and cognition have been established at background levels of population exposure, 72,73 clearly indicating widespread exposures are a cause for concern. The main route of PCB exposure is through the food chain. Because the half-lives of PCBs range from 5 to 15 years, 74 dietary PCB exposures need to be reduced throughout childhood and reproductive years to limit adverse developmental effects on the next generation. 68,75
Because breast milk contains relatively high levels of PCBs, breastfed infants are exposed to a substantial portion of a total lifetime dose of PCBs within the first few months of life. Although transplacental PCB exposures are quantitatively small compared with breast milk exposures, it is nonetheless these prenatal exposures that have proven harmful. PCB exposures in breast milk from mothers with relatively high PCB body burdens are not without some cognitive and immunologic effects, but these effects are compensated for by the cognitive and immunologic benefits of breastfeeding. 72,76,77 Considering all currently available knowledge regarding risks, benefits, and alternatives, breastfeeding continues to be recommended without qualification. 78,79 The benefits of breastfeeding can, however, be improved by the same dietary measures needed to reduce fetal exposure to maternal PCBs. 68 Intake of PCBs, as well as the companion pollutant dioxin, can be reduced by minimizing consumption of high-fat animal products, particularly cheeses and processed meats. These should be replaced by animal products that are low in fat, such as nonfat milk and lean meats, fish and poultry, and/or by vegetarian foods including grains, beans, fruits, and vegetables.
IN HARM’S WAY
Routine Exposure of Fetus and Child to Possibly Unsafe Industrial and Environmental Chemicals
The substances discussed above are unique in being well studied and relatively well understood. In reality, few household and environmental chemicals to which the fetus and child are routinely exposed have undergone even minimal screening for adverse effects on the developing brain. The intensive study of the few well-scrutinized substances was in each instance triggered by a toxicologic catastrophe. In each case, subsequent research revealed progressively lower toxic thresholds, culminating in the discovery of toxicity at background population exposures with disturbing implications for public health. Were it not for the occurrence of high-dose epidemics, current population impacts of lead, mercury, and polychlorinated biphenyls (PCBs) might well be unrecognized today.
The potential for similar impacts from exposures to other commonly encountered chemicals is indeed troubling. Approximately 80,000 chemicals are currently in commercial use, 80 and the great majority were synthesized in the past 50 years. They are therefore entirely new to the human environment in the evolutionary time frame. Among these chemicals, only 12 have been adequately tested, according to the standards established by the Environmental Protection Agency (EPA), for their effects on the developing brain. 81 Indeed, for most of the 3000 chemicals produced in highest volume (over 1 million lbs/yr), the public record holds very little or no basic toxicologic screening data and no data at all regarding effects on the developing nervous system. 82 Meanwhile, the number of chemicals registered for production grows by 2000 to 3000 per year. 80 Despite vast ignorance as to the human health impacts, more than 2.5 billion pounds of toxic chemicals, nearly half of them known or suspected neurotoxicants, 83 were reported to have been directly emitted to the environment by large industrial facilities in 1997 alone. 84 These emissions provide a crude but nonetheless valuable indicator of potential exposures through air, food, and water contamination. Further potential for harmful exposure is created by the vast quantities of chemicals used in manufacturing and/or incorporated into products from which exposures may occur during transport, use, and after disposal. For example, in Massachusetts alone, over 500 million pounds of neurotoxic chemicals were used by industrial facilities in 1997. 85
Failure of Current Regulatory Framework to Protect Children
Currently there is no requirement to test chemicals for possible effects on brain development—not even in the registration of pesticides, one of the strictest areas of chemical regulation. 86 However, even for those few chemicals that have undergone some degree of examination, studies in both animals and humans have important deficiencies.
Prospective epidemiological studies, the best source of human toxicity information, are costly, require very long time frames, and are rarely available. Animal studies commonly underestimate human vulnerability to neurotoxicants because of the obvious difficulty testing uniquely human cognitive, language, and behavioral functions within animal models. In the case of lead, mercury, and PCBs, animal studies underestimated the levels of exposure that cause effects in humans by 100- to 10,000-fold. 87 In addition, the importance of genetic variability in determining susceptibility to environmental exposures is ignored when using genetically similar animals for testing.
Current testing protocols also underestimate toxic threats by exposing subjects to only one chemical at a time, although children are exposed to complex mixtures of chemicals throughout development. 88 It is now well established that such multiple chemical exposures can be far more damaging, or cause damage at lower levels of exposure, than single exposures generally addressed in animal models. 89–93 Testing chemicals in combinations, however, would exponentially increase the number of tests to be performed. For example, to test 10% of commercial chemicals, or 8000 chemicals, in combinations of three, 85 billion tests would be required. 94 Comprehensive testing of chemical combinations is clearly not feasible.
Protecting Child Development from Toxic Threats
A historical review of toxic chemicals reveals a disturbing pattern. As a rule, these chemicals are recognized as harmful long after their use has become routine and exposures widespread. In some cases, toxic chemicals have become entrenched global contaminants by the time their human health consequences were understood. Because the fetus and developing child are most sensitive to the effects of these insidious exposures, our children in particular bear the risks of regulatory policies that largely consider chemicals safe until proven harmful.
Whereas improved chemical testing is essential, there are inherent limits to toxicity testing. Therefore, with mounting evidence of toxic threats, it becomes increasingly important to protect the fetus and child from unnecessary chemical exposures. In the realm of public policy, child development can be better protected by a more public health-oriented approach to the regulation of household and environmental chemicals. Such an approach would introduce appropriate precaution at all phases of the life cycle of these substances, including their production, use, and disposal. Meanwhile, providers, parents, and all who care for the developing fetus and child can help reduce exposures to a wide variety of known and suspected neurodevelopmental toxicants that are commonly found in consumer products, food, the home, and wider community. 95
FOOTNOTES
*For the purpose of this discussion, developmental disabilities are broadly defined to include learning, behavioral, emotional, sensory, speech, and neurodevelopmental impairments, as well as cerebral palsy and delays in growth and development.
Cited Here
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