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With 1 in 88 American children now affected by autism, The Autism Puzzle is the first book to move beyond the distractions of the vaccine debate to address compelling new evidence that autism may be the result of the pairing of environmental exposures with genetic susceptibilities that together impact the brain development of children.
Journalist Brita Belli brings us into the lives of three families with autistic children, each with different ideas about autism, as she explores the possible causes. She interprets for readers compelling evidence that environmental toxins—including common exposures from chemicals mounting in our everyday lives—may be sparking this disorder in vulnerable children. Belli calls for an end to the use of hazardous materials—like toxic flame retardants used in electronics and furniture—insisting that we cannot afford to experiment with our children. The Autism Puzzle puts a human face on the families caught in between the debates and offers a refreshingly balanced perspective.
|Publisher:||Seven Stories Press|
|Product dimensions:||8.10(w) x 5.50(h) x 0.80(d)|
About the Author
BRITA BELLI is the editor of E - the Environmental Magazine—the largest independent magazine dedicated to green issues. She is the author of The Complete Idiot's Guide to Renewable Energy for Your Home and editor of EarthTalk: Expert Answers to Everyday Questions About the Environment. Her articles have appeared in Plenty Magazine, MSN.com, Treehugger.com, Fairfield Magazine, Colorado Springs Independent, Black & White City Paper, Illinois Times, and Monterey County Weekly.
Read an Excerpt
The Autism PuzzleConnecting the Dots Between Environmental Toxins and Rising Autism Rates
By Brita Belli
Seven Stories PressCopyright © 2013 Brita Belli
All right reserved.
Urban Exposures, Chemical Concentrations, and the Question of Race
Thanks to years of public health campaigns and plenty of media coverage, many people are aware that certain types of fish are contaminated by mercury. Mercury released through emissions from coal-burning power plants and municipal and medical waste incinerators takes to the air and is carried along, sometimes for miles, before settling in soil or water. The inorganic mercury is absorbed into microorganisms in the water and converted to an organic substance, methylmercury, which is then consumed by fish. Big fish like shark, swordfish, king mackerel, and tilefish eat small, contaminated fish and accumulate high concentrations of toxic methylmercury. Both white (albacore) and canned light tuna contain mercury, too, with a January 2011 investigation from Consumer Reports finding that “children and women of childbearing age can easily consume more mercury than the Environmental Protection Agency considers advisable simply by eating one serving [about 2.5 ounces] of canned white tuna or two servings of light tuna per week.
Women who eat large quantities of such fish, both during and after pregnancy, can readily pass that mercury on to infants through umbilical cord blood2 and through their breast milk. 3 Pregnant women exposed to methylmercury from fish—particularly canned fish—have shown a greater likelihood for giving birth prematurely, 4 and a child born with low birth weight (4.4 pounds or less), such as happens when babies are born premature, is five times as likely to be diagnosed with autism as a child born at normal weight.5 Recognizing that mercury from seafood “may harm an unborn baby or young child’s developing nervous system,” the Food and Drug Administration (FDA) has advised women to limit their consumption of certain fish while pregnant.
Knowing of these dangers, many women choose not to eat fish high in mercury during pregnancy. But most populations exposed to toxic chemicals are not made aware that their food, water, or air could be poisonous. The likelihood of chemical exposure is deeply intertwined with a community’s socioeconomic status; factories that spew pollution are often allowed to operate with impunity alongside poor communities whose residents aren’t given the choice to opt out by simply avoiding contaminated items.
An early example of what can occur when factories pollute unchecked happened in Minamata, Japan, a small village of rice farmers and fishermen who depended on fish and shellfish from the Minamata Bay and the Shiranui Sea. In 1907 the Chisso Corporation opened a carbide plant on the shores of the bay. The townspeople initially welcomed the factory with the hope that it would bring economic prosperity. In 1930 the Chisso factory turned its attentions to the production of materials that could be used for Japan’s growing military needs—specifically acetaldehyde, or ethanol, a needed energy source for a country without its own oil supplies, and polyvinyl chloride (PVC), which was used for airplane parts. As the factory rapidly expanded its production, it dumped increasing amounts of untreated waste into local water supplies, contaminating the bay and the sea with methylmercury from 1932 to 1968. As the chemical bioaccumulated in the local fish and shellfish, widespread mercury poisoning—Minamata disease, as it came to be called—seeped into the village.
It was the cats they noticed first—acting crazy, falling into the sea, as if they were committing suicide. The first official case of Minamata disease was recorded in 1956, when two sisters, ages five and two, exhibited symptoms that included convulsions, muscle contractions, twisting and repetitive movements of the hands and feet, and sudden screaming fits. They were determined to have an unknown disease of the central nervous system. Soon researchers from Kumamoto University discovered that many residents living around Minamata Bay showed an inability to grasp small objects and difficulty with hearing, seeing, walking, running, and swallowing. Once the symptoms began, they could progress within weeks to massive convulsions, insanity, coma, and death. 7 A black-and-white image of a mother and child known as “La Pieta de Minamata” has come to symbolize the heartbreak. The mother’s head is wrapped in a scarf, her shoulders bare, her face lit ethereally, as she cradles and bathes her profoundly disabled child. The child looks, in fact, to be a young man, his neck muscles strained, legs and arms shortened and deformed, hands shriveled and bent.
The National Institute for Minamata Disease reports that as of 2001 there have been nearly 3,000 certified patients with the disease—some 1,784 of whom have died—and more than 10,000 with “applicable conditions such as sensory disorders or a high consumption of marine products.”8 Not until April 2006, nearly fifty years from the first report of the disease, did sufferers and their caregivers receive a formal apology from Prime Minister Junichiro Koizumi for the Japanese government’s failure to stop the pollution. Many victims are still fighting legal battles for compensation.
The Minamata tragedy was clearly linked to the Chisso factory, but it is often difficult to pin symptoms and diseases on exposure to chemicals from one particular source. People living in highly polluted urban areas are subject to a host of environmental contaminants that can lead to preterm birth. Pregnant mothers are more likely to give birth prematurely, or give birth to babies who are small for their gestational age, when they live near highways and are exposed to the associated air pollution, including carbon monoxide, nitrogen dioxide, sulfur dioxide and particulate matter.
Sharon Sandifer-Holmes, a special education teacher who has several family members with autism, grew up with six siblings in a crowded apartment in an African-American community in the Bronx. There, environmental contamination was a constant presence, from the smog to the rusted pipes to the peeling lead paint in her mom’s pre-war high rise, a subtler type of toxic exposure to which Sharon and her family never gave a second thought. But lead dust rises to the surface of lead paint and ends up on the floor, where children can easily ingest it in the normal course of crawling and putting objects in their mouths. Lead exposure is strongly linked to problems with cognitive functioning, including impaired learning and memory, mental retardation and developmental delay, psychiatric disturbances, seizures, and pre-term delivery. 11 Dr. Mark Mitchell, the founder and president of the Connecticut Coalition for Environmental Justice (CCEJ), a group that works to educate urban communities about existing pollutants and to give those communities a say before new polluting industries are ushered in, notes that “If you rent your own housing, you don’t have control over when it’s painted or how it’s painted. . . . So children are much more likely to be exposed to chipping and peeling paint.”
Sharon was the one to take care of her youngest brother when it became clear he had severe autism. Six years older than her brother, she took on the role of teaching him as much as she could—how to say the alphabet and count to ten, how to tie his shoes. She learned to brush off the inevitable stares that followed her brother whenever they were out in public. Now in his midthirties, and with their mother no longer able to care for him at home, Sharon’s brother is in a home for special needs adults full-time. Sharon’s aunt and her nephew—both of whom were born and raised in the Bronx—also have autism.
Still living in the same apartment, Sharon gave birth to a son, James. In 1997 James failed to meet early milestones like walking and talking, but despite her familiarity with the signs of autism, Sharon didn’t immediately make the connection. James was born seven weeks early, so Sharon assumed her son would be a little behind developmentally; she didn’t know that premature birth is a risk factor for autism. 13 But the difference between James and other kids his age grew too pronounced to ignore. He didn’t start walking until he was thirteen months old. He didn’t look his mother in the eyes, or show her any affection. “I was like, ‘Wow, something is not right here,” Sharon says. “Plus the fact that it was in my family, the light bulb went off in my head. I’m like, ‘I need to get him checked. I need to get out of that denial stage and take the first step.’”14 She made an appointment for James at the Kennedy Child Study Center in the Bronx, where they confirmed that he had PDD, a catchall term that means James showed severe impairments in thinking, language, affection, and social interaction. In other words, he is autistic.
By the time James turned six, Sharon had fallen in love and was pregnant with her second son, Chris. She moved to Bridgeport, Connecticut to live with her husband, affectionately known as “Big Chris.” They live on a quiet, tree-lined street in one of a string of brick townhouses with matching white awnings not far from the former Remington Arms Factory. Flowering bushes and a pinwheel or two brighten the small, fenced front yards. It’s quiet here, and the neighbors are neighborly. For Sharon, Bridgeport is an improvement over the crowded Bronx apartment. But the Bridgeport Harbor Station—a coal-burning power plant that burns 997,370 tons of coal per year and is located between the city’s downtown and South End neighborhoods—produces over 3,000,000 tons of carbon dioxide emissions per year according to 2006 data, along with over 2,000 tons of nitrogen oxide emissions, nearly 3,000 tons of sulfur dioxide emissions, and 54 pounds of mercury. Families like Sharon’s living within a mile of the plant have an average income of just $11,400, and 87 percent of those living in the plant’s vicinity are people of color. Jacqui Patterson of the National Association for the Advancement of Colored People (NAACP) Climate Justice Initiative took a walking tour of the Bridgeport Harbor Station and its surrounding neighborhoods in April 2010 and reported seeing “the highest mountain of coal” she’d seen in her many visits to urban coal plants; it was left uncovered and resulted in a film of coal dust over her car. Residents reported the same coal dust regularly coated their cars and kept them from opening their windows or hanging out their laundry.
The coal-burning power plant is just one of many toxic burdens the city’s largely poor and minority urban residents must bear. An aerial map of the city shows it dotted, chicken pox-like, with brown-field sites—abandoned parcels of former industrial land that are now polluted—208 of them with leaking underground storage tanks. The massive thoroughfare of I-95, which bisects the city, sends nearly 130,000 cars and trucks barreling through Bridgeport each day as they pass between New York City to the south and Boston to the north. 17 Meanwhile, Bridgeport RESCO Company, a waste-to-energy plant on the city’s west side, has failed to monitor for heavy metal emissions in the past, burning a massive pile of construction debris called “Mount Trashmore” between 1992 and 1993 that included asbestos and toxic metals “without extra monitoring of air emissions.”
“In Bridgeport, you can have industrial facilities in the middle of a residential block,” says Dr. Mitchell of the CCEJ. “It was set up originally so people could work where they live and they could walk to work [one of hundreds of city factories producing items such as sewing machines, brass parts, Frisbie pies, gramophones, and corsets]. But because of the toxicity of industries, it’s not workable any more. There needs to be a buffer. So in many places in the 1920s, the zoning started moving toward separating the residential from the commercial. But other cities didn’t. Bridgeport is one of them.” At a former chrome plating facility in Bridgeport, Dr. Mitchell saw children playing inside an abandoned building where they could be exposed to chromium 6, a serious toxin associated with cancer, skin ulcers, and kidney damage.
In the city’s north end sits the sprawling remains of the Remington Complex—the former GE arms factory, composed of thirteen interconnected buildings five stories high spread across more than seventy-six acres. Once, it was the largest munitions manufacturer in the world. Now, the decrepit, blackened brick buildings with broken windows and rusted metal balconies are stacked like giant, duplicate Lego structures, devoid of activity—unless you count the rumored ghostly presence of workers who lost their lives there in molten metal accidents and deadly explosions. Hazardous wastes produced at the plant were initially stored onsite in leaky drums containing cyanide, mercury, and PCBs.
Could a child’s risk for developing autism be tied to exposure to such persistent environmental toxins? One study looking at autism cases in San Francisco found a substantial link between mothers living in areas of high environmental air pollutants and their likelihood of having children with autism. The researchers matched the health records for children born in 1994 in six counties in San Francisco—284 of whom had autism—with relevant pollution data. Where environmental air pollutants including heavy metals like mercury, cadmium and nickel; industrial solvents like trichloroethylene (or trichloroethene, TCE, used to clean metal parts); and gases like vinyl chloride (used to make PVCs, which are in many plastic pipes, wires and packaging materials) were highest, the risk factor for autism increased by 50 percent. 23 The hazardous air pollutants studied came from sources as varied as car, plane, train and ship emissions; dry cleaners, gas stations, and large industrial manufacturing facilities; and home cleaning products.
The Agency for Toxic Substances and Disease Registry (ATSDR) and the EPA are required to maintain a list of substances from industrial facilities that pose the greatest threats to human health. The entire list contains a whopping 276 priority hazardous chemicals. Mercury is ranked third behind arsenic and lead in terms of frequency, toxicity and potential for human exposure. Vinyl chloride ranks fourth. In the San Francisco study, subjects were exposed to so many overlapping chemicals that researchers were unable to tease apart data linking individual chemicals with autism rates. Instead, they categorized compounds as either metals or solvents. They were also unable to take into account the subjects’ personal habits, such as smoking or eating contaminated food. However, they concluded that, as such limitations in exposure estimates are “unlikely to vary by case status, the effect estimates are probably shifted toward the null.”
This was not the first study to link higher autism rates with environmental toxins, specifically exposure to heavy metals. A 2004 study in Texas found that for every 1,000 pounds of environmentally released mercury, there was a 43 percent increase in the rate of special education services and a 61 percent increase in the rate of autism. Children in urban districts were found to be particularly at risk for autism; relative to rural districts, urban districts showed a 473 percent higher rate of autism. Suburban districts had a 255 percent higher rate of autism compared to their rural counterparts.
And stress makes people more vulnerable to toxic assaults. Black mothers are more likely to be affected by the stress of struggling to make a living than white mothers. One 2006 study relating particulate exposure to low-birth-weight babies reported in the journal Pediatrics that among Georgia mothers who participated in the study, there were 69 infants born preterm—31.9 percent of these infants were born to white mothers, 68.1 percent of them were born to non-white mothers. Another study in the American Journal of Epidemiology analyzing race, neighborhood deprivation (neighborhoods whose residents exhibit low incomes, high unemployment rates, and a tendency not to finish high school) and preterm births reported 2004 vital statistics data showing that 13.7 percent of infants born to black mothers were low birth weight, compared to 7.2 percent for white mothers, with factors like income, education and housing playing a significant role. The study went on to note that “Preterm birth . . . is responsible for two thirds of infant deaths and approximately half of subsequent childhood neurologic problems in the United States.” Even when researchers control for factors like maternal smoking, the racial disparity in preterm birth rates remains, leading researchers to conclude that larger neighborhood factors, such as living conditions and the stressors of poverty, racism, violence, and exposure to toxins and contaminants, are at play. One of the lead researchers who looked at neighborhood deprivation and preterm births, Dr. Patricia O’Campo, says those affected have a lifetime of issues ahead. “Babies born early have a high risk of subsequent adverse developmental health problems,” O’Campo says. “And a whole lot can happen between giving birth and when a child is assessed with interventions.” A premature baby literally has less brain matter evident at ages seven to fifteen than his or her carried-to-term counterpart; and males are “most vulnerable to adverse neurodevelopmental outcomes.” But recent studies have revealed something else about such infants: if early interventions and innovative teaching programs are applied—if a parent knows about such services and has access to them—the child can develop normally and succeed in school. Women living in low-income, toxic, and high-stress environments, then, are at a double disadvantage, with both an increased likelihood to give birth to babies prematurely, and less access to the services that can improve their child’s development when it is most critical. “There’s a lot of recent information about psycho-social stress and toxins,” Mitchell says. “Hundreds of studies [have been] done. If you live in a bad neighborhood, the stress from racism, the stress from poverty. Poverty is not nearly as important as the inequality of income. So if you make much less than the people around you than that’s much more stressful than if everybody were poor. If you live in a drug-infested neighborhood, if you’re exposed to a certain level of toxins, your body will have more of a reaction to the toxins than if you don’t have the stress level.”
A poor city could hardly be more juxtaposed with wealthy neighbors than Bridgeport, Connecticut’s most populous city, where more than 70 percent of residents are black and Hispanic, and 20 percent live in poverty. Meanwhile, Fairfield, Connecticut, just over the border, was ranked in the top ten best places to live by CNN’s Money Magazine, thanks to its five beaches, high-performing schools, low crime, upscale restaurants, and winding, leafy streets that showcase one perfectly manicured lawn after another. Passing through it on I-95, Bridgeport’s visible cityscape offers little to welcome potential visitors but empty brick warehouses, a belching smokestack, and vacant lots. Its small downtown, a collection of historic bank buildings and storefronts from a more prosperous era, is eerily lifeless at night despite lofty ambitions for revitalization from each subsequent city administration.
Bridgeport is similar to many cities across the country where minority residents live with a daily onslaught of chemical exposures from power plant smokestacks, contaminated factories, and outdated school buildings; from highways and congested streets; and from old apartment high rises where walls and windows still contain lead paint. For Sharon, those exposures would have been most worrisome when she lived in the Bronx, during the time when she was pregnant and first raising her infant son. But the Bronx could just as easily have been Chicago’s Pilsen or Little Village neighborhoods, each home to an outdated coal-burning power plant that together (as of 2009) release 90 pounds of mercury and 265 pounds of lead per year into surrounding densely populated communities; or Houston, Texas, which boasts some of the most consistently polluted air in the country thanks to major traffic and a concentration of chemical industry and power plants; or Pittsburgh, Pennsylvania; Birmingham, Alabama; Detroit, Michigan; Los Angeles, California—all of which rank among the most polluted cities in the US with record levels of air pollution and particle emissions.8
Sharon works for a Bridgeport public elementary school with kids who have a range of learning disabilities, including autism and attention deficit hyperactivity disorder (ADHD), and emotional problems. She sees that many city kids are not getting diagnosed early enough—often not until they are twelve or thirteen, according to their individualized education plans, which are used to define shortcomings and differentiate instruction for special needs kids. The children need services they aren’t getting. Mostly, she says, the parents don’t know what to do or are in denial. “They just think their kids are going through something and they’ll grow out of it,” Sharon says.
Since Sharon took care of her autistic brother and works with autistic children, she has an advantage over most parents of autistic children. Looking back, Sharon realizes her son was likely having small seizures in his sleep around the age of twelve, because when James woke in the morning his tongue would be chewed on either side. But it wasn’t confirmed until she received a phone call from the bus driver one morning that James had had a small seizure. After that, the seizures came with more frequency and intensity. The spasms lasted less than a minute, but they occurred several times a day. One day, he had five seizures in the span of twenty-four hours. When James first experienced multiple seizures, Sharon rushed him to the emergency room where he was kept overnight and administered medicines intravenously. Now he visits a neurologist every three months, and since starting anti-seizure medications, including Topomax and Trileptal, has improved.
Inside the family’s home is a coffee-colored sectional couch with a large matching ottoman. When James comes downstairs, he pauses by the ottoman, rubbing the corner. After walking by, he changes direction, so he can touch the ottoman again. When he’s uncomfortable, he makes high, whining noises, grabs his ear repeatedly and looks away from the person speaking to him. He rocks in place. But when his mom asks James about his notes, he becomes excited, talking in a flurry of words, proud, suddenly, and forgetting for a moment that there’s a stranger in the room. James loves to write notes; every day, over and over, he writes a note to the woman with a little boy who lives across the street—a family he’s never officially met. The note reads, “Dear lady from 312, for Christmas I want potato chips, Frosted Flakes, chicken nuggets.” “He’ll write the note fifty times a day,” Sharon says, “and the note will say the same thing all of the times.” When James comes home from school, he runs up to his mother, nearly bursting, saying, “Mom, mom, this is what I wrote for you at school, guess what I wrote?” And Sharon unfolds the note and reads: “Dear Mom, for Christmas I want . . .”
Sharon’s ability to recognize the warning signs for autism early meant that James has been able to get the help—both at school and from doctors—that will allow him to steadily become more capable and communicative and to overcome life-threatening complications like seizures. That’s not always the case, particularly in urban districts. The signs of autism are often present from birth: the child isn’t making eye contact or responding to his name, he’s not babbling by age one, not playing with toys, and seems not to hear. But as Sharon has noticed in the schools where she’s taught—where the large majority of students are black and Hispanic, where all kids qualify for free meals and many homes are run by a single parent—a parent not aware of these signs can miss out on critical early intervention.
Black children, according to one study, are being diagnosed with autism an average of 1.4 years later than white children when they are brought in for testing, losing valuable treatment time. When researchers looked at groups of families on Medicaid in relation to how autism was diagnosed, they found that black children were nearly three times more likely to receive another diagnosis on their first visit to a specialist. Most often, they were instead deemed to have conduct or hyperactivity disorder. And a family’s insurance status plays a role, too. Those who had been on Medicaid for more than a year, as opposed to less than a year, were 3.4 times as likely to receive a diagnosis other than autism.
When the CDC looked at rising autism numbers nationwide in 2006, it found that the median age for autism diagnosis was between four and five years old, despite the fact that the kids in question showed concerning developmental shortcomings prior to age three. The finding prompted the CDC to launch an autism-related public awareness campaign called “Learn the Signs. Act Early.” Once a diagnosis has been made, school districts are required to provide services for special needs kids, including specialized education, or, if that is not available, to bus kids to schools with the necessary services. The Individuals with Disabilities Education Act (IDEA) does more than require these services—it works to ensure racial balance in the way such funds are distributed. However, since the law’s inception in 1975, officials have noticed a troubling trend—black males, particularly those with behavioral problems, have been increasingly pushed into special education classrooms without an academic reason. It is evident that minority communities need the tools both to recognize and describe their child’s autism behaviors. Doctors, teachers, and specialists, for their part, should be more attuned to their own biases when it comes to diagnosing.
In the national autism conversation, the issue of race has been largely overlooked. Wendy Fournier, president of the National Autism Association, wrote that she’s increasingly concerned about how autism has gone undiagnosed in minority communities, adding, “At the conferences we go to, there are no black people there, no minorities. It’s kind of freaky.”
From celebrity advocates like the much-quoted actress Jenny McCarthy, whose child has autism, to promotional materials for leading autism groups, the face of autism is overwhelmingly white. The perceived imbalance has helped fuel the notion that the rise in autism reflects a parental and media hysteria, not an actual increase. That notion appeared to be vindicated by a California study in January 2010 in which researchers looked at the birth records of some 2.5 million babies born in California between 1996 and 2000, 10,000 of whom were later diagnosed with an ASD. Rather than finding clusters of autism cases around areas of high pollution and toxicity, researchers uncovered the opposite: autism cases in the state were clustered in the wealthiest cities and suburbs, places like San Francisco, Modesto, Mission Viejo, and Beverly Hills, and Thousand Oaks in Los Angeles. These are places where home values regularly exceed half a million dollars, and where residents are largely wealthy, white, and educated. The media response to the University of California, Davis study was immediate: environmental causes, it was reported, had little to do with autism clusters. Rather, these were educated parents pushing for special services because they had access to specialists and the means to pay for them. As a result, children in these well-to-do neighborhoods had autism rates nearly double those of surrounding regions.
What was largely missing from the story and related commentaries was that these families seeking and receiving early autism diagnoses and treatment did so because they had the education and means to identify the disorder and get help for their children. Other families—particularly black, minority, and low-income families—did not. The study unwittingly highlighted the fact that families who needed services were not being screened, diagnosed, or treated. Recognizing the signs of autism begins with the parents. A follow-up study done in March 2010 confirmed that parental knowledge about how to identify autism and seek treatment was critical in getting children diagnosed. Diagnosis happened more often when parents talked to other parents familiar with autism and were referred to area specialists. The resources for treating autism are out there, but, reports the study, in order to obtain them, “parents have to recognize the behavioral symptoms of autism, identify and reach a physician capable of identifying autism, and learn how to navigate the complex world of state developmental service departments, school systems, and other service vendors. Obviously, this knowledge is achieved, not ascribed.”
As autism becomes more universally recognized—and de-stigmatized—the racial gap is closing. The CDC findings on autism rates reflect a greater prevalence for autism among white children, particularly boys, but they also point to steadily climbing numbers in black and Hispanic populations. Between 2002 and 2006, the numbers of white children with autism jumped 55 percent; among black children, 41 percent; and among Hispanic children, 91 percent. Arizona’s numbers reflected the most significant jump in Hispanic kids with autism—144 percent—a result, researchers later surmised, of the state doing a better job at recognizing and diagnosing autism in a population that had been seriously under-diagnosed. 47 The latest study of autism prevalence conducted in a community in South Korea that relied on in-person screenings of all children between ages seven and twelve (55,266 in total) instead of simply counting how many kids were enrolled in special education classes found that numbers were much higher than previously estimated. Published in the American Journal of Psychiatry in September 2011, the study found that one in thirty-eight children, or 2.64 percent, had autism—and two-thirds of the children who met the criteria had not been diagnosed and remained in mainstream schools and classrooms. Bennett Leventhal, one of the study’s authors and deputy director of New York’s Nathan Klein Institute for Psychiatric Research, said, “There’s no reason to think that South Korea has more children with autism than anyplace else in the world.”
Autism is on the rise in immigrant populations as well. Dr. Daphne Keen, a developmental pediatrician consultant and senior lecturer at St. George’s University of London, noticed that a disproportionate number of immigrant parents were coming to clinics with children on the autism spectrum. She began asking other colleagues in the UK and abroad about what she’d noticed, and they’d all seen similar trends. So Keen and other researchers launched a study, published in April 2010, that combed through UK data to see if they could connect the dots. They found that immigrant parents, specifically those who had migrated to the UK from the Caribbean and Africa, were giving birth to children with autism at much higher rates than children of non-immigrant parents. Among the 428 children studied during a six-year period, the risk of increase for autism in children of Caribbean immigrant parents was five times higher than for the general population. The children of black immigrant mothers were five times as likely to have autism as children in the general population; the same did not hold true for children of black mothers in the UK in general, showing that immigration was the critical factor. There were also substantial increased risks for the children of Asian immigrants.
A study in the mid-1970s in Australia found that children of Greek and German immigrant parents were more likely to have autism. In the 1980s and 1990s, other studies found increased autism risks for children born to immigrants, particularly in Sweden. But this was the first time that researchers had the extensive population and health records to draw such definitive conclusions. Such disparities could not be explained by race; they could only be explained by environmental factors. Immigrants were subject to unique stressors, such as social isolation and adjustment difficulties, and may also have been more susceptible to the particular toxins in their new home countries as a result of that increased stress. It’s possible that epigenetics plays a role; a stressful event like immigrating to a foreign country could carry epigenetic consequences.
Because the findings are so new, the exact causes driving these higher autism numbers among immigrants is still unknown. But as in the San Francisco and Texas studies, there’s strong evidence linking environmental contamination and higher rates of autism. However, since autism research relies on community health records, and accurate health records, in turn, are dependent on a family’s access to and use of services, study results are often skewed. Until there is comprehensive nationwide screening for autism and universal early healthcare services, the rates of autism will continue to be under-diagnosed, misdiagnosed, or diagnosed late in poor and minority communities—the very communities most at risk for elevated levels of toxic exposures.
Excerpted from The Autism Puzzle by Brita Belli Copyright © 2013 by Brita Belli. Excerpted by permission of Seven Stories Press, a division of Random House, Inc.
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Table of Contents
Introduction The Missing Percentage: Why Genetics Alone Can't Explain the Steady Climb 1
1 Uncounted Numbers: Urban Exposures, Chemical Concentrations and the Question of Race 13
2 Foreign Bodies: How We All Became Carriers of Mercury, Triclosan, and Flame Retardants 29
3 Dumped On: When Chemicals Act in Combination 49
4 Gut Reactions: Bowel Issues, Alternative Treatments, and Life-Saving Support 71
5 Birth Complications: Weighing the Risks of Inductions, Medications, and Early Cord Clamping 91
6 Our Chemical World: The Long Reach of Plastics and Pesticides 111
7 Unanswered Questions: Avoiding Toxins and Taking Action 147
About The Author 213