Living Downstream

I first learned to see air when an art teacher began coming to our grade school. Of all the ideas she introduced, none made more sense to me than the concept of the vanishing point—an invisible place on the horizon where parallel lines mysteriously converge. Simply by choosing a point and drawing in perspective a house or a road, I could draw air. This was a great discovery. And the Illinois landscape was full of such points through which all objects seemed to be striving to disappear. Grain elevators along a railroad track. A plowed field. The silver towers and looping cables of high-power lines. Everything eventually vanished into air.

What I never figured out was how to represent air’s transformative properties. In rural Illinois, how objects appear depends on how much air they are viewed through. A brown chip in the sky turns, a half-mile closer, into a circling hawk. Fluttering black specks turn into black handkerchiefs and then into a flock of crows. The dead body on the side of the road eventually becomes a scrap of carpet.

In the fifth century B.C., the Greek philosopher and physiologist Empedocles declared that the atmosphere was not a void but a living substance. A thousand years later, his theory was animated by Paracelsus himself (of “dose-makes-the-poison” fame), who professed that air was inhabited by elemental beings he called sylphs. I am thinking of these two scholars while driving through central Illinois during a period of record-breaking cold. It is many degrees below zero—dangerously cold—equipment malfunctioning, cars seizing up, and hourly warnings against venturing outdoors issuing from the radio. I should not be out myself, but it seems important to see the landscape at its most unmoving: Its constituent molecules vibrating at their slowest recorded speed. The earth with all its seeds frozen down to many feet. Water only a memory.

Leaving the engine running, I step from the car onto the stone floor of a cornfield. Only the atmosphere seems alive. Every inhalation brings pain, every exhalation a puff of crystals. Whatever sylphs are, they instantly find the cracks between scarf and collar, glove and sleeve. In seconds, I am exposed, although still standing fully clothed. And yet never is this element more invisible. Even objects at the vanishing point seem distinct and permanent, untransformed by miles of air.

Far from Illinois, the White Mountains lie across upper New Hampshire like a crooked crown. Their westernmost peak, Mount Moosilauke, rises above a tract of trees familiar to every student of ecology, the Hubbard Brook Experimental Forest. Here, researchers have used large-scale, long-term field studies to trace the slow cycling of nutrients through an entire living community. Much of what we know about the ecological pathways of nitrogen, phosphorus, and calcium, for example, derives from work carried out in these woods. Some of the first investigations of acid rain were conducted here as well.

A research team led by the biologist William H. Smith of Yale University discovered something else about the forest floor of the famed Hubbard Brook. Its newly fallen leaves and needles, as well as the composting earth beneath, contained detectable amounts of both DDT (0.8 pounds per acre) and PCBs (2.3 pounds per acre). Even more remarkably, neither of these long-banned chemicals had ever been used, distributed, or produced in the immediate area where the samples were collected. Soil and leaf litter sampled from nearby Mount Moosilauke were found to be likewise contaminated—all the way up to its tundra-covered summit. Tellingly, the level of contamination rose with elevation and was greater on west-facing slopes. Such patterns are consistent with atmospheric deposition.

Smith and his colleagues thus postulated that molecules of DDT and PCBs were being carried into Hubbard Brook by prevailing winds. Their origin, however, remains obscure. Storm tracks that pass over major centers of agriculture and industry in the United States also pass frequently over New England. Quite possibly, regional air masses are spiriting these semivolatile, long-lived molecules from landfills, dump sites, and farm fields to this remote, pristine forest. It is also possible that global air currents are the transporting medium. Like undocumented aliens, these chemicals may have been swept in from other countries, even other hemispheres. Studies conducted in rain-fed bogs across eastern North America support this possibility. These peculiar habitats receive all their input of pollutants from the atmosphere, and not from ground or surface water. Therefore, they function as a living map, revealing in detail the historical and geographical contours of atmospheric deposition. And because peat preserves organic compounds almost completely, they also function as living archives.

More evidence for the role of global circulation comes from the world’s trees. A survey found traces of twenty-two different organochlorine pesticides—including DDT, chlordane, and endosulfan—in tree bark gathered from ninety different sites around the globe. Bark is a remarkably oily tissue and therefore readily absorbs oil-soluble pollutants from the air. That trees growing in the agricultural regions of the midwestern and eastern United States should bear residues of pesticides in common use there is hardly surprising. However, researchers also found insecticides in trees growing in the Arctic. And they also found them in the bodies of the people who live there. Indeed, the highest concentrations of the most villainous chemicals of the twentieth century are inside the bark, blood, and tissues of the organisms living the farthest from the sources of these chemicals. This phenomenon is known as the Arctic Paradox.

As described by journalist Marla Cone in her 2005 book Silent Snow, this paradox is explained by a form of chemical nomadism called global distillation. When persistent organic pollutants are released in warmer climates, they evaporate and are carried by winds to cooler areas, where they condense and descend back to earth. These trespassers overwinter in soil, snow, or water. When the summer sun revaporizes them, air currents blow them further toward the pole. They then drift downward once again. During this process, the various chemical contaminants are spatially partitioned: those substances that evaporate at the lowest temperatures keep revaporizing and are thus continuously drawn to northern latitudes and higher altitudes. Finally, in the Arctic, they can ascend to the skies no more, and this is how the most pristine corner of the earth has become the most chemically contaminated. The rising and falling movements of global distillation explain not only why chemicals used in rice paddies eventually end up in the skin of Arctic trees but also why fish in Yukon Territory’s Lake Laberge became so full of carcinogenic toxaphene—a pesticide used in cotton fields—that the Canadian government was forced to ban angling there. Global distillation also explains why, during negotiations for the United Nation’s Stockholm Convention on Persistent Organic Pollutants, the most powerful testimony came from a delegation of Inuit mothers. They spoke about ecological genocide.

The phenomenon of global distillation shows that not all of the dangers from carcinogens in our air supply come from breathing. Some also come from eating. Poisons dumped and plowed into the earth are released, molecule by molecule, into the air, where they redistribute themselves back to the earth and into our food supply. In short, because of air, we each consume suspected carcinogens released into the environment by people far removed from us in space and time. Some of the chemical contaminants we carry in our bodies are pesticides sprayed by farmers we have never met, whose language we may not speak, in countries whose agricultural practices may be completely unfamiliar to us. Some of the chemical contaminants we carry with us come from long-defunct products of industry—objects manufactured, used, and discarded by people of a previous generation. When we sit down to eat a meal of, for example, freshwater fish, we are linked to all these people through the medium of air.

Conversely, chemicals dumped and sprayed in our own neighborhoods, fields, and landfills have drifted to distant territories and found their way into the diets of the people who live there. I sometimes think of this multitude of connections while walking through Illinois corn and bean fields. I wonder where the chemicals sprayed in these fields when I was growing up here now reside. On what mountainside, in what forest or lake bottom, in whose bodies do they lodge now?

Of all the toxic chemicals released by industry into the nation’s environment in 2007, more than one-third was released into air. These emissions include ninety-one million pounds of known or suspected carcinogens. When vehicle exhaust is added to the mix, air’s burden of carcinogens grows larger. According to the International Agency for Research on Cancer, ambient air in cities and industrial areas typically contains a hundred different chemicals known to cause cancer or genetic mutations in experimental animals. And while air pollution in the United States has improved since the Clean Air Act of 1970, 60 percent of Americans—186 million of us—live in areas with unhealthful levels of air pollutants.

These are facts not in dispute. How much airborne carcinogens actually contribute to human cancer, however, remains an elusive question. Air can evade the rigors of scientific analysis through at least three means. First, its fluidity makes exposure very difficult to quantify. Wind speed and direction, as well as wind flow along river valleys, over hills, and around buildings, significantly alter the transporting path of airborne carcinogens. Residents of a single metropolitan area may all drink water from the same river and buy their food from the same supermarkets, but they may not all breathe the same air. Those who live downwind from the local industrial park may live in a very different atmosphere than those who live upwind. A centrally located air-monitoring system cannot account for differences in microclimate.

Secondly, there exist whole classes of air pollutants that we do not even attempt to monitor at all. Chief among these are fine (less than 2.5 micrometers) and ultrafine (less than 100 nanometers) particles. Some are so small that an electron microscope is required for viewing them. Fine and ultrafine particles are nevertheless visible: they are the haze that blurs the sunlight of a summer day. Well, not exactly. What we are seeing are not the specks themselves but the scattering of light waves they cause. Far more dangerous when inhaled than gritty generic particles, fine and ultrafine particles can slip past the defenses of the lung’s cilia, glide straight through lung tissue, and enter the bloodstream. Here they can have many effects. Making blood platelets sticky is one—and is probably the mechanism by which fine and ultrafine particles contribute to heart disease.

In spite of their vanishingly small size, fine and ultrafine particles come in many varieties. They may sport highly complex architectures or be as simple as dots of elemental carbon (soot). And particles need not be solids. Many take the form of superfine droplets. Some are combinations of different liquids within a single droplet. Some are solids wrapped with liquid jackets. Some are liquids suspended inside solids—like chocolates with a liqueur center. Fine and ultrafine particles can be metals, oils, acids, hydrocarbons, or all of the above. They are mixtures of mixtures. The EPA regulates particles above 2.5 micrometers but does not attempt to regulate the fine or ultrafine ones. They are simply too hard to measure.

The third reason for uncertainty is that air is a transmutational medium. As in an alchemist’s flask, the atmosphere concocts new materials from the ingredients placed into it. Recent evidence suggests that some of the major carcinogens in air are synthesized when organic chemicals released from various sources react with each other and are transformed into entirely new substances. Many may not even be identified yet. Currently, a team of U.S. and Chinese researchers are looking at air pollutants that may be morphing into carcinogens on their way across the Pacific Ocean from Asia to the United States. Thus, a simple laundry list of air emissions—such as the Toxics Release Inventory—cannot account for the presence of all the cancer-causing agents to which we are exposed.

Of these various pollutants that appear, literally, out of thin air, the most notorious is ozone. This molecule is created naturally up in the stratosphere from the interaction of ultraviolet radiation with oxygen. The resulting layer of ozone protects us from excessive UV exposure, and, thus, with good reason, we concern ourselves with its disappearance. At the earth’s surface, however, ozone is a noxious, unnaturally occurring irritant to eyes and lungs. With equally good reason, people who live in cities during the summer concern themselves with rising levels in its daily parts-per-million concentration. (Molecules of ground-level ozone are too heavy to rise into the upper reaches of the atmosphere and take the place of their faltering compatriots, upon whose presence all life depends.)

Although it’s a major ingredient of urban smog, ground-level ozone is not emitted into the air by a known polluting source. Instead, it’s created when sunlight catalyzes a reaction between two kinds of vapors: nitrogen oxides, which are emitted from tailpipes and smokestacks, and volatile organic compounds, which rise into the air when houses are painted, cars refueled, roads paved, and clothes dry-cleaned.

In the classic sense of the word, ozone is not a carcinogen. Nevertheless, in the complex unfolding of cellular events that typifies carcinogenesis, ozone seems to play a supporting part. A powerful poison, ozone causes inflammation of the airways and thereby interferes with the body’s ability to sweep foreign particles—some of which may be carcinogenic—out of the lungs. Ozone also hampers the activities of the lungs’ macrophages. Part of the immune system, these amoebalike scavengers offer a first line of defense against a variety of pathogens and foreign substances. In studies of laboratory animals, ozone appears to magnify the effect of other lung carcinogens and influence the carcinogenic process itself. Lung tumors in ozone-exposed mice have distinctly different genetic mutations than do those from mice that have breathed clean air.

In the attempt to understand how substances in air may contribute to cancer, the issue of ozone raises some vexing questions. How do we assess exposure to airborne pollutants that emerge from chemical recombinations of other airborne pollutants? How do we quantify the cancer-causing potential of a substance that enhances the cancer-causing potential of other substances? How many cancer deaths do we chalk up to ozone? What is the body count?

The most recent estimate we have of cancer diagnoses attributable to air pollution derives from a 2009 EPA investigation called the National Air Toxics Assessment. Although it does not take into account the questions raised above, this report looked closely at air contaminants within all counties within the United States and concluded that all of us—all 285 million U.S. residents—have elevated cancer risks from exposure to air pollution. This risk is not evenly distributed, however. Counties within southern California, Ohio, West Virginia, and parts of Indiana and Illinois had significantly higher risks for air pollution-related cancers than, say, North Dakota. The average of the estimated risks from all the 500 counties within the United States is 36 in a million, meaning that for every one million of us, 36 people will contract cancer from breathing. The EPA researchers didn’t carry out the math any further, but I will. Thirty-six times 285 is 10,260 cancer patients.

With a five-year survival rate of only 15 percent, lung cancer is so swiftly fatal that we rarely hear stories of its victims. While those diagnosed with breast cancer form support groups, write books, lobby Congress, and organize rallies, gala benefits, and races-for-the-cure, those with lung cancer tend to vanish quietly from our midst. The small public presence afforded them is usually a posthumous one. Guilt and blame also silence lung cancer patients, who are seen as having brought about their own misfortune.

Whether we hold individual consumers or corporate producers responsible, the primacy of tobacco in the epidemiological portrait of lung cancer is indisputable. Smoking is the dominant cause of lung cancer. Nevertheless, there is more to the story of lung cancer than cigarettes. If other factors seem minor in comparison, it is only because tobacco is such a major killer. But lung cancer among nonsmokers is the sixth most common cause of cancer death in the United States. Not all of these deaths are cigarette independent. About 20 percent (three thousand deaths each year) are thought to be attributable to secondhand tobacco smoke. So shocking is this statistic that it has rightfully prompted substantive changes in laws governing smoking in workplaces, airplanes, restaurants, and other public domains. However, the majority of nonsmoking lung cancers remain unexplained. While air pollution is not the only possible cause, it is one that unavoidably affects us all, and it is one that may interact with and potentiate the effects of other factors. On these bases alone, this topic deserves thoughtful inquiry. Several lines of evidence suggest its role may be significant.

The first comes from doctors’ offices. Oncologists who specialize in lung cancer are reporting increasing numbers of nonsmokers among their patients, as well as increasing cases of a specific kind of lung malignancy not strongly associated with tobacco in men. Called adenocarcinoma, it is distinguishable from oat cell and squamous cell carcinomas, both strongly linked to smoking.

Meanwhile, epidemiologists have been focusing on understanding the urban factor in lung cancer. Studies from the United States and Europe consistently find higher rates of lung cancer among nonsmokers living in urban areas than among those living in the countryside. Areas with chemical plants, pulp and paper mills, and petroleum industries also show elevated rates of lung cancer. Truck drivers and other workers who inhale diesel exhaust on the job have higher rates of lung cancer. And a cohort study of five thousand chimney sweeps in Sweden found increased mortality from lung cancer and other tumors that was not explainable by smoking habits but that was related to exposure to carcinogenic soot. In Utah, where smoking rates are very low, researchers compared lung cancer rates in two counties that were similar in all respects, except that one them then became home to a steel mill. Initially, lung cancer rates were indistinguishable, but, within fifteen years, cancer mortality in the now-polluted county was higher. On a larger scale, a prospective study of nearly a half-million U.S. residents found that the risk of death from lung cancer was higher in parts of the country where density of particles in the air was higher.

As ports of entry, the long tunnels and spongy rooms of the lung are only the first place where airborne carcinogens meet human tissues. Those carcinogens absorbed across the lung’s membranes are carried in the bloodstream and deposited throughout the body. Much less is known about the relationship of these contaminants to other forms of cancer, but the question is provoking increasing interest.

By-products from the burning of fossil fuels are under particular suspicion. Breast cancer, as we have seen, was first linked to potential sources of air pollution in Long Island. Subsequently, associations have been found between exposure to traffic exhaust during puberty and risk of early-onset breast cancer. Perhaps not coincidentally, a growing body of evidence suggests that tailpipe emissions have estrogenic activity. Air pollutants may also alter breast density in ways that raise the risk for breast cancer. A 2007 review of the literature concluded that the risk of breast cancer associated with exposure to engine exhaust and other aromatic hydrocarbons is roughly equivalent in magnitude to some of the well-known and well-established risks for breast cancer, such as late age at first childbirth and sedentary lifestyle. Corroborating evidence comes from the laboratory: members of a chemical family of combustion by-products called aromatic hydrocarbons—of which benzo[a]pyrene is one—cause breast cancer in animals. According to researchers at Albert Einstein College in New York, aromatic hydrocarbons inhaled by the lungs can become stored, concentrated, and metabolized in the breast, where the ductal cells become targets for carcinogens.

Bladder cancer, too, has been linked in several studies to air pollution. The strongest evidence comes from Taiwan, where researchers found positive associations between air pollution, especially from petrochemical plants, and the risk of dying from bladder cancer. An investigation of bladder cancer deaths among children and adolescents in Taiwan found that almost all those afflicted lived within a few miles of three large petroleum and petrochemical plants.

Closing a lethal circle, air pollutants have also been implicated in promoting the spread of cancer from other organs to the lung. For example melanoma-afflicted mice who breathed air polluted with nitrogen dioxide developed more tumors in their lungs than those who breathed clean air. They also died sooner. Not lung cancer per se, these tumors are metastases, secondary growths from cancer cells shed from the original tumor. They are carried by the blood to the lungs, where, like planted seeds, they take root. As cancer patients know, metastases to the lung are an ominous sign. The first capillary bed encountered by blood leaving most other organs, the lung is the most common place for cancer metastases to take hold. And somehow—at least in mice—breathing nitrogen dioxide seems to facilitate this process.

The pathologist Arnis Richters, of the University of Southern California, believes that at least two sinister mechanisms are at work here. First, nitrogen dioxide impedes so-called killer T cells, whose function, among others, is to rid the body of wandering tumor cells. Second, nitrogen dioxide causes blisters to form deep in the lung’s airy chambers, where such errant cells can then become trapped. “Since many cancer patients have circulating cancer cells,” says Richters, “it is possible that noxious air pollutants may play a more important role in dissemination of cancer than is realized at the present time.”

I am driving through my favorite section of town, the old neighborhood north of the post office. It was Pekin’s original town site, but I like it for a different reason. All the east-west streets have women’s names, and not just ordinary ones: Cynthiana, Henrietta, Sabella, Caroline, Catherine, Matilda, Lucinda, Amanda, Charlotte, Susannah, Minerva, and the one I, as a child, most revered—Ann Eliza. All of these streets dead-end at the river.

I have my sister’s two sons in tow, and we stop to pick up treats at Patsy’s Bakery. It is a Sunday morning at the end of February, the first warm day in months. The church parking lots are all full. We head for the river, zigzagging as we go so we can hit all the girl streets. As we do, the smell that is almost always present here gets stronger. I’m half thinking about the research papers I’ve been studying.

I have thought a lot about how to describe this smell, but I cannot. I can smell it more acutely now than I could when I lived here, although it is probably less potent than in earlier decades. It is still too familiar for words. A complicated smell, it seems to contain more than one odor. It is . . . pungent. After watching the barges and the fishing boats for a while, we swing onto Route 9 and head over the Pekin bridge.

On the west bank of the Illinois, the floodplain spreads out like a dance floor in a pool hall. It’s mostly corn and bean fields now—all the way up to the power plant and the coal piles and the access roads and the railroad yards and the bait shops. I love this river valley and the bluffs that rise above it, the backdrop of my childhood. I want the boys to love these landscapes, too—but with full knowledge rather than denial, in the terribly difficult way that one is asked to love alcoholic parents: not abandoning them to wretchedness, not enabling their self-destruction, not pretending there is no problem. I don’t know how to explain this to my young nephews, but maybe I don’t have to. Maybe we adults need only demonstrate an attitude of passionate attention about where we live.

“Let’s check out the west bluff.” I turn right onto Route 24 and then left onto a narrow side road, steep as any mountain grade, and downshift. Even in second gear the car stutters, and what’s left of our doughnuts tumbles backward into our laps. Suddenly, we are in thick woods that draw a curtain on the river’s floodplain behind us.

At the top of the ramparts, we emerge back into the sunlight and find ourselves in Tuscarora, an unincorporated scattering of homes that follow the topographical contours of the bluff. These eventually give way to more corn and bean fields—a mirror image of the east bluff. Not so, claim my two companions, who believe the west bluff is hillier and therefore more fun to drive on. I’m not persuaded, but it’s a good argument.

In the nineteenth century, many good people—medical doctors and officers of the government among them—believed that infectious diseases were brought on by bad air. These were followers of the miasma theory of disease causation. Air was thought to be “corrupted” when it passed over decaying organic matter—swamps, sewage, dead bodies. Breathing the poisonous odors emanating from such places was, according to the miasma school of thought, injurious to the body and had the power to trigger terrible physical maladies.

The miasma theory was eventually supplanted by its rival, the germ theory. But before its drift into obscurity, miasma’s disciples managed to usher in significant reforms in public health policy, namely, closed sewage systems, clean drinking water, and deep burial of the dead. These did much to deter epidemics even before the real, microscopic causes of disease were discovered. The miasma theory, although mistaken, saved many thousands of lives.

I follow Route 24 east over the McClugage Bridge. Here the river is nearly three-quarters of a mile wide, and at the exact center we cross from Peoria back into Tazewell County. This border fascinated me as a child. A line in the middle of a river! How did they know exactly where it was? Stories about my childhood are fascinating to my current company, including my old fear of drawbridges and my enchantment with tugboats. And the fact of their fascination fascinates me. This is where we come from.

Still, I wonder if I should be bringing the boys down here at all. The younger one has asthma—as does his mother, who developed it as an adult. A secretary at the local grade school, Julie is astonished, she says, at the number of children with inhalers in their backpacks. On the days that she must send unusually high numbers of wheezing children home from school, my sister has begun to take note of what the weather is like, which way the wind is blowing, how the air smells, and how labored her own breathing is. Perhaps it is once again time, we both agree, to look at the environment to understand what ails us. Perhaps it is time to risk being right for the wrong reason—as did our predecessors who successfully prevented the spread of infectious disease by cleaning up pollutants in the absence of complete knowledge about the microbes they contained.

Increases in childhood asthma and the clustering of lung cancers around cities with dirty air are telling us something. Suppose we do nothing until the exact mechanisms are elucidated, until exposures are definitively ascertained, until the precise combination of air pollutants and their specific interactions with each other and with the tissues of our respiratory airways are exhaustively understood. Then are we not mimicking those who, at one time, could just as well have claimed that there was not sufficient reason—on the grounds that science had not yet identified any specific biological agent responsible for cholera—to keep human excrement out of the drinking water?