During brain development, which begins in the fetus and continues into adolescence, a precisely timed sequence of cell division, migration, differentiation, myelination, synapse formation, programmed cell death, and synapse pruning unfolds. Disruption or alteration of this process by chemical exposure or other environmental factors can lead to various outcomes (developmental delays, learning disabilities, attention deficits, etc.), depending on when in development the exposure takes place and its duration (Koger, Schettler, & Weiss, 2005).
Methylmercury, for example, a developmental neurotoxicant, shows various effects—including mixtures of developmental delays, learning disabilities, attention deficits, seizures, and mental retardation—depending on the amount of exposure, when in pregnancy the fetus is exposed, and for how long the exposure lasts. (Go online for an interactive graph showing the effects of exposure to several chemicals at different times in prenatal development.)
Each toxicant, therefore, has its own "window of vulnerability." Animal studies show that changing the timing of exposure by even a few days can dramatically change effects on the developing brain (e.g., Miller & Ferriero, 2009). This concept may be familiar to communication sciences and disorders (CSD) professionals, given the more than 50-year acknowledgement that, depending on timing, a rubella infection in a pregnant woman can lead to auditory and visual disability and birth defects in the fetus (e.g., Kohlmoos, 1953).
The prevalence of developmental disabilities in U.S. children rose 17% between 1997 and 2008, increasing from 12.84% to 15.04%, according to analysis of National Health Interview Surveys data (Boyle et al., 2011). Rates of autism spectrum disorders and attention deficit hyperactivity disorder grew the most. Concurrent with the increased prevalence of developmental disabilities is growing evidence for connections between neurotoxicants and disabilities, with a list of chemicals now known to be—or strongly suspected of being—neurotoxic (see chart [PDF]). Many more chemicals have not yet been tested for neurotoxicity, so this list could continue to grow.
It's not practical to expect CSD professionals to memorize all the various neurotoxicants and their effects. It is, however, worthwhile to note the number of neurotoxicants and the strength of the evidence showing connections to disabilities, the range of these disabilities, and the wide array of neurotoxicants that can contribute to them.
Also noteworthy is the fact that children are more vulnerable than adults to toxic substances, in part because they're smaller and they put more objects in their mouths [Antoniadis, Gilbert, & (Gagnon) Wagner, 2006]. Children's ability to metabolize substances is more limited, and an infant's immature blood-brain barrier is not as effective at keeping toxic chemicals from the brain, at least for several months after birth. Nor does the placenta block many chemicals from crossing from the mother into a fetus, as described by Koger et al. (2005).
In addition to individual behavior change, one vehicle for minimizing children's exposure to these substances is continued chemical policy reform that limits the production and use of toxicants in products. In the United States, the elimination of lead from paint in 1978 and from gasoline in 1975, for example, will eventually have a huge protective effect on health, although the effects of existing lead residues from prior use will last for decades or even centuries to come.
For CSD professionals, a more direct, immediate means of limiting children's exposure may be educating families of children with developmental disabilities. Professionals can help families prevent further exposure in affected children and also protect subsequent pregnancies and younger siblings. In addition, by familiarizing themselves with common neurotoxicants and their effects, CSD professionals can play a key role in improving quality of life and outcomes for affected individuals and their families.
CSD professionals should be aware of the risks of exposure to several substances, including alcohol, nicotine and tobacco smoke, lead, pesticides, mercury, and solvents. A summary of the effects and routes of exposure for these toxicants is presented here. Additional substances, including cocaine and methamphetamine, also are recognized contributors to developmental disabilities and delays (Frasier, 2011; Salisbury, Ponder, Padbury, & Lester, 2009; Wells, 2007), but are beyond the scope of this article.
Alcohol (ethyl alcohol or ethanol) consumption, even in moderation, has been recognized since the 1970s as a contributor to disability and birth defects (Hanson, Pytkowicz Streissgutha, & Smith, 1978). The effects of alcohol clearly demonstrate windows of vulnerability, as doses too small to seriously affect the mother's brain can have devastating effects on the fetal brain and nervous system (Gilbert, 2004).
In addition, alcohol consumption during pregnancy has been associated with preterm delivery (Albertsen, Nybo Andersen, Olsen, & Grønbæk, 2004), a risk factor for developmental disabilities. Even modest consumption during pregnancy—an average of one drink per week—has been associated with neurological effects in children (Sood et al., 2001).
The effects of prenatal exposures cannot be reversed—but CSD professionals working with at-risk individuals and families can help prevent exposures in the next generation. Alcohol consumption is largely an individual choice, but because of its addictive nature, awareness of the problem does not necessarily lead to changes in behavior. Societal and cultural decisions to limit access to alcohol, as well as to address alcohol use during pregnancy and alcoholism, are needed to protect children from preventable disability. Professional medical and education groups can play a part in these decisions.
Nicotine and tobacco smoke exposures involve not only individual tobacco use, but second-hand and third-hand exposures. Third-hand smoke is defined as "residual tobacco smoke contamination that remains after the cigarette is extinguished" (Winickoff et al., 2009). Exposure is associated with cognitive impairment, congenital malformations, and low birth weight, itself a risk factor for developmental disabilities (March of Dimes, 2008).
Reducing tobacco product use, as with reducing alcohol consumption, is made more complex and
difficult by its addictive properties. Society can take steps to restrict use in areas that subject pregnant women and children to second-hand and third-hand exposures. However, unless at-home use is addressed through education, incentives, and cultural shifts, pregnant women and children will still likely be subjected to exposures several hours a day.
A culture shift seems to be in process: More than 20 states have legislated bans on smoking in workplaces, restaurants, and bars (Centers for Disease Control and Prevention, 2010), and several jurisdictions (Arkansas, California, Louisiana, Maine, and Puerto Rico) ban smoking in private vehicles when a child is present. Similar bans have been proposed in at least 20 other states (Public Health Law Center, 2010).
Lead has been a known contributor to developmental disabilities for decades, but even though much has been done to raise awareness and address sources of exposure, lead remains a serious contributor to disability in children. Common sources of exposure include lead paint chips that children ingest and/or inhale and that contaminate house dust, soil contaminated by exhaust from vehicles burning leaded fuel or from industrial activity, household water contaminated by lead solder in pipes, and many toys and other products made of vinyl and plastic. Even very small exposures to lead can cause permanent harm to a developing brain and nervous system; many professionals consider that there is no detectable level of lead in blood that is safe (e.g., Centers for Disease Control and Prevention, 2011; Gilbert & Weiss, 2006). Children should have blood lead levels tested at a young age, ideally in the first year of life, with remediation if the blood lead level is above 2 µg/dL. Because lead persists in the environment long after the source of contamination is removed, ongoing clean-up efforts are also needed.
Pesticides, even at moderate direct exposure, have been linked to learning, behavioral, and developmental disabilities (Schettler, Stein, Reich, Valenti, & Wallinga, 2000). Direct contact can occur through spray drift; residue in homes, at schools, and on lawns, gardens, athletic fields, and agricultural fields; and residue on clothing, shoes, hair, and other articles from household members who work with pesticides. New evidence shows that prenatal exposure is associated with nervous system and cognitive disturbances (Bouchard et al., 2011; Engel et al., 2011; Rauh et al., 2011). Families can take several measures to reduce exposure (for more information about exposure prevention and integrated pest management, see "Resources" below):
Greatly reduce use of pesticides in favor of less toxic methods of controlling pests.
Securely lock away any pesticides for home use.
Remove shoes at the door to prevent pesticides from being tracked indoors.
Reduce dietary exposure to pesticides by eating organically grown food (Lu et al., 2006).
Pesticides (or classes of pesticides) listed in the accompanying chart include atrazine, chlorpyrifos, cyanazine, DDT, diazinon, herbicides, lindane, methyl bromide, metolachlor, organochlorine pesticides, organophosphates, and pentachlorophenol.
Mercury is associated with cognitive impairment, congenital malformations, and low birth weight. A pregnant woman or child eating contaminated fish is the most common route of exposure leading to developmental effects. Of fish that children tend to eat, white albacore tuna is the most contaminated; children in some cultural and ethnic groups with diets different from the "typical American" diet may have higher exposure (see "Resources" below for information on sport-fish and commercially produced fish consumption). Other sources include dental amalgam; some drugs and related products, including mercury-based skin creams and teething powders; and broken mercury-containing household items, such as thermometers and fluorescent light bulbs, including the energy-saving compact bulbs. Some cultural and religious rituals also use mercury.
The most effective way to reduce mercury exposure is eliminating contamination of fish and seafood. Only policy and legislative action by state and federal governments will reduce the mercury released by coal-burning power plants, cement factories, and incinerators. Supporting these policy and legislative actions is an important step toward protecting children's health. Educating parents about the safe clean-up and disposal of fluorescent light bulbs, and replacing mercury-containing switches and thermometers with safer alternatives are also important actions.
Solvents are used in industrial applications, including as fuels and in building finishes, adhesives, and cleaning solutions. Solvents also are found in many cosmetics and personal care products, aerosols, and anesthetics. Whether used as intended or intentionally inhaled ("sniffed") for intoxication, solvents are hazardous to health. Exposures to solvents—anesthetic gases, carbon disulfide, chloroform, ethylene glycol ethers, hexafluoroacetone, methyl chloride, tetrachloroethylene, toluene, trichloroethylene, trihalomethanes, and xylene—are associated with most of the developmental disabilities listed in the chart.
Regulation and oversight of solvents in workplaces, as well as proper use, ventilation, and disposal of solvents are needed to protect the health of workers, families, and consumers. Replacing harmful solvents with more healthful alternatives is also a valuable preventive step. Green chemistry principles are driving the creation and use of many replacement substances for solvents and other chemicals (U.S. Environmental Protection Agency, 2011).
Studies, especially with animals, provide evidence that an enriched, nurturing social environment can help mitigate the effects of exposure to some toxicants, such as lead (Schneider, Lee, Anderson, Zuck, & Lidsky, 2001). New discoveries also are beginning to show that toxic exposures, as well as nutritional and social environments, can cause changes in gene expression, even without changes to the DNA sequence of genes. There's some evidence that these "epigenetic" changes may be passed on to future generations (University of Utah, n.d.). Thus, professionals may have an opportunity not only to identify exposures, but to reduce their impact in current and future generations by taking action with families and on policy.
Exposure, especially during windows of vulnerability, can create or exacerbate developmental disabilities. Although many of these disabilities are not reversible, CSD professionals have an opportunity to advise parents and caregivers to prevent continued and additional exposure. In addition, professionals can participate in research efforts and influence social and legislative policies and actions to reduce exposures for future generations. CSD professionals can, for example:
Take an exposure history with patients and their families to assess past and current risks. A fact sheet for health care providers
[PDF] from Physicians for Social Responsibility provides more information.
Provide materials to families that may be at risk to educate and guide them in removing exposure risks from their environments. The Learning and Developmental Disabilities Initiative (LDDI) website has a number of resources, including Practice Prevention Columns and fact sheets designed for parents and caregivers
Advocate for protective action locally and nationally. Join LDDI
, which works on issues of learning disabilities, autism, developmental disabilities, and mental health. Membership is free and includes timely information about science-based teleconferences, publications, events, and more.