My Quest to Understand What Caused My Children’s Birth Defects

A journey into my family history, the chemical industry, and genetics

IIt’s 1989. I’m 26, 19 weeks pregnant, and I really need to pee. The technician calls my name and I follow her to the examining room where I undress and slip under the cold white sheet on the examining table. After some discussion about morning sickness, she applies gel to the wand and places it on my small baby mound. She gently presses the wand over my full bladder. I feel a slight release of warm urine between my legs. She presses the wand a little harder, then takes another pass around my mound before returning it to its cradle and telling me, “Wait here, I’ll be right back.”

“Is everything okay?” I ask.

“The doctor will explain.”

I’m frightened and alone, no longer worrying about needing to pee.

Is my baby alright?

The answer is no. What the technician saw, my doctor explains, is a sign that my baby is developing with numerous birth defects. Namely, my baby is developing spina bifida — a neural tube defect in the upper lumbar region where the baby’s spinal cord hasn’t closed — and anencephaly, meaning a major portion of the baby’s brain, skull, and scalp was missing.

Long hours turn into endless days. My husband, Steve, and I meet with a geneticist who asks questions about our family history — most of which I can’t answer because I’m adopted — and lays out the baby’s dire prognosis and our options for addressing it.

We ask what caused the baby’s neural tube and brain defects. The geneticist offers no clear answer, only speculating that the “anencephaly was likely caused by things mom came into contact with.” Something I ate or drank, or perhaps a chemical I was exposed to during pregnancy. She means these words to be reassuring. She means my future pregnancies probably won’t be at risk.

I’m far from reassured. All I can hear is: You did something wrong to cause this.

Abortion is not always a simple case of wanting or not wanting a child.

She tells us the baby has a 50/50 chance of surviving to full-term. If the baby does survive, he or she will be paraplegic, or even quadriplegic. The baby will also be severely cognitively impaired, require a brain shunt, and will likely die within six to nine months of birth.

That’s option A.

We ask about terminating the pregnancy. The doctor looks down at her notes and replies, “It’s late, but you still have that option.” Steve and I exchange clueless looks.

“Go home and sleep on it,” she says, as if sleeping is an option.

Faced with two options, one bad and the other worse, we choose worse — or is it bad? At 21 weeks, the doctors sedate me and proceed to disassemble the growing child inside my womb before sucking the remains out of me with a vacuum. I mention these details not because I am opposed to abortion. I’m not. I mention them because I asked the doctor what the procedure involved and I continue to live with this visual and the trauma of ending a life.

Abortion is not always a simple case of wanting or not wanting a child. I desperately wanted the one I was carrying. The complex layers beneath that decision are often overlooked in the contentious debate over abortion, which is another story altogether.

After the procedure, I ask my obstetrician the baby’s sex — something the ultrasound technician hadn’t looked for once she’d found the abnormalities.

“A girl,” my obstetrician, Dr. Hansen, tells me.

Steve and I leave the hospital and head for Windansea Beach. We hold hands and cry. We decide to give our daughter a name: Caitlyn.

After the abortion, I fall into a depressive stupor. I spend days wracking my brain, trying to figure out what I might have done to cause my baby’s defects. Was it because I kept forgetting to take my prenatal vitamins? Could it have been the two beers I drank at the Indigo Girls concert before I learned of my pregnancy? Maybe it was my twice-a-week tennis lessons.

TTwenty-eight years later, in March of 2017, I’m driving down Highway 1 in Southern California listening to NPR’s All Things Considered when I hear a story that makes me bolt upright. Scott Pruitt, Trump’s former Environmental Protection Agency administrator, is lifting a ban on the pesticide chlorpyrifos. Numerous studies — including one longitudinal study on the neurodevelopmental effects of indoor pesticide exposure — have linked the chemical to neural tube defects and brain malformations.

“Until the late 1990s,” the reporter says, “chlorpyrifos was the active ingredient in household flea bombs.”

The words flea bombs land like a punch. In addition to the two beers I drank and the tennis lessons I didn’t give up, my husband and I had set off flea bombs in our condo before we knew Caitlyn was growing inside me. That year had been particularly rainy by San Diego standards, and wet weather breeds fleas. Our house and pets were infested, and my husband’s skin was covered in welts from flea bites. We were broke, so instead of calling a pest control company, we purchased flea collars for our cats and two flea bombs to fumigate our condo — one for upstairs and the other for down. We followed the instructions on the label, closing all windows and leaving our condo for a set number of hours. When we returned home, the chemical odor was so strong that we opened all the windows and left for a few hours more.

Could this chemical have caused Caitlyn’s neural tube and brain anomalies? Part of me doesn’t want confirmation that I, in fact, did do something wrong. The other part of me can’t help but begin researching chlorpyrifos on the internet.

CChlorpyrifos is an organophosphorus insecticide used to control household cockroaches, fleas, and termites. It’s also the active ingredient in some pet flea and tick collars. It is structurally similar to nerve gas developed by Nazi Germany. Human and animal studies link chlorpyrifos exposure to structural damage to the brain, diminished IQ, neurobehavioral deficits, and brain tumors in children. It has also been linked to heart disease, lung cancer, Parkinson’s disease, and the lowering of sperm counts.

While conducting research, I fall down several rabbit holes that lead nowhere before stumbling upon a rich vein of information. I learn that in 1989, when I was pregnant with Caitlyn, virtually all the leading home flea treatments contained organophosphates, chlorpyrifos being the primary one. When chlorpyrifos is released from a container to treat a large area in the home — the manner in which we used it — it volatilizes and then settles back on the surface of any object in the vicinity, e.g., a child’s toy, or the plate a pregnant mother’s eats from. I was likely exposed to chlorpyrifos by breathing, eating, and drinking the substance, by touching surfaces in my home after we set off the flea bombs, and by touching the cats’ flea collars.

The EPA finally banned indoor use of the pesticide in 2001.

I dig for more information about the manufacturer of chlorpyrifos, Dow Chemical. Dow first started to produce chlorpyrifos in 1965. Originally, they branded it under two names: Dursban and Lorsban. By the late ’80s, reports began to surface at Dow that the metabolic breakdown of chlorpyrifos caused central nervous system abnormalities (hydrocephalus and dilated brain ventricles) and other abnormalities (cleft palate and skull and vertebral abnormalities) in fetuses. Dow waited as long as seven years to forward these findings to the EPA, which first learned of them in 1994.

Dr. Janette Sherman, an activist, physician, and author, uncovered Dow’s hidden reports via a Freedom of Information (FOIA) request from the EPA. In 1995, Dow was fined for withholding 249 reported incidents of chlorpyrifos poisoning from the U.S. government.

Informed by Dr. Sherman’s case studies, both the EPA and the FDA set tolerance levels for chlorpyrifos in the ’90s. The EPA finally banned indoor use of the pesticide in 2001. However, the agricultural use of chlorpyrifos was still permitted, despite evidence showing that the chemical sickened farmworkers who applied it and contaminated drinking water supplies in farming communities.

II begin sending emails to lead investigators on chlorpyrifos studies. Eventually, I am directed to Betty Mekdeci, Executive Director at the nonprofit Birth Defect Research for Children. Mekdeci explains to me the difference between teratogenic studies conducted by the chemical and drug industries versus those conducted by non-industry scientists. I learn that chemical industry studies are purposefully designed to avoid certain developmental markers and therefore rarely produce reproductive effects. And once a product goes to market, it’s difficult to convince the FDA to pull it even if subsequent non-industry studies suggest it has deleterious effects on consumers.

Finally, I read a longitudinal study mentioned in the NPR story and discover how researchers used magnetic imaging to reveal that children exposed to chlorpyrifos in the womb had persistent changes to their brains throughout childhood.

By this point, I felt it was likely that my exposure to chlorpyrifos led to Caitlyn’s birth defects. I interviewed Eric Johnson at Scripps Research Institute and the late John Casida at UC Berkeley, two scientists specializing in toxicology and genetics. Based on studies they were familiar with, they believed my hypothesis had merit.

InIn 1991, after losing another pregnancy to a blighted ovum, I get pregnant again. This time, I’m assigned a “high-risk” obstetrician. My first ultrasound is reassuring: a normal heartbeat, with all signs pointing toward a healthy fetus. I decide that if my second ultrasound goes well, I’ll tell my family I’m expecting.

The technician for my second ultrasound is Min, the same one who discovered Caitlyn’s troubles. Like a recurring nightmare, within minutes of the exam, I can tell by the look on her face that something isn’t right. Just like the last time, she excuses herself, returning minutes later with a radiologist. He takes over the controls, traversing and pressing my belly with the wand before performing a vaginal ultrasound. He does not speak, and keeps the screen directed away from me.

Finally, he places the wand in its cradle and directs his gaze at me. “I’m sorry,” he begins.

Somehow, I make it to the obstetrician’s office across the quad from radiology. My doctor is on vacation so I’m seen by the obstetrician covering for her. He repeats what the radiologist has already told me: There is no longer a detectable heartbeat and the amniotic sac is elongated, suggesting that I am in the midst of miscarrying.

“Go home, drink a pitcher of margaritas and wait,” he tells me. “If you don’t miscarry by Monday, come back and we’ll perform another D&C.”

Because I’d forgotten my purse at the radiology clinic, I return to Min’s office, where she beckons me to follow her down the hallway, out of the receptionist’s earshot. I tell her what the obstetrician said. She whispers, “If you don’t miscarry over the weekend, wait until Dr. Hansen returns before you do anything. I have a feeling — nothing based on medicine — that you won’t lose this baby.”

I continue to search for definitive answers as to whether my children’s brain malformations are related to chlorpyrifos exposure.

I don’t drink a pitcher of margaritas or miscarry over the weekend. Instead, I wait until Wednesday before returning to the office to hear Dr. Hansen’s assessment. Everyone in the office appears to know I am about to lose another baby.

Dr. Hansen enters the exam room with a sorrowful expression on her face. Feigning optimism, she says, “Before we do anything, let’s have a quick listen.” She places the doppler on my underbelly. Crickets. She moves it upward, just below my rib cage, and stops. I hear — or imagine — a faint sound, but nothing like a heartbeat. She turns the doppler 90 degrees, and there’s the sound again, only this time it’s louder, and rhythmic.

We look at each other and both begin to cry. There is life inside me.

I wish I could tell you that the remaining months of my pregnancy were smooth sailing, but that’s just not how I roll. I spot heavily throughout the second trimester, so much that I decide to search for my birth parents to learn more about my medical history. I call my “uncle” Lester, my parents’ adoption attorney for my brothers and me, to explain my circumstances. Fifteen minutes later, he calls me back with the notes from his interview with my birth mom. He reads them to me over the phone, including her maiden name.

With the help of a private investigator friend, I track down Rose Sciuchetti, the woman who placed me for adoption because she couldn’t afford another child and refused her abusive boyfriend’s marriage proposal. Rose and I meet on my 29th birthday at her home in Elmhurst, Illinois. She tells me everything she knows about her family’s medical history, including her clinical depression and a bout with ovarian cancer. She is unaware of any birth defects or pregnancy complications in our family history.

SStuart is my first child to be born. He arrives on April 17, 1992. Just as I’m delivering my stubborn placenta, Stuart is taken from us for “further evaluation.” The following day, Stuart undergoes a six-hour operation to repair a tracheoesophageal fistula — his esophagus is connected to his trachea instead of his stomach, where it belongs. He recuperates for three weeks in NICU before I’m allowed to hold him again. He is diagnosed with VATER Syndrome, a satellite of birth defects including, in his case, the fistula, a wonky urethra, two hiatal hernias, a cockeyed aortic arch, and a questionable kidney. As he matures, Stuart is considered a “failure-to-thrive” infant, which means his growth is decelerated or arrested. The condition is associated with abnormal growth and development. And sure enough, Stuart consistently reaches developmental milestones far behind schedule. At 13 months, we discover he has an anaphylactic allergy to peanuts; at 15 months, that he has asthma; and at 21 months, that he has severe reflux, which explains his colic and recurrent pneumonia. By the time Stuart is 10, he’s endured 19 surgical procedures, three of them major.

Stuart’s chronic health issues subside for four years, until, at age 14, he begins waking up with nausea. After one fateful afternoon spent riding roller-coasters, Stuart complains of a violent headache that does not abate. We relay this to the pediatrician — the mention of nausea, in particular, causes her to turn on her heel and order an MRI.

Stuart and I fly to New York for a consultation with a supposed “miracle worker” I’ve read about in an online support group only to realize we’ve been woefully misled.

My son is diagnosed with two brain malformations: Chiari I, which translates to a skull that is too small for the brain, and basilar invagination, a condition in which a vertebra at the top of the spine moves into the brain cavity, compressing the brainstem and spinal cord. The head of UCLA’s pediatric neurosurgery tells us he can fix the Chiari but wouldn’t touch the basilar invagination “with a 10-foot pole.”

A week before his 15th birthday, surgeons remove a piece of Stuart’s skull to allow his brain some breathing room. Over the course of several weeks, his symptoms appear to improve. Then they return with a vengeance. He stops attending school and is prescribed opioids for pain. He can barely walk.

My marriage doesn’t survive. Still, we form a united front when it comes to Stuart. The UCLA surgeon is at a loss, so we seek out another geneticist. We tell her about Caitlyn, wondering whether there was any connection between her and Stuart’s brain malformations since both are congenital and involve the central nervous system. She tells us they’re unrelated.

Stuart and I fly to New York for a consultation with a supposed “miracle worker” I’ve read about in an online support group only to realize we’ve been woefully misled. After a nine-hour wait in the Chiari Institute waiting room, Dr. Paulo Bolognese, the neurosurgeon who evaluated Stuart, tells us he can’t do anything about the basilar invagination but would like to try an experimental procedure on my son’s spinal cord.

“I’m so confident in the surgery,” he tells us, “I’ve even performed it on my own son.”

Later, we learn of the Institute’s suspect marketing practices. The online support group I’d thought of as independent was in fact run by a former Chiari Institute patient who refers most new support group members to the Institute in coordination with its marketing department. In 2008, the Institute is sued after a patient is prepped for surgery and Bolognese is nowhere to be found. Both Bolognese and Milhorat, two of North Shore University Hospital’s “highest-volume surgeons” at the time (earning a combined $10 million in 2007), are then named in a class action suit for medical malpractice. Eventually, they are both suspended.

After further research and several phone consultations with neurosurgeons in Great Britain and the U.S., I finally find a neurosurgeon who is able to perform the basilar invagination surgery. We travel to Iowa City to meet with him. He describes a high-risk surgery that involves entering the brain cavity through the soft palate at the back of the throat, then removing bone that is compressing the brain stem, and finally stabilizing the skull and spine by fusing the two with bone that has been removed from another part of the body. He estimates Stuart will spend a month in the hospital followed by six months in a brace molded to fit his upper body.

JJust after Stuart was born, Steve and I discussed whether to have more children. Steve’s dad offered unexpected, unsolicited, and harshly worded advice: “You’ve aborted the retarded baby and had a defective baby, maybe you should just stop at one?” His cruel remark and my own “wanting to get it right” instinct lead me to try again sooner rather than later.

Steve wasn’t opposed to more children; he just thought we should wait a year or two. “Stuart’s a handful,” he said, and “your mom has cancer, and I just started my new job.”

That all made perfect sense, but let’s just say nursing is an unreliable form of contraception. We learned we were expecting soon after Stuart’s first birthday.

Spencer is born on December 23, 1993, without complications. He’s chubby and pink, sleeps like nobody’s business and as he matures, he proves to be everything Stuart is not: an early walker, easygoing, athletic, lighthearted, and most notably, healthy. Oh, sure, there have been a few broken bones, and a scary night in the E.R. for whooping cough — but relatively speaking, he’s my wash-and-wear child.

Fast-forward 20 years, to 2013. Spencer is a college student in Bellingham, Washington, and complains of a severe headache with nausea and vomiting. My second husband, Ain, and I travel to meet him in Portland, Oregon, where Stuart is attending college. When Spencer begins to shake uncontrollably, we rush him to the E.R. We explain his symptoms to doctors and mention Caitlyn’s and Stuart’s medical issues. The E.R. doctor immediately orders an MRI.

Two days later, Spencer is diagnosed with a congenital condition called cavernous venous malformation (CVM), a golf-ball-size tangle of veins and arteries deep within his brain. It bled, causing Spencer’s headache.

I take Spencer to a vascular neurosurgeon in Seattle who specializes in microsurgery. After looking at his MRI, he explains that given the location of the CVM, surgery would be highly risky and may do more harm than good. Because it was a one-time event, he says, we might want to take a “wait-and-see” approach. He recommends an MRI every six months.

Over the next three years, Spencer’s MRIs show little to no growth. He mountain bikes at every opportunity, works on his engineering degree, and is named Employee of the Year two years in a row at his campus outdoor center. The frequency of his headaches increases, though none rise to the level of high-risk brain surgery. Everything seems more or less okay — until I get a fateful call from my ex-husband, Steve. His tremulous voice immediately tells me something is wrong.

AAin and I arrive at Seattle’s Harborview Medical Center ICU around noon the next day. Spencer has suffered a hemorrhagic stroke. Steve recounts details of the emergency airlift from Bellingham to Seattle as we watch our son sleep, his arms and legs in restraints, an IV hooked up to his left arm. I sit down and cusp Spencer’s hand with both of mine. He does not respond. Over the next hour, he occasionally mumbles gibberish, something about a goat farm and Fidel Castro.

Spencer recovering from brain surgery at Seattle’s Harborview Medical Center in 2016. Photo: Amy Roost

Suddenly, without warning, Spencer bolts upright with all his muscles flexed. He pulls his left hand free of the restraint and yanks the IV out of his arm. He thrashes about, trying to free his other limbs. Ain, the nurse, and I try to hold him down. The nurse yells for a crash cart. An orderly and Spencer’s roommate, Nick, join in the effort to restrain Spencer while the nurse frantically attempts to restart the IV. A doctor lifts Spencer’s eyelid to reveal a fixed and dilated pupil. The sound of plastic bags being ripped open fills the room. All of us are holding our breath but Spencer is gasping for air, his skin turning scarlet red then a deep purple. His bare chest heaves, revealing every rib. I watch from the foot of the bed while pressing his feet into the mattress. Time is collapsing. I’m losing him. The nurse shouts, “It’s in.” The doctor orders propofol, then more propofol, and more still, until finally Spencer’s body relaxes enough to insert a breathing tube.

They perform an emergency craniotomy. Three days later, the neurosurgeon tells us the “wait-and-see” period has come to an end.

SStuart and Spencer have each survived their multiple brain surgeries. Stuart graduated from college with a physics degree and now works for NASA. After nearly a year of rehabilitation, Spencer returned to college, something his doctors predicted would never happen. Both of them suffer physical side effects from their respective operations: Stuart has mobility and chronic pain; Spencer has a short-term memory deficit. But they’re alive and I still get to love on them.

You may be asking yourself, as I have over the years: What are the odds that I’d have three children with what doctors say are unrelated brain malformations? I’ve never been good at math but I’m pretty sure the odds are astronomical. I also believe the odds that they are related are far greater than the odds that they are not. My own hypothesis is that my exposure to chlorpyrifos caused the anomalies in all three of my children.

After filling out an online questionnaire offered by Birth Defect Research for Children, I consult the organization’s director, Betty Mekdeci, again to get her thoughts on my family’s history.

I want to do everything in my power to ensure that what happened to my children doesn’t happen to their own children.

“You have three malformations that are very similar in that they are affecting the brain and could have the same etiology, that is clear,” she says. I press her about my chlorpyrifos hypothesis, and while she is careful not to give it her full-throated endorsement, she explains that because of its chlorinated structure, chlorpyrifos can be stored in body fat, and that it’s possible I harbored what she calls a “body burden.”

“You go to the body’s resources to build a baby,” she explains. Fat is one of those resources and studies have shown that, for instance, dioxin — a chemical contaminant that is a byproduct of the chlorpyrifos production process, and one of the most potent and poisonous contaminants (it’s in Agent Orange) — has been detected in body fat and seminal fluid 30 to 40 years after exposure. Questions about grandparents were recently added to the birth defect registry questionnaire, because of what is believed to be dioxin’s multigenerational effect on the immune system. Mekdeci goes on to explain that certain enzymes are known to play a role in the detoxification of the body, and some individuals lack these enzymes. She suggests that I submit my 23andMe raw data on the Genetic Genie website to see if I am one of those individuals.

It takes less than 10 minutes to upload my data, receive my “Detox Profile,” and discover that I have a gene variation known in genetics parlance as GSTP1 i105v rs1695 GG. Translated, this means my body does not produce enough of the detox enzymes that protect cells against the toxicity of many compounds including pesticides, heavy metals (present in many pesticides), herbicides, solvents, steroids, and many other harmful environmental pollutants. In fact, some health professionals recommend individuals with my genotype minimize their exposure to pesticides and heavy metals.

OOther than to satisfy my own curiosity, why does digging up the chemical industry’s sins — and the secrets of my family history — matter?

It matters because Stuart and Spencer, now 26 and 24, may want to have families of their own one day. I want to do everything in my power to ensure that what happened to them doesn’t happen to their own children.

It matters because the government is no longer working for the people or public health when a $1 million donation by Dow Chemical to the Trump Inauguration happens to coincide with former EPA Administrator Scott Pruitt rejecting the advice of his agency’s chemical safety experts and reversing the Obama era’s prohibition against agricultural uses of chlorpyrifos. Fortunately, environmentalists and public health advocates were quick to file suit. A federal appeals court has issued a stay effectively banning the agricultural use of the chlorpyrifos until the case is settled. The EPA has appealed the court’s decision and the $800 billion chemical industry lobby will undoubtedly hire the best lawyers money can buy.

It matters because Dow continues to sell chlorpyrifos without proper warning labels in developing nations.

It matters because even though the household use of chlorpyrifos is banned, we are still exposed to chlorpyrifos when it is applied to the grounds around our homes or offices to control for termites. Children are especially sensitive to this type of pest control because they are more likely than adults to play outside and put their hands in their mouths, and because their bodies break down chemicals differently than adults’.

More broadly, it matters because the Trump administration is engaged in an all-out assault on the agencies charged with using independent, evidence-backed science to protect our nation’s public health. Chlorpyrifos is but one example. Lead, arsenic, ozone, beryllium, mercury, and silica are others. The Trump administration should be protecting the public from known and emerging threats to our health, safety, and well-being. Instead, it is loosening EPA, CDC, FEMA, NOAA, USDA, and OSHA regulations. Many in the White House, and in Congress, are supported by the chemical, agricultural, and other business interests.

II continue to search for definitive answers as to whether my children’s brain malformations are related to chlorpyrifos exposure. And while I may never have proof, I know this much is true: It is dangerous for pregnant women and children to come into contact with chlorpyrifos.

I can’t change what happened to my own children, but by sharing my family’s story and the findings of my research, I can alert an unsuspecting and vulnerable public to everyday invisible hazards — and the dangers of a government that overlooks them.

An earlier version of this story appeared here.

Essays, anthologies, and memoirs, oh my!!

Get the Medium app

A button that says 'Download on the App Store', and if clicked it will lead you to the iOS App store
A button that says 'Get it on, Google Play', and if clicked it will lead you to the Google Play store