09/13/2009 07:01 pm ET Updated May 25, 2011

Dangerous Hours: Toxic Tap Water and the Fetus

Thanks to the New York Times, it seems we're beginning a national concern about toxic water, a fearsome chapter in our national Book of Devils -- toxic air, toxic food, toxic life styles, and now toxic drinking water.

Of course the people who hawk for various industries will tell us it's all a mirage, just eat, drink, and be merry -- keep the cash registers ringing and all will be well. Regulation by government? Forget about it. That's socialism, they tell us. The hawkers hawk the mantra even when their own children are at risk. That's the way it is, our American insanity.

So far the focus is on children already born, hardly a word about the unborn, the embryos, the fetuses, the most vulnerable of the vulnerable. Yes, the embryo and fetus are extremely vulnerable, and the consequences are chilling.

The human egg cell (ovum) is the largest cell in the body, on average 145 microns in diameter (average human hair width is 100 microns, or 0.1 millimeters), which means it's visible to the naked eye. The ovum is about 15 times larger than ordinary cells, such as skin cells and liver cells, but it's still no larger than a dot, smaller than the period at the end of this sentence. The profound glory of human reproduction, the wonder of wonders, is that under the right circumstances over about 277 days of gestation, this biological dot is capable of turning itself into a 7-pound infant ready to scream at you to look smart and give it some food and attention.

But why is prenatal development so vulnerable to damage?

With the fusion of a sperm cell and an ovum at fertilization, the phase of the human life cycle of prenatal development starts the long and wondrous journey from a single cell (the ovum) to the trillions of specialized and organized cells of a new individual at birth. What we're looking at is a cascade of many thousands of events, a cascade with special vulnerabilities at special times -- and the possibility for several vulnerabilities at any single time. A cascade is a succession of sequentially interdependent events, each event both triggered by the event preceding it and itself acting as a trigger for the next event. But the cascade of prenatal development is more complicated. It involves not only multiple events occurring and interacting at any instant before the next set of multiple events is triggered, but also multiple interactions with the local cellular environment. And these local interactions can themselves be necessary triggers in the cascade. The ovum starts with a genome. Throughout development, as the number of cells derived from the ovum continues to increase, the genome in each cell is the same, but which genes are turned on (expressed) changes in time, producing specialized (differentiated) cells or new triggers for subsequent events -- release or take-up of special biochemical entities, rearrangements of cells into tissues and organs, migrations of cells to new locations in the developing embryo and fetus, appearance of specialized cell organelles, and so on.

The cascade of development is essentially chemical, involving not just a few kinds of molecules but hundreds of thousands of kinds of molecules, organizing, rearranging, moving from one place to another, enhancing (catalyzing) the synthesis of themselves and other kinds of molecules. The kinds of molecules in the cascade are so numerous that we've hardly yet catalogued even a small fraction of them. Biochemists estimate that a single cell may contain as many as a hundred thousand different proteins, carbohydrates, and lipids, and no one anywhere has yet identified more than a small fraction of that number. The cascade of prenatal development is thus a cascade of gene expression events, chemical events, and cellular events -- and the whole mix moves forward by both internal triggers and triggers brought about by interactions with the local cellular environment.

So the first important cause of prenatal vulnerability is complexity: the sheer complexity at many levels of prenatal development means that an enormous number of different and important process points are available for disruptive effects.

Another important cause of prenatal vulnerability is pace, the high rate of cellular proliferation necessary to transform a single microscopic cell (the fertilized ovum) into a 6- or 7-pound newborn infant consisting of trillions of cells specialized and arranged to constitute the human body externally and internally -- albeit in the small of the infant. For example, it's estimated that in the developing brain and nervous system of the prenatal human, about 250,000 new neurons are generated each minute at the peak of cell proliferation during gestation.

The high rate of cell proliferation means a high rate of metabolism, chemical synthesis, cellular rearrangements and migrations, conversion of maternal nutrients into fetal cells and tissues, and so on. In prenatal development, everything is happening rapidly. If any special process has its rate changed up or down by an unscheduled impact with the local environment, the consequence may be anything from a subtle bending of development in one direction or another to a lethal corruption that kills the embryo or fetus. In general, the metabolism of embryos is different from that of adults, and the fetal construction of an organ can be affected by chemicals that have no apparent damaging effect on the normal adult functioning of that organ.

The third major cause of prenatal vulnerability involves size and simple physics. If a small permeable mass -- a cluster of cells, for example -- is exposed to a chemical, that chemical can reach all parts of the mass quickly by simple random diffusion. With larger masses, the diffusion time to reach all parts increases dramatically. But as late as the 6th week of gestation, the human embryo is still only a quarter of an inch in length and has no developed circulatory system, and any freely permeating chemical that gets into the embryo by any route will quickly diffuse throughout the embryo to affect every embryonic cell. Throughout the embryonic period, until the 10th week of gestation, the situation is not much better. At the 10th week--when we begin to call the developing embryo a "fetus" -- we're dealing with an embryo/fetus only about two inches in length, indeed recognizable as a vaguely human form, but still small enough for simple diffusion to quickly distribute any permeating chemical entity throughout its body.

Small size facilitating distribution by simple diffusion is one of the reasons the early weeks of prenatal development are so vulnerable to certain chemical effects. The other important reason is that those early effects can be multiplied as the cascade of development proceeds. For example, there's mounting evidence that a critical window of vulnerability for fetal alcohol spectrum disorder occurs very early--during and shortly after the blastocyst stage--and that alcohol affects early gene expression in the developing embryo. It appears that concentrations of alcohol too low to produce gross morphological disruptions may still cause subtle changes in the connections between nerve cells in the developing brain. Evidence indicates that among the results of those changes are cognitive deficits in children whose mothers drank alcohol during pregnancy.

The high vulnerability of embryos and fetuses to toxic chemicals is known to every biologist on the planet. Maybe now it will be known to everyone else and something will be done to reduce these insidious dangers to unborn children. We will see what happens.

Meanwhile, it seems to me that "pro-life" people who shout concern for the unborn ought to be marching in the streets demanding free prenatal care for every pregnant woman, and also demanding local, state, and federal regulations and protections against the mangling of fetuses by toxic environmental chemicals. Until that happens, maybe "pro-life" is an exercise in hypocrisy.

(Portions of the above text are adapted from Dan Agin: More Than Genes: What Science Can Tell Us About Toxic Chemicals, Development, and the Risk to Our Children. Oxford University Press. October 2009.)