No one has ever taken a vacation who took along a baby. You can go out of town with a baby, you can even leave the country or be on the lam with a baby, but you are never on vacation. Mothers who don’t breast-feed usually leave baby with dad or a sitter when they go out of town, but a nursing mother hasn’t any choice. A bottle-fed baby is inseparable only from the nearest supermarket, but a breast-fed baby is inseparable from the breast.
Many women find it easier to keep themselves on hand than to keep the pantry stocked with infant formula. I do. And more and more women are now aware that artificial formula can’t substitute for human milk. Mother’s milk is a great natural resource: it’s in endless supply in a healthy mother, it’s always the right temperature, it costs less than a thousand calories a day to manufacture and absolutely nothing to deliver, and it’s almost always perfectly suited to the consumer.
There is only one flaw in this otherwise ideal consumer product: it is vulnerable to contamination. And because of that, I took a trip—not a vacation—with my four-month-old nursing baby to a pesticides laboratory in South Texas to find out if my milk contains something it shouldn’t. Nothing less could have prodded me to travel with a baby.
The Human Milk Study has thirteen laboratories across the country, one of them in Texas. The study, the second of its kind (the first was done in 1975-76), is monitoring the incidence of seventeen substances—sixteen pesticides and one industrial pollutant (PCB)—in mother’s milk samples across the nation. The study’s purpose is to identify any pesticides that might be approaching dangerously high levels. The labs do not take unsolicited samples as part of this study, but the Texas lab, under the guidelines of another of its projects, works with people who suspect they have a pesticide problem. Since they are equipped to analyze milk, they accepted my sample. They could tell me what I wanted to know: did my milk have high levels of pesticides?
What I had read recently led me to believe that even I, a fastidious consumer of health food and a confessed coward when it comes to handling so much as a can of Raid, might have picked up some pesticides and that my nursing son might be taking in chemicals that could cause him to develop cancer or some undiagnosable organic or behavioral disorder. A 1950 test showed that 24 women who occasionally used DDT sprays had residues in their milk ranging from zero to 770 parts per billion. (The World Health Organization has recommended 50 ppb as the maximum safe level of total DDT concentration in cow’s milk.) A 1971 test of people in rural Colorado found levels of two DDT derivatives that ranged from 19 to 386 ppb and from 7 to 109 ppb, and a 1972 test from South Carolina found three DDT derivatives almost universally in those tested (it also found high amounts of dieldrin and PCBs). DDT, which was first used in 1936, was banned by the Environmental Protection Agency (EPA) in 1972; however, it is a “persistent” pesticide—a polite way of saying it will be around for a long time.
The report that struck closest to home was made by Patrick O’Keefe, a Harvard chemist working on an EPA-funded project in 1976. O’Keefe was concerned with rangelands, including some in West Texas, that were being sprayed with 2,4,5-T, the defoliant containing dioxin, which is similar to the notorious Agent Orange used in Viet Nam. Dioxin is such a poisonous substance that its toxicity is measured in parts per trillion. O’Keefe found that half the milk samples he took from mothers in San Angelo contained between 0.5 and 1 part per trillion. Safe levels for dioxin in humans have yet to be established, but the chemical is suspected of having caused miscarriages in women in Oregon forest areas sprayed heavily with 2,4,5-T. On the basis of these miscarriages, the EPA imposed an unprecedented ban on 2,4,5-T this year—a sort of “guilty until proven innocent” sentence. However, exemptions to the ban include spraying on rangelands and rice fields, which means 900,000 acres of Texas farm and ranch land will continue to receive seasonal doses of 2,4,5-T.
The Texas Tech School of Medicine’s pesticides laboratory is in San Benito in the Valley, an area whose rural landscape belies a history of heavy, sophisticated pesticide applications to cotton and food crops. The EPA contracted with the lab to participate in the Human Milk Study. Because the pesticides they are looking for—chlorinated hydrocarbons and organophosphates—are lipid (fat) soluble, milk is used for analysis. It is easily available for study but it is not a perfect test vehicle, because it restricts the testing to women and the fat content of milk varies throughout the day and during a feeding.
A larger problem with the study is that it tests for so few substances. Approximately two thousand compounds compose an EPA list of restricted chemicals, of which thirty are pesticides; there are about fifty substances suspended or severely restricted because they are known or suspected carcinogens. All the pesticides, or their derivatives, under investigation in the Milk Study come from one or the other list. In addition to these pesticides, the study is looking for PCBs (polychlorinated biphenyls), a wide-spread industrial pollutant used in transformers, brake fluid, and capacitors, among other things, that has entered the ecosystem through dumping into water supplies.
A friend, also a nursing mother, endured the flight to the Valley with baby and me; this was her first vacation from her daughter, whom she hoped to wean by a gently enforced separation. We were a motherly crew, eating supper at Sambo’s in Harlingen. Discreetly nursing baby Jeff, I tried with one hand to construct and hold together a cheeseburger. Sue Ellen’s chef’s salad somehow failed to live up to my idea of a Rio Grande Valley chef’s salad—it might as well have been from Chicago. It crossed my mind that the lettuce and tomatoes had probably been sprayed with a cousin of one of the pesticides the chemists would look for in my milk the next day.
On Friday, a gray, misty morning, Jeff and I set off for San Benito, six miles from Harlingen. I found the pesticides laboratory on one of the streets that intersected the main boulevard, in a white stucco building. I wrestled baby and carseat out of the car and went in.
I had sent a frozen sample of my milk down to the lab on the plane a couple of days before. When I met Ed Gomes, the director of the laboratory, he was thawing the tiny jar of milk, preparing to show me how the analysis was made. While the milk thawed, Ed sketched the lab’s history for me. He has been with the lab since it opened fourteen years ago. It was then part of the Texas State Department of Health. Texas Tech took it over in 1976 and shortly thereafter the EPA contracted with Tech for the lab’s participation in the Milk Study. The lab, as part of its Pesticides Incident Monitoring Program, also tests the blood, urine, or fat tissue of people exposed to various poisons, people who spray chemicals with tractors and crop dusters, people who load airplanes and trucks. They also check people who have no occupational exposure to chemicals but who may have come in contact with something by accident. While I was in San Benito, Dr. Bill Elliott, one of the lab’s chemists, was called to Crystal City, where a pesticide wholesale outlet had caught fire. Elliott went to collect soil samples from the area and blood samples from the firemen.
Another project—the Prospective Cancer Study—is in the earliest stages of operation and will take years to accomplish its lengthy detective work. The project would isolate people from the Valley with a known twenty-year exposure to pesticides and compare their cancer rate to the greater Texas population. Dr. Leland Parks, the assistant projects director, later explained to me the lab’s involvement in other activities. However, the most obvious one—that is, a follow-up of the medical histories of the children nursed by mothers participating in the Human Milk Study—is still only in the talking stage.
With the preliminaries over, Ed donned a white lab coat and moved Jeff and me out into the lab, where he introduced us to his staff. Vaughn Cox, whom he called his right-hand man, is a round-faced youth with a red Prince Valiant haircut and red Vandyke beard. He was working on testing procedures for 2,4,5-T residues in urine.
“This is where it will all be made clear to me,” I thought. “This is where I’ll get some answers. If my milk has anything in it, if…” I didn’t finish the thought. I shifted the baby to my other shoulder and rocked him. Everything about him—his round littly body, his downy head, and clumsy movements—felt unfinished and uncorrupted. His innocence seemed almost shocking in this harsh and sophisticated place.
Ed Gomes checked to see that the tiny bottle of milk was thoroughly thawed. He weighed out seven grams of milk into a centrifuge bottle while I looked for a chair, settled in, and began to nurse my fussy baby as inconspicuously as circumstances would allow. Most of the sample would be examined for chemicals, but a small part would be used to determine the percentage of lipids in my milk. The lipid content is important because the pesticide residues—“if any,” as Ed reiterated—would be measured against the lipids in the milk. He added acetone to the bottle, then put it in a centrifuge to separate out the solids.
After taking the sample out of the centrifuge, he filtered the liquid through a separatory funnel, an elegant piece of glassware shaped like an inverted teardrop. What came out of the funnel was a clear-looking acetone solution. “The pesticides, if there are any, are in the acetone now,” Ed explained. “We’ll repeat the whole process two more times to make sure we’ve got them all.” After that, he added a mixture of hexane and water to the solution, shook it, and let it separate out like vinegar and oil. Somewhere in the watery hexane was my milk and the pesticides.
Several other complicated steps followed, then Ed discarded part of the solution, transferred part into other vessels, and held back part for the lipid test. Despite his patient elucidation, I had the impression I was watching a skillfully played shell game: “Your milk is in this flask, and now…it’s in this beaker. Now, in this test tube over here.” All along I was convinced, wrongly of course, that it had been poured down the drain hours ago.
Finally he put a small portion into a glass column to filter out the first of the pesticides. This first “fraction” would contain any signs of dieldrin. He would filter two more fractions, each of which would carry within it a group of chemicals he was testing for. The purpose of this elaborate procedure was to set up the contents of my milk in known sequences so Ed could run them through a machine called a gas chromatograph.
While we waited, Ed extracted a little glass cup from an oven. An almost invisible film coated the glass; that film was the lipids in my milk. The percentage was lower than ordinary, the average being about 3 to 3.5 per cent. Mine registered only 1.7. After some speculation about how I had reared a 21-pound four-month-old on low-fat milk, we decided Jeff either ate too often or else this sample was the watery “fore” milk from the early half of a feeding; the “hind” milk, which is produced late in a feeding, is fattier.
Vaughn brought a small tube of clear liquid—what remained of my milk—into the room containing the gas chromatographs; these machines measure minute amounts of chemicals, then transcribe the measurements onto graph paper. He injected some of the contents into one gas chromatograph and an equal dose into another machine. He would check the graphs from both against each other to verify the accuracy of each machine, and then compare those to the model patterns made by the chromatography of “Standard 10,” a sample made up of known quantities of the pesticides the lab is investigating.
Vaughn held Jeff while Ed and I hovered over the paper as the first fraction rolled off. Ed measured the ink peaks on the graph paper. Something that looked like a pesticide registered on the first machine, but the other failed to match it. “If it’s not exactly the same on both machines, it doesn’t count,” Ed asserted. No dieldrin.
Vaughn gave the baby back to me and “shot” the second fraction. The needle moved slowly over the steady outpouring of paper. No HCB, no Mirex. But a little series of four bumps caught Ed’s attention. He measured their height and the distance between them. Then he checked the pattern forming on the sister machine. They both indicated PCBs. Polychlorinated biphenyls. “The amount is very, very small,” Ed said. By his calculations, less than 11.7 parts per billion. “Remember what I told you?” he asked. “One part per billion, if you can picture it, is one one-thousandth of a teaspoon of sugar in a boxcar full of sand—twenty tons of sand. One teaspoon is about one part per million.” He tried to impress upon me how small an amount that was. It didn’t help.
All I could think of was how careful I am about what I eat and what chemicals I expose myself to, but I should have suspected that no amount of virtuous living could make me immune to some contamination. The insecticides on Ed’s list and the PCBs are old chemicals, still hanging around in the environment, some after nearly forty years. The DDT derivatives are so pervasive that trying to figure out the source of one’s exposure to them is futile. I had been exposed to Western civilization—that’s about as specific as I could get.
I asked Ed and Vaughn to put these unexpected findings into perspective for me, but the analyses of the Milk Study had just begun. They couldn’t interpret for me. I would have to compare my numbers to those of the 1975-76 study. Even then, no one could tell me if the levels in my milk are going to harm my baby. Suddenly I felt too tired and disheartened to wait for the third fraction to play out on the graph paper. My back ached from holding the baby, I had run out of diapers hours ago, and the ink needle on the chromatograph didn’t seem to be moving perceptibly. Ed offered to finish the test that evening and I gratefully accepted his plan.
That night at the Holiday Inn, I lay in bed in the dark, the baby curled up close to me nursing. When I put my sleeping baby in his crib and went back to bed, the first tiny doubt entered my mind. Should I be nursing this baby? Should I give up this dearest of relationships and run out now and buy a can of Similac?
The next morning I found the irrepressible Mr. Gomes looking tired but working away. In blue jeans and a gimme cap with a chemical brand name appliquéd over the bill, he looked a bit more like a Little League coach (which he has been) than a chemist. He showed me the readout for the last fraction: DDE (a derivative of DDT), a little less than 12 ppb. Ed’s youngest son, Michael, called asking for advice about transplanting pepper plants. It gave Ed and me an excuse to talk about his opinion of pesticides.
“I use them,” he told me. “If you’ve ever tried to grow vegetables, you know you need them.” I confessed to using Sevin dust on my own garden. Michael called again. I said good-bye. Ed needed to get back to his tests; I wanted to get back to Austin.
Bad news followed me home. A few weeks after my trip to San Benito, I talked to Ed Gomes on the phone. He was concerned that the low lipid content of my milk may have given us a false reading on the pesticide content. I sent him another sample, this one taken after a feeding, containing milk we hoped would show a higher fat content. It did. The butterfat rose to 3.64 per cent, more than double the previous count. The pesticides residues rose too: p,p′-DDE (50.4 ppb), p,p′-DDT (0.690 ppb, well below the WHO maximum level), dieldrin (2.63 ppb), beta-BHC (6.74 ppb), HCB (0.670 ppb), oxychlordane (2.08 ppb), trans-nonachlor (3.59 ppb), and PCB (35.0 ppb).
My initial reaction was shock. I spent the rest of that afternoon feeling uncomfortable in my body, like some kind of leper. When I finally realized I couldn’t postpone nursing my baby, I decided the only choice was to come to terms with this new information. I talked with Gomes again and he explained how I could mathematically adjust my whole-milk amounts and compare the fat-adjusted figures to those in the 1975-76 Human Milk Study from the Southwest Region, so I started doing some quick division. PCBs were not investigated in the study so I had nothing to go on there. In the other categories, for whatever solace it provided, I didn’t register at the high end of the ranges. If I had to be contaminated, at least I wasn’t highly contaminated. I just hoped it was good enough.
I told my pediatrician at Jeff’s four-months checkup what I had found out in San Benito. He said, “I’d like to tell you not to worry, but, of course, that’s not very practical. You’ll worry anyway. But I can tell you what the American Academy of Pediatrics has to say about pesticides in milk and I agree with them.” What they say is that when mother and infant are healthy, breastfeeding is the preferred form of infant nutrition in the absence of any evidence that low-level pesticide residues present short-term health hazards. They concede that the long-term effects are not known.
That’s the catch: what constitutes a low level and how long is long-term? “High” levels of PCBs, as demonstrated in the Kyushu, Japan, epidemic in 1968, cause chloracne (cola-colored skin), ocular discharge, enervation, hypotonia, apathy, and other even vaguer symptoms in infants. Dioxin’s minute quantities apparently cause liver disease, depression, irritability, miscarriages, and birth defects. But no one has determined the effects of small amounts of DDE, PCBs, HCB, or any of the other pesticide acronyms, whether in infants or in their mothers. And because the traces of these chemicals are so widespread (DDE and PCBs are now the most common pollutants in the world), and my children will undoubtedly ingest or absorb them without any help from me, and because the amounts in my milk are so small, I will continue to breast-feed my baby, although I’ll never feel quite the same about it.
Whenever Jeff has a grumpy day now for no apparent reason, I worry that he might be feeling the insidious effects of those “low-level” residues. Though I have never been a great meat-eater, I have given up even more in an effort to get off the top of the food chain, where the largest concentration of chemicals accumulates. I read labels and reject foods grown in areas of the country that I know are chemical hot spots. But there’s no escaping some contamination—it is irrevocably part of the world my sons have inherited from me.
