CHAPTER SIX

Asthma (and Intergenerational Equity)

WE MOVED. From a log cabin by a beaver lodge to a Victorian house by a fire station. From a frog-filled hollow to a kidfilled village. From cords of wood and a wellhead to a water main and a sewer bill. From a sleeping loft and a back deck to three little bedrooms and a front porch. From a lease to a mortgage.

The only thing that was staying the same was floor space. The new house, like the cabin, was just over a thousand square feet. A cottage, really. And a not entirely charming one. There were broken windows, Edgar Allen Poe–like shrubbery, and dry rot. But Jeff had construction skills. Top on his to-do list was to build, in the branches of the sturdiest of the backyard walnuts, a tree house commodious enough to serve as the rec room that didn’t come with the main house—and private enough to be a hide-out for those with sibling complaints.

Of the two of us, I was the one less filled with elation. Indeed, I’d walked into the real estate closing ceremony preceded by the same sense of teeth-gritting doom that I’d felt while walking to my Ph.D. oral exams. Giving up my life-long identity as a rakish renter felt like a final concession to parenthood. Family life was no longer going to be one big, extended camping trip. But even I could see that, sooner or later, bedrooms would be useful. And, frankly, the middle-of-the-blizzard burn accident had made physical isolation less alluring.

There was one other insight that kept me turning the pages of all the closing documents and signing my name on each one: Life in the woods with two children—one going on six and the other turning three—had increasingly meant life in a car. The ditched, shoulderless road that connected us to the rest of the world not only murdered newts and toads, it carried trucks and a 50 mph speed limit. Nobody could tricycle along it, and trips to obtain groceries, Band-Aids, and cash involved carseat buckles, books on tape, and drive-through windows. I could see where this was going. Every library visit, music lesson, play date, soccer game . . . would involve driving. Living with the foxes and the beavers would increasingly mean operating a machine whose emissions undermined the conditions that foxes and beavers needed to live. The contradiction was hard to justify. So we chose a small home in a walkable village with a bus line that connected us to Ithaca where Jeff would be teaching art (at the school our kids would attend).

The advantages of our new habitat were soon apparent. A sidewalk stretched from our door out to a craggy maple tree and then connected with another sidewalk that headed down the block toward Main Street. Here was a track, upon which the wheels of a stroller could roll, that linked me to coffee, library books, postage stamps, hardware displays, bank tellers, and a bus stop. The fields of our new CSA farm lay within biking distance. So did a state park with a swimming beach and hiking trails. Three blocks away, a music conservatory operated out of an old church; it offered piano lessons and dance classes. The built environment and open spaces surrounding our new house seemed to provide the best elements of both rural and urban life.

I sat on the front porch (spongy floorboards) and grinned. To be sure, the village sidewalks—century-old slabs of stone—were neither plumb nor true, but this was evidence that they had outlasted a generation of street trees whose roots must have lifted them and then, in dying, set them down uncrumbled but askew. Looking at the misalignments, I tried to guess where trees had stood in 1840. From a geologist neighbor, I learned that our sidewalks are a form of shale—the mother of slate—created from marine sediments. That’s when I noticed the marks of a vanished ocean on the walks’ rippled surfaces.

The kids were not interested in geology lessons. They seemed bewildered. Faith especially was lonesome for the cabin and for a particular tree behind it—a cherry—that she considered a special friend. Elijah, too, seemed subdued. He was also coughing. In fact, he had been coughing for a couple weeks now—even before the move. This was not unusual. Whenever respiratory infections blew through our household, it was Elijah who suffered the worst. Long after the rest of us had recovered, he would slog along—colds morphing into bronchitis—and he was sometimes still coughing when the next round of pathogens swept in and the cycle started anew. But this time, he wasn’t sick and seemed to have no other presenting symptoms. Just the cough.

I touched his forehead, and he looked up at me. My chest hurts.

 

Lungs are two vineyards separated by a heart. Inside their lobes, hanging like clusters of grapes from the ends of delicately branching airways, are the lung’s alveoli. Here is where the Earth’s gaseous layer and the inside of our body meet.

It is not a small space. (The combined surface area of all 300 million air-filled alveoli—the estimated average for a pair of healthy, adult lungs—exceeds the total area of our skin by a factor of twenty-five. That’s about the size of a tennis court.) But it is an intimate space. The diameter of a human hair is about 70 microns. The width of the alveolar membrane is . . . one micron. On one side of the micron, atmosphere. On the other, blood. The vanishing thinness of the alveolar boundary is what makes breathing our most ecological act.

The exchange between organism and environment that goes on across that border—within the ribs’ bony cage, behind layers of recoiling elastic fibers, inside the spongy lobules of the lungs—is at once highly protected and terribly exposed. As my old human anatomy textbook notes, respiration provides us with “methods of expressing emotions, such as laughing, sighing, and sobbing.” At the same time, chemical pollutants have greater access to us at the respiratory junction than anywhere else. The substances we inhale into our permeable alveoli—that subsequently enter us—are a function of our energy policy, our systems of transportation, the Clean Air Act, tobacco regulation, trends in home decorating, dry cleaning practices, pest control methods, and laws governing workplace exposures. Big policy issues swirl around the wellspring of laughter, sighs, and sobs.

Because the boundary between environment and organism is an air-water interface, keeping the alveoli inflated is a tricky business. Wet surfaces want to cling together—like pages of a book left out in the rain. To counteract this tendency, special cells coat the alveoli with surfactant. This slippery fluid prevents lungs from sticking together and collapsing during exhalation and allows carbon dioxide to exit the blood plasma through the alveolar membrane and flow into the atmosphere. Moving in the opposite direction, during inhalation, is oxygen, which jumps the alveolar micron, enters the bloodstream, and is quickly embraced by red blood cells. (Less soluble in water than carbon dioxide, oxygen relies on hemoglobin to ferry it around.) Meanwhile, specialized lung cells with janitorial duties wander through the alveoli and sweep up any inhaled debris. They are called, satisfyingly enough, dust cells.

Lungs enjoy a leisurely development. Unlike the heart, they are not needed at all during prenatal life, when the placenta serves as the site of gas exchange, so they take an unhurried approach to getting their anatomical affairs in order. Lung buds sprout during the fourth week of pregnancy. As the tubular airways begin to grow out in all directions, the lungs resemble two jacks in a child’s game. The alveoli do not form until late pregnancy, and the ability to make surfactant comes last of all. At birth, the alveoli must suddenly make the transition from water to air and, like a sky full of parachutes, undergo rapid inflation. The just-in-time production of surfactant allows for this. This is not to say the fetal lungs are collapsed during the aquatic life of pregnancy. They are, as we now know, fully expanded—but full of fetal lung fluid rather than air.

Compared to those who arrive via Caesarean section, babies born vaginally have an easier time of it. The stress of the birth process itself stimulates their adrenal glands to produce glucocorticoids, which, in turn, enhances surfactant production. Stress is not always bad. (As mentioned in Chapter 2, glucocorticoids also play a role in glucose metabolism and cancer prevention. They are a steroidal family of multitaskers.)

Premature babies are the ones caught in the roughest spot. They have far fewer alveoli at the ready, and, if born before 32 weeks, they lack surfactant to inflate the ones they do have. Injections of glucocorticoids can hasten the maturation of lung tissue in preemies, but the speed comes at a cost: Their lungs will ultimately contain fewer alveoli. Thus, with or without steroid treatments, preterm birth is a severe disruptor of lung development. If born too soon, you grow a different pair of lungs than you would if you weren’t. These differences persist into adulthood and increase the risk for chronic lung diseases at all stages of life. And one of these diseases is asthma.

 

Elijah’s delicacy went beyond his lungs. He was prone to eczema, and he’d had a couple of mild but noticeable reactions to routine vaccinations. I’d convinced our family medical practice to spread out the inoculation schedule and administer his boosters one at a time rather than in clusters.

And then, out of the blue, while accompanying his dad on an afternoon of errands, he suffered an inexplicable bout with hives and anaphylactic shock. Thanks to a quick-thinking medical receptionist, who sent Jeff straight to the emergency room after hearing his report (“he’s covered in spots and complaining that his hands and feet hurt”), we’d averted disaster. By the time I joined Jeff in the ER, I didn’t even recognize my own son. His eyes were puffed shut, and his hands belonged to Mickey Mouse.

And so we entered the world of allergists and EpiPens–spring-loaded syringes full of epinephrine that work to counteract anaphylaxis. These would, from here on out, accompany Elijah wherever he went. Hypervigilance comes with this territory, especially since, in our case, the triggering agent was a phantom one. The allergy test results came back inconclusive. As did the pulmonary tests. Although Elijah didn’t exhibit the classic asthmatic wheeze, he certainly had hyperreactive airways. We were told that he might outgrow this. Conversely, it could worsen and develop into full-blown asthma. Or perhaps he had a cough-variant asthma already. Either way, watchful waiting was the byword.

To be on the safe side, we followed the allergist’s advice and eliminated dairy and nuts from his diet. We instituted higher standards of housekeeping. To avoid respiratory infections, we initiated obsessive handwashing rituals and swift quarantines of the sick. I pursued conventional medical approaches. Jeff pursued the alternatives. Thus, in addition to the allergist, Elijah was under the care of a homeopathic healer and a Russian acupuncturist. Gradually, over the span of a year, he seemed to improve. But it was a long time before a case of the sniffles did not always lead, inexorably, to sleepless nights of coughing, croup, vaporizers, and steamy showers. And often enough, it still does.

To parent a child with allergies and asthma is to enter a paranoid and all-consuming world. In this, we were not alone. Many other parents in Faith’s school were living here, too. Jeff, the lunchroom supervisor and after-school coordinator as well as the art teacher, became aware of just how many kids were coping with these conditions. He knew exactly whose names were written on the EpiPens and asthma nebulizers stashed in the nurse’s office. On the front door of the school, a poster of a peanut shell with a slash through it told all who entered, even the preliterate, that children with peanut allergies were members of this community. For a few years, the school not only disallowed peanuts but banned all tree nuts from the premises to accommodate two students with life-threatening nut allergies. Ergo, no lip balm (palm oil). We reflexively read the fine print on the back of hand lotion bottles and boxes of crackers. And breathed secret sighs of relief when those boys graduated.

 

Asthma has its own taxonomy, and many different forms exist. One type is simply triggered by inhalation of respiratory irritants. (Adult-onset asthma is often this type.) By contrast, atopic asthma, like eczema, is a kind of allergy. Which is to say, it’s an inflammatory disorder.

Inflammation—from the Latin, to set on fire—is the least discriminatory part of our immune system. While other elements of immunity bring sophisticated approaches to the surveillance of foreign enemies and devise elaborate sting operations to apprehend them, the motto of inflammation is burn ’em out and shoot ’em dead. When it comes to homeland security, inflammatory immunity is a vigilante mob wholly uninterested in the presumption of innocence until proven guilty. That’s not a bad approach if, for example, you have no skin on your feet. With open wounds, there is no time to sort out the innocent bystanders from the truly wicked. A kill-anything-that-moves credo is useful—up to a point. The problem with go-go inflammatory agents is that they can easily overdo it or head out after the wrong enemy—sometimes mistaking benign things like cat dander for dangerous pathogens. The result is an allergic reaction.

This is exactly what happens with atopic asthma. Following sensitization to some kind of allergen or irritant, the lung’s airways become hyperreactive. Further exposure provokes inflammation, which serves no good purpose at all. Chronically inflamed airways become obstructed and narrow, and breathing becomes difficult. During an asthma attack, the smooth muscles around the airways contract sporadically, constricting airways further. Different asthma sufferers have different triggers. The common ones include dust, dust mites, mold, pollen, pets, gasoline vapors, perfume, and cold air.

What sensitizes the lungs to the triggering agent in the first place? Asthma triggers are not the same as asthma causes. But neither are they independent of each other. Here is where the terrain of asthma gets complicated, and sorting out the causal chain of events is like following a trail through the woods that loops back around on itself.

The weight of the evidence suggests that experiences in prenatal life or infancy can alter the development of both the immune system and the lungs in ways that heighten inflammatory responses. The result, in many people, is asthma. But by what molecular pathway? No one knows, but some evidence suggests that both stress and chemical exposures can be part of the story. Stress can disrupt the developing adrenal gland. Adrenal hormones communicate with that part of the immune system involved in inflammation. They also, as we have seen, play a role in guiding lung development (glucocorticoids). Reprogramming the adrenal gland, which affects both how the developing lung gets constructed and how it responds to allergens, is one of a number of potential influences on lung and immune system development. At the same time, exposure to environmental chemicals can also influence programming of the immune system as well as alter the branching pattern of respiratory airways and the architecture of the alveoli in ways that undermine pulmonary functioning throughout life.

In other cases, a pollutant may aid and abet inflammatory responses. This appears to be the case with phthalates, the plasticizer used to soften PVC. In their ability to incite the infiltration of white blood cells, phthalates fan the flames of inflammation. Lab studies reveal how the phthalate DEHP may act as the agent provocateur of wheezing: When metabolized, DEHP induces the production of an enzyme whose job it is to make inflammatory weaponry out of subcellular materials. In so doing, phthalates issue a treasonous call to arms.

Certainly phthalates are linked to child asthma. In a groundbreaking 2007 study that examined chemicals in indoor air, researchers identified six household activities consistently associated with child asthma: recent painting, renovation, cleaning, and the acquisition of new furniture, new carpets, or new wallpaper. Digging deeper, the team discovered that two chemical suspects were repeatedly found at the crime scene: formaldehyde (an airway sensitizer that is found in textiles and in the glues holding particle board together) and phthalate plasticizers in house dust. These results corroborated an earlier Swedish study that had uncovered an association between asthma and phthalates in children’s bedrooms: The higher the phthalate levels, the higher the risk for asthma.

Because phthalates are hormone disruptors as well as respiratory irritants, the Product Safety Improvement Act, passed by Congress in 2008, now bans six types of phthalates from children’s toys. But this law does not protect children from phthalates leaching from flooring, carpet backing, or wallpaper, for example, nor does it offer them protection during prenatal life, which would require limiting exposures of their mothers.

 

The upside of renting is that is allows for blithe inattention to large parts of one’s surroundings. Like bathtub tiles. It doesn’t matter if they are too fussy, too retro, too pink, or exactly reflective of one’s taste in home décor. Because you can’t change them anyway. And there is no danger that anyone else is going to read into the tilework a statement about your stylistic sensibilities because . . . you are a renter! When I held a lease, I could safely ignore the furnishings and go back to whatever paragraph I was working on. Or head outside for a run. Or plan a camping trip.

Inattention had been my lifelong approach to many objects around me: flowerbeds, shrubbery, mailboxes, crown molding, newel posts. (Newel post. That was a new term for me.) But suddenly, as a homeowner, I had to have opinions about everything. Was the light fixture above the dining room table to my liking or not? More to the point, why did it flicker when the kids jumped on the beds?

Worse than figuring out stylistic preferences, I was now responsible for the maintenance of every damn thing. I had never before in my life examined a fuse box with a flashlight. Or peered into soffits. Or cared about the pitch and capacity of gutters and downspouts. Or wondered if the venting system for a sump pump was up to code or not. (Not was the unfortunate answer to that query.) Our semiruined carriage house, which, in my renting days, I might have appreciated as a Romantic object of decay, was stressing me out. And its surly inhabitant, a raccoon with an attitude problem, I viewed as an agent of entropy. In some hidden way, it was undoubtedly hastening the decomposition of the foundation. Surely, the homeowner thing to do was evict the raccoon. But I didn’t.

Then I realized the obvious: Having responsibility for our surroundings allowed Jeff and me to align them with ecological principles. Heat. Light. Food. Waste. I now possessed much more control over their cycles and flowcharts. In fact, I could redesign the household—not with the fantasy of creating an organic pod within an otherwise toxic world but with the aim of running a laboratory, an incubator for sustainable ideas.

In this, Jeff was way ahead of me. He had prior experience gutting rooms and repurposing them—albeit with different ends in mind—because he had once worked as a contractor for a highend decorator. His clients wanted wine cellars and wainscoting and had decided opinions about wine cellars and wainscoting. So Jeff didn’t believe me when I announced that I had no opinions whatsoever about doorknobs. (The one in the bathroom had come off in my hand.) He was right. As he described to me the many ways by which doors could open and close—and in which heat, light, and children flowed through doorways—I realized I did have opinions. I just never knew I had them.

Our approach to home renovation was to pay cash. That meant making changes gradually. It quickly became apparent that there were different categories of work competing for our money and Jeff’s time. There were things that would make the house more energy efficient—and contribute to future environmental goals—and there were things that would contribute to the current health, safety, and happiness of the occupants. Devinylizing the house—which would improve indoor air quality for Elijah and protect us all during (God forbid) a house fire—fit into the latter category. Insulation and window replacement, the former.

Stripping the walls of vinyl wallpaper was a cheap, fast, and easy decision, as was ripping out the vinyl-backed carpeting. But replacing the vinyl kitchen floor was deferred for a while out of a need to capitalize a project from category one: The replacement of a fickle and wildly inefficient boiler, which the plumber said dated back to the Kennedy administration. (When I relayed this news to my tax accountant, he responded blandly, “Well, at least it’s a Democratic boiler.”)

Time passed. Finally, during a summer vacation, we got to the kitchen floor. Having sent the kids to the tree house and me to my office, Jeff began the work of ripping out the PVC tiles. He soon called me to take a look. Under the floor he was removing there was another floor and under that one, still another. The middle layer was a handsome, black and speckled tile floor that, Jeff guessed, dated back to the 1930s. I conjectured that it might be real linoleum. We imagined for a while what the kitchen might look like if we simply restored it. But the more Jeff excavated, the more we could see how damaged it was. By the basement stairs, a big swath of it lay in shards. Those broken pieces allowed us a glimpse into what appeared to be the original floor—a green-painted, wide-planked wood floor. Hardwood maybe. We looked at each other. That could be nice. Jeff said that he would crowbar up the top two layers of flooring and call me when he was finished.

Back in my office, listening to the sound of floor demolition, I began to wonder if the street were being repaved. I smelled asphalt but couldn’t see any dump trucks up or down the block. Then something clicked in my mind. Asphalt tile. It was a type of early synthetic flooring manufactured in the first half of the twentieth century. I had read about it while researching the history of PVC. So I typed “asphalt tile” into an online encyclopedia for building inspectors, and up popped a photograph of what looked exactly like the speckled black floor in our kitchen. And under the picture was a warning: If uncovered during a renovation, this flooring should not be disturbed as it may contain up to 70 percent by weight asbestos fiber.

Asbestos. The mineral with jagged, microscopic fibers that lodge deep into the lungs when inhaled. First identified as a death trap in 1898. Easily released into air when disturbed. Known cause of lung cancer and mesothelioma.

Just at that moment, Jeff called me. I think you should see this, Sandra. It’s backed with some kind of fiber.

 

It turns out that dialing 911 is an appropriate thing to do in situations like these.

With the help of the fire chief, who arrived at our house within minutes after I called, Jeff sealed off the kitchen from the rest of the house, created a negative airspace using fans, and located an EPA-certified lab to help with remediation. At night, he slept in a tent in the backyard. The kids and I moved into a nearby hotel. I signed them up for day camp and worked at the library. In the evenings, we hiked to the waterfall and picnicked at the beach. Forthcoming yet nonchalant about the problem that made us flee the house, I tried to make our exile seem like an adventure. We are just being extra careful. Still, it was hard to explain why we couldn’t go home. Faith asked if daddy and I were getting divorced. Elijah cried.

Ten days later, the kitchen was covered with a layer of new (formaldehyde-free) plywood. Air sampling conducted throughout the house showed no traces of asbestos. The kids and I checked out of the hotel.

It was a sober homecoming. Jeff and I both felt like nominees for Worst Parent of the Year. Somehow all of our respective experience in home renovation and environmental health had not helped us avoid a serious environmental health hazard while conducting home renovation. In attempting to remove one respiratory threat from our son’s life, we very nearly exposed him to a much worse one—and may indeed have exposed ourselves. We created a mess that required our entire year’s renovation budget to solve. What was wrong with us? We had so carefully tested the house for lead and radon—and indeed asbestos—before we signed the purchase offer. Why had we not done due diligence on the black floor before ripping it out? If only I had entered “asphalt tile” into the search engine ten minutes sooner.

By the way, Jeff said. The green floor was covered with lead paint.

There was nothing to do but laugh. Essentially, our manyfloored kitchen was a toxic archive of every terrible building material of the twentieth century: lead (destroyer of brains); asbestos (destroyer of lungs); and PVC (see Chapter 5). As a partial explanation for how such a thing could even happen, I found this sentence in the online encyclopedia for building inspectors:

One reason that so much asbestos was used in flooring tiles was simply the wish to find an application for asbestos waste product from asbestos mining operations.

A long time ago, somebody made a decision to turn kitchen floors into a burial ground for mining waste. Not so long ago, a father unfamiliar with this decision—who was not even born when the decision was made—inadvertently released it into his kitchen. And had to empty our bank account to clean it up.

This is how one generation with unresolved environment problems leaves unexploded ordnance for future generations to trip over.

 

To talk about asthma’s statistics requires facility with millions and billions. Asthma accounts for 14.4 million lost days of school every school year. (It’s a leading cause of school absenteeism.) It affects 7.1 million children—and each year, it kills 600 of them. (It’s the number one chronic childhood disease.) Asthma carries an impressive price tag: $20.7 billion in annual costs. (It’s the number one cause of child hospitalization and visits to emergency rooms.)

What role environmental pollutants play in the story of child asthma is a hotly debated question. The most reliable guess is that it accounts for 30 percent of cases, but because asthma, like cancer, is a disease with multiple causes, that’s a soft number. Nevertheless, evidence for a contributing role of pollutants comes from multiple sources. The first is time trends. Since 1980, childhood asthma has doubled in incidence, and severity has worsened. A doubling in the rate of a disease over a twenty-five-year period means that it’s unlikely that dust, mold, or smoking is driving the trend. As a recent analysis of the issue points out, our homes have not become twice as dusty or twice as moldy. Moreover, asthma rates do not differ between humid and dry regions. Cigarette smoking is down, yet asthma rates are up. What about exposure to airborne contaminants?

At first glance, air pollution, like house dust, seems to have a reasonable alibi. Outdoor air quality has also mostly improved during the time span in which child asthma has worsened, as gauged by the falling levels of those air pollutants regulated by the EPA. Nitrogen oxides, sulfur dioxide, and vaporous compounds are down. Ozone (smog) is also down—although not by a lot. Particle pollution yields a more complicated picture. Particles were down, but then rose again after 2002, mostly because of coal-fired power plants.

But the air pollutants we monitor and regulate under the Clean Air Act are only a tiny fraction of the total. Diesel exhaust, for example, contributes to the air we breathe high levels of ultrafine particles (less than 2.5 microns), which are sticky and act as miniature taxicabs for other noxious chemicals like formaldehyde and sulfuric acid. Ultrafine particles and chemical hybrids are not routinely measured in outdoor air. So perhaps asthma is related to them—or something else in our air not monitored and regulated.

Or perhaps children today show greater immune sensitivity to the air pollutants we do monitor and regulate.

Or perhaps the sensitizing exposure is not a classic air pollutant. Evidence from both epidemiology and lab animal research has uncovered links between pesticide exposure and asthma. Organophosphate pesticides in particular can induce spasms in bronchial tubes and contribute to airway hyperreactivity by altering the functioning of nerves that supply the muscles of the airways. As we have seen (Chapter 3), children are exposed to organophosphates through their food and possibly also when they are sprayed into their environment. One such pesticide, chlorpyrifos, was banned for household pest control in 2001, precisely because of its ability to interfere with children’s neural pathways (more on this in Chapter 8), but it is still used in agriculture and in urban pest control.

Other clues can be found in the demographics of the disease. Asthma disproportionately affects poor children, black and Hispanic children, and urban children. Children born prematurely are at increased risk for asthma, as are obese children. The concurrent rise of pediatric asthma with increased rates of preterm birth (now 12.5 percent of all births) and obesity (now affecting 16.9 percent of children) certainly suggests possible connections.

Children living in polluted areas also have higher incidence of asthma. But children living in polluted areas are more likely to be non-white and poor—making difficult the task of teasing apart socioeconomic factors from environmental exposures. Nevertheless, geographic patterns in Europe also show connections between asthma and air pollution. A recent study shows that Dutch children who live near busy roads are more likely to have asthma. (They also have more ear, nose, and throat infections, more colds, and more flu.) These patterns mimic those found in California: Asthma rates double among children with the closest residential proximity to busy traffic lanes. And, independent of home location, California children who attend schools located on busy roads also have elevated rates. (Poverty also matters: Given the same exposure to traffic-related air pollution, kids of lower socioeconomic status are more likely to develop asthma. Poorer children have higher inflammatory markers, suggesting they are living closer to the threshold of disease.)

So there are two things we can say with a high degree of certainty. One: Outdoor air pollution is geographically associated with high rates of child asthma. Two: Outdoor air pollution exacerbates asthmatic symptoms. When air pollution goes up, the lung functioning of asthmatic children goes down, and hospital admission rates go up. We even have molecular evidence for this trend: On bad air days, asthmatic children have increased markers of inflammation in the condensation of their exhaled breath. And their lung functioning gets worse.

But can outdoor air pollution cause asthma? Answering this question requires painstaking studies that involve following asthma-free children over time and noting who gets asthma and under what conditions. These sorts of prospective studies have been carried out by teams of researchers in both New York and California. All together, they show that, indeed, early-life exposure to fine particles, ozone, diesel exhaust, and a group of combustion byproducts called polycyclic aromatic hydrocarbons is associated with the onset of asthma. In particular, prenatal exposure is a risk factor for its development.

Teams of investigators at Columbia University’s Center for Children’s Environmental Health have been monitoring cohorts of children since before their births. (These are the scientists from Chapter 1 whom we saw equipping pregnant women with personal air monitors.) In a study published in 2009, they report that exposure to traffic exhaust during pregnancy reprograms a gene in ways that increase a child’s chances of developing asthma.

Similarly, researchers in California followed a group of children from early life onward and discovered that traffic-related air pollution was associated with the onset of asthma. This 2008 study was particularly convincing because an air pollution monitor was placed outside the home of each child in the study. (Earlier studies had relied on centrally placed air monitors.) In a 2010 study, a team of California researchers followed a cohort of asthma-free kindergarteners. Those who attended a school with high levels of air pollution—independent of the levels of air pollution at their homes—were 45 percent more likely to develop asthma. Furthermore, California children who participated in at least three outdoor activities in communities with high smog (ozone) levels were 30 percent more likely to develop asthma.

 

Air pollutants impede the breathing of children in a variety of ways. Particulate matter buried deep in the lungs can excite the release of cytokines. These are proteins that can call a state of emergency, deputize immune cells, and send them off after the bad guys. Cytokines are the sheriffs of inflammation. More cytokines means a twitchier respiratory system. In addition, prenatal exposure to air pollutants can alter the development of immune cells. Polycyclic aromatic hydrocarbons (emitted by cars and coal-burning power plants) can change the ratio of white blood cells in the umbilical cord, skewing the nascent immune system in a more inflammatory direction.

Air pollution can also interfere with the treatment of asthma. Asthma drugs work by relaxing muscles that wrap airways, compelling them to dilate. But air pollution can continue to provoke inflammation, constricting airways.

Even among asthma-free children, air pollution stunts lung development. Up to 80 percent of the alveoli in an adult lung develop after birth, with alveolation continuing until at least age eight. Some pulmonologists believe air sacs are still forming during adolescence. But, as of age 20—at the outside—you have all the respiratory surface that you will ever have. Air pollution causes permanent changes in developing pulmonary structures. The result is less surface area for respiration and a smaller lung volume.

Studies show that teenagers in southern California who grow up in more polluted places have smaller lungs and diminished lung functioning. These alterations raise the risk of chronic obstructive pulmonary disease in later life and, in childhood, raise the risk for bronchitis. And with rising levels of air pollution also come rising rates of middle ear infections.

 

Did you ever dream that you had to go back to school and take a math exam? This actually happened to Jeff in his waking life. All certified art teachers in the state of New York must have on their transcripts passing grades for college-level coursework in math and science. Such requirements were not in place for art majors in the free-wheeling academic world of our youths—not even, apparently, for the art majors of Amherst, his very serious alma mater. Thus, some number of decades later, he had to make up the deficits. He was a good sport about it all—tackling college algebra first and then astronomy.

I was surprised at his choice of astronomy. Of all the sciences, it’s the one I know least about, so I was not in a position to be helpful. But he believed it would be the most visual field of study and thus most compatible with the way his own mind worked. And soon he was interpreting Hubble telescope imagery and had no need of my assistance anyway.

There was an unexpected benefit to all this required knowledge. Through direct observation and some kind of calculation involving math, Jeff figured out the angle of the moon as it passed over our house and cut a hole in the roof over our bedroom so that moonlight would trace a path directly across our bed. (And installed a skylight in the hole.) This was a home renovation firmly in category two—improves happiness of occupants—although a case could be made for number one—aligns household ecosystem with environmental goodness. An open skylight, Jeff noted, would serve as our summertime air conditioning, drawing cool air up the stairwell at night.

And so all four of us took to the bed to engage in astronomy, looking straight up through the ceiling, through miles of air and atmosphere, into the firmament above. Moon. Stars. Clouds.

Sometimes Jeff gave lessons on the properties of light.

Sometimes we all just lay together in silence.

Sometimes, if we didn’t know where one child or another had disappeared, Jeff or I would find him or her supine on our bed, staring up. Night or day, it became the preferred place to have a private talk, check the weather, or recoup during a time out. The moon-aligned skylight brought a measure of infinity into a small house.

On the first night that I awoke to a waterfall of silver in my eyes—my husband breathing next to me, my children breathing in the next room—I realized I was home. This was my house. And I matched my breathing to theirs.

 

By all the pathways we have seen, air pollution wrecks the health of the whole family. First, air pollution during pregnancy is linked to lower birth weight and preterm birth. Both of these conditions, all by themselves, raise the risk for childhood asthma. Second, air pollution—both the indoor kind and the outdoor kind—makes children’s asthma worse, and growing evidence suggests it serves as a direct cause of the disease. Third, air pollution reprograms pulmonary development in ways that stunt lung growth, a condition with lifelong consequences. Fourth, air pollution alters immune functioning. And fifth, it increases the frequency of bronchitis and ear infections. In short, early-life exposure to air pollution sows suffering for children and misery for parents. It diminishes respiratory health, fills up emergency rooms, incurs medical costs, and steals time, money, energy, and sleep.

The air pollution-asthma link is also part of a much larger story. Among adults, air pollution contributes to cancer (with tobacco smoke, radon, and diesel exhaust among the substances conferring the greatest risk). Lung, breast, and bladder cancers all have demonstrable links to air pollution. Air pollution also contributes to diabetes. More specifically, in both the United States and in Europe, traffic-related air pollution has been identified as a risk factor for type-2 diabetes in women. Again, its ability to induce inflammation, which contributes to insulin resistance, appears to be the link.

In addition to all this, according to the EPA, about 20,000 Americans die prematurely each year from cardiovascular problems attributable to exposure to air pollutants, most notably, the byproducts of fossil fuel combustion. Small sooty particles (those less than 2.5 microns)—which can easily cross the alveolar threshold and enter the bloodstream—are thought to be largely responsible. By multiple mechanisms, their inhalation contributes to heart attack, stroke, and high blood pressure. Fine and ultrafine particles, for example, make clotting factors in the blood stickier and more prone to coagulation. Stoked by air pollutants, chronic inflammation also irritates nerves, altering their electrical signals, which in turn, contributes to abnormal cardiac rhythms.

In other words, the combustion of fossil fuels reprograms not just the lungs and immune systems of our children but the pace and tempo of our own heartbeats.

 

These results raise some questions. Given the breadth and depth of the evidence published in the scientific literature, why are we not reading about the dangers of ozone and diesel exhaust—and traffic and coal-burning power plants and phthalate-laden flooring—in parenting magazines? The ones I pick up in the doctor’s office waiting room (while waiting to see if Elijah has bronchitis yet again) or in the pharmacy (while waiting to refill the EpiPen prescription) have lots of information about managing asthma with medication but none about preventing it through the provision of cleaner air.

Why is the only person interested in talking with me about our local coal-burning power plant a childless college student out canvassing for an environmental group?

Why is there no analysis of the proposed amendments to the Clean Air Act in the Web sites of online support groups for mothers of children with asthma and allergies? I entered “clean air act” into the internal search engines of many such sites and came up with nothing. (On the other hand, the testimony of the American Lung Association’s director before the U.S. Senate Committee on Environment and Public Works provided an excellent overview of the issues.)

So why can’t parents become conversant with the Clean Air Act and its National Ambient Air Quality Standards, whose various rules affect our children so intimately? The American Petroleum Institute certainly is.

Originally passed in 1970, the Clean Air Act is the federal law that requires air pollution limits to be based on the latest available science. As the science shifts, so too must the law. And therein lies a mighty battle, with arguments over what constitutes “maximum available control technologies” and who should receive exemptions, and so on. Yes, it’s complicated, but so is figuring out a vaccination schedule for an allergic child or staying au courant with ever-evolving car seat/booster seat regulations. (These vary by state, by type of vehicle, and by weight, height, and age of the individual child.) And yet I’ve seen plenty of articles in parenting magazines, online and off, that help shepherd families through the byzantine intricacies of car seat rules. I’ve seen none about what cars are doing to our air.

In 2009, more than half of Americans lived in counties that received failing marks for either ozone or particulate matter. Given the direct consequences for children, that news, when it broke, should have been a big topic among parents: What needs to be done to bring half our nation into compliance with the Clean Air Act? Instead, what children with asthma, and their parents, heard about air pollution was how to “limit their exposure as much as possible by decreasing their time outside when particulate levels are high.” (A government Web site, www.airnow.gov, allows you to monitor your local particulate levels.) But physical activity is exactly what we and our children are supposed to be doing more of in order to avoid obesity, which in turn is linked back to increased asthma risk in children.

Surely, growing up indoors and sedentary is not the answer to air pollution. There is no substitute for clean air. And we can’t go shopping for some. And since the only way to ensure that our children have access to healthful air is by not polluting it—why aren’t mothers of children with hyperreactive airways across the land marching on Washington, demanding investments in green energy and public transportation?

Happily, there are plenty of evidence-based reasons to believe that political action would bring quick benefits. When air quality improves, children’s respiratory health rebounds. In Switzerland, an 11-year decline in airborne particulate matter was followed closely by immediate improvements in children’s lung functioning. Likewise in China, after the government closed a polluting coal-fired power plant in 2004. In Atlanta, while traffic was reduced for the 1996 summer Olympic games, ozone levels fell by 25 percent, and child hospital admission for asthma fell by 19 percent. When the steel mill in Provo, Utah, closed down in the mid-1980s, hospital admissions for children with asthma dropped by half.

And when it reopened, they went back up.

 

Just when I felt truly settled in to our skylit Victorian cottage—the piano teacher’s phone number committed to memory, the origin of the basement leak identified, peace with the carriage house raccoon brokered—along came a job offer in a different time zone.

At first I viewed the invitation in the way a sober alcoholic might view an offer of a drink. You don’t know who you’re dealing with, pal. As though the offer of a steady salary, an academic post, and retirement benefits were wicked temptation. I worried that I was still too much in love with sleeping bags and on-theroad-again adventure. The job description seemed perfect. My first interview was a laughter-filled conversation with colleagues whom I could easily imagine at a potluck dinner. And Jeff could be considered for a post in the art department at the same university.

Soon we were on a sleeper train heading for the Midwest—the kids each promised a turn in the top bunk in exchange for open-mindedness. Jeff and I both had campus interviews scheduled. Mostly, we hoped, as a family, to get the lay of the land, and look at the area schools, neighborhoods, food co-op, public library.

During the train ride, I pored over local air quality data. There were a couple of things I had noticed during my first interview that were bothering me. One was the coal-burning power plant on campus, and the other was an old-style trash incinerator downtown that served as the municipal utility. Among the nation’s incinerators, this was a famously polluting one. Indeed, the dioxin generated by it had been traced all the way to northern Canada (using a computer model that could also have been used to model dioxin emissions from the Illiopolis PVC inferno). What I learned was troubling, but I set it aside on the grounds that all communities have their environmental issues.

Here were the highlights of our visit: Jeff was offered a position. He was also invited by the city council of a nearby town to consult on a public art project. We were all treated to a dinner of local, organic foods. Faith made a friend, attended a day of fourth grade, and impressed a geography teacher by correctly identifying the location of the Snake River (Idaho). I received a standing ovation for my public lecture. The provost apologetically rescheduled our meeting because an asthma attack landed her in the emergency room. And Elijah started coughing. He coughed during the whole week of our visit, and when we came back home, he stopped.

 

Sometimes when I’m faced with weighty decisions, scraps of Scripture enter my mind—indelible remnants of a childhood spent in a hymn-filled Methodist church. Within my youth group, I was the resident expert on the fifth book of the New Testament, The Acts of the Apostles, which is where, said I, the plot got truly complicated. But as the train rattled east again, the words that came to me were from the second book, the gospel of Mark:

For what shall it profit a man, if he shall gain the whole world, and lose his own soul?

Soul is a Germanic word, perhaps referring to the sea. In Latin, spiritus, which means to breathe, as in inspire. In Greek, psyche, to blow, as in air, referring to the breath of life. In Hebrew, nephesh: life, the soul, which is to say, that which breathes. My son, who had once floated in a sea within me, needed to breathe. And no salary or retirement benefit was profit enough to compensate.

I turned the job down, fully aware that for many parents—and for myself at an earlier stage in my own life—the choice between a job and a child’s well-being too often comes without the option of favoring the latter. But as long as I could squeak out a living, I couldn’t choose to relocate an asthmatic child near a trash incinerator. For clean air, I was willing to forego retirement benefits.

 

Lungs exist at a place where two environmental crises meet.

Their ability to respire—to exchange oxygen for carbon dioxide across a membrane as fine as gold leaf—is compromised by the toxicity of emissions from fossil fuel combustion. About half of these emissions come from power plants (coal and natural gas) and another third from transportation (petroleum). The chemical adulteration of the planet with toxic pollutants derived from coal, gas, and petroleum is one crisis.

At the same time, the combustion of fossil fuels contributes heat-trapping gases to the atmosphere—most notably, carbon dioxide. These are destabilizing the planet’s climate. Global climate change is, thus, the second crisis.

But the problems of toxicity and temperature are not independent of each other. Higher global temperatures accelerate the creation of toxic lung pollutants, such as ozone, nitrogen dioxide, particles, and carcinogens. And they accelerate the evaporation of liquid pollutants, like gasoline. By raising the heat, you raise the air’s toxicity. Higher temperatures also increase levels of pollen, dust mites, and fungal spores. In all these ways, climate change is an asthma trigger.

I have now walked us right into the blockbuster topic of global warming, and there are many dozens of things I could say at this point. Global warming is a Biblical epic with a cast of thousands, from polar bears to floods, and many complicated subplots. It is easy to feel that you’ve arrived late to the theater and find the storyline confusing. It is easy to wish you could skip this show altogether. (As if.)

For the legions of busy, multitasking parents who walked into the middle of the climate movie, here’s what’s already happened: In 2007, the Supreme Court ruled that heat-trapping gases fall under the Clean Air Act. In 2009, the EPA declared that six of these gases constitute a threat to human health but has not yet regulated them because it’s waiting for Congress to pass climate legislation.

For the sake of this discussion, I’m going to focus on just two other scenes of the movie that each relate to the air we breathe—with others to come in the next chapter.

Scene One: In a 2008 study, Stanford University engineer Mark Jacobson demonstrated that upticks in the average temperature of the planet lead to significant increases in human deaths due to air pollution. Specifically, an increase of one degree Celsius (1.8 degrees Fahrenheit) kills, each year, an additional 1,000 Americans from exposures to ozone and particulate matter—and leads to many more cases of asthma.

This is not a possible threat; this is an outcome already measurable. The combustion of coal and oil has already increased the global temperature by nearly one degree Celsius, with much of that increase occurring in the last few decades. Global climate change is, thus, already contributing to the burden of child asthma and, unless mitigated, will add even more rocks to the pockets of asthmatic children in the years to come.

In 2009, a year after the Jacobson report, members of the European Respiratory Society—physicians—called for immediate political action on climate change on the grounds that the deterioration of air quality wrought by higher temperatures is disproportionally killing their patients—people with asthma and other chronic respiratory infections. Whereas a one-degree increase in average ambient temperature results in a 1 to 3 percent increase in the premature deaths of the general public, it leads to a 6-percent increase in deaths among people with preexisting respiratory conditions.

In other words, if you have a child with asthma, he or she is two-to-six times more likely than everyone else to perish from global warming-induced air pollution.

Those are the stakes.

In the same year, on this side of the Atlantic, researchers from the Columbia Center for Children’s Environmental Health convened a remarkable conference that explored the ways in which both environmental crises—the crisis of toxic chemical exposure and the crisis of climate change—interact to erode the health of children.

Of particular interest was how climate change magnifies the problem of toxic exposures. Overseeing this event was molecular epidemiologist Frederica Perera, who has been studying the effects of prenatal chemical exposure for thirty years. Perera oversees the long-standing studies of mother–newborn pairs—including the 9/11 cohort and mothers and children in China and Poland—the results of which we’ve already explored. It is Perera’s team that installs individual air monitors in the backpacks of pregnant women and traces the flow of air pollutants from mother to child, recording the damage to fetal blood cells along the way.

If anyone deserves to feel overwhelmed by the power of climate change to magnify the toxic effects of air pollutants, it would be Perera. But that was not the note she struck in her remarks at the conference. First, she meticulously documented the myriad impacts of fossil fuel dependency on child health and development—lower birth weight, preterm birth, stunted lung growth, developmental delays, cancer, asthma, allergies, heat stroke, drowning, malnutrition, diarrhea, malaria, encephalitis, and psychological trauma. Then she meticulously documented how the economic costs of doing nothing exceed the cost of mitigation—through investments in green technology and greater efficiencies in power generation, building design, and transportation. In other words, quitting fossil fuels would both save us money and avert disaster. Win–win. Her conclusion was urgent but hopeful: “Our addiction can be cured. We do not have to leave our children a double legacy of ill health and ecological disaster.”

Another conference speaker, climate strategist Michel Gelobter, put a finer point on the addiction analogy: Fossil fuels are like cigarettes for the planet. “They take money out of our communities, they pollute our environment, they kill children, and they waste our lives.” A smoking cessation program for the planet necessitates nothing less than the remaking of the economy and the will to leave the remaining oil and coal in the ground and do something different. Devoted to realizing this vision, Gelobter said that his work was inspired by a deeply felt appreciation for the injustice of climate change. “Some people have used more of the atmosphere than they had a right to, than was sustainable, and are precluding the use of that atmosphere and those resources for others, have precluded it, and will continue to do so unless we take action.”

Essentially, the unrestricted burning of fossil fuels is turning air into the atmospheric equivalent of an asbestos-filled kitchen floor. While I listened to Gelobter talk about intergenerational inequity to an audience full of Ph.D.s and M.D.s, it occurred to me that my children had simpler words for it: That’s not fair.

It also occurred to me that Perera and Gelobter are the voices that parents of children with asthma and allergies need to hear while waiting for prescription refills in the pharmacy. All 12.4 million of us.

 

Here is the second scene from the climate movie: It’s set in the top layer of the ocean, which has absorbed 93 percent of the excess heat trapped by global warming gases.

Floating around on the surface of the high seas are plankton. By definition, they are drifters, blowing where the currents send them. Some of them are animals. Some of them are plants. Both groups are struggling.

The animals—zooplankton—have two problems. First, they depend on plant plankton (algae) for their food source, and when the foundation of the food chain is in trouble, everybody north of the foundation also suffers. But zooplankton also have a second, separate problem. Many members of the zooplankton community are the larval forms of various shell-bearing species. They spend their youth at sea as directionless wanderers. Then they settle down and calcify. But now they are having trouble doing that.

About a third of the carbon dioxide contributed to the atmosphere from cars and power plants is absorbed by seawater. Here, it turns into carbonic acid. This transformation is changing the pH of the ocean’s surface—indeed, has already changed it, from 8.2 in 1750 to 8.1 today. (The pH scale is logarithmic. Each whole pH value is ten times more or less acidic than the preceding one.) And an increasingly acid ocean makes it difficult for marine animals to secrete shells. (They dissolve.) An acidifying ocean thus endangers corals, oysters, barnacles—along with their seafaring offspring, the zooplankton.

The zooplankton’s green counterparts, the phytoplankton, also have a problem. Because they are restricted to the sunlit surface of the ocean—indeed the upper layer is the only place where plants grow in the open ocean—phytoplankton depend on upwelling of water currents from the deep to bring them nutrients—like nitrates—otherwise lost to gravity. This planktonfilled surface layer is warming up, and its higher temperature inhibits its ability to mix with the cooler, nutrient-dense layers below. As a result, in eight of ten ocean regions, the abundance of plant plankton is declining.

Given that phytoplankton are microscopic, how do we know this? Satellites keep track of the changing color of the ocean’s surface, but the better data come from a decidedly low-tech oceanographic instrument called a Secchi disk. And, thanks to 100 years of its continuous use by oceanographers, researchers can construct a timeline of plankton density. This shows that the world’s plankton stocks are waning.

A Secchi disk is a black-and-white plate the size of a Frisbee that is mounted on a tape measure and lowered into the water from the side of a ship or boat. The point at which the disk disappears from view is called the Secchi depth. It’s an indirect measure of how much chlorophyll is in the water. The shallower the Secchi depth, the murkier the water, and the greater the density of chlorophyll (phytoplankton). The deeper the Secchi depth, the clearer the water, and the lower the density of plankton. Secchi disks, standardized tools of oceanographic observation, are used on lakes as well, which is where I’m familiar with them. You gently slip the disk into the water on the shady side of the boat and watch as it disappears into the green depth. The point at which the black-and-white pattern disappears into the greenness is where you stop and take a reading.

Out in the open ocean, Secchi depths are increasing. According to a 2010 analysis of a more than a half million oceanic readings going back to 1899, global phytoplankton stocks are down 40 percent. The 1950s marked the beginning of their decline, which has continued at a rate of 1 percent a year. The investigators found a strong correspondence between this long-term trend and warming temperatures on the surface of the ocean.

 

Phytoplankton make half the oxygen we breathe.

 

Back at home, lying under the skylight, Elijah and I watched a windstorm. Leaves blew by. Birds that looked like leaves blew by, as though not flying under their own power. Twigs and spruce cones pelted the shingles.

Where does the wind come from?

It wasn’t the first time a child asked me this question, but it’s one I’ve always loved to consider. And I knew where it would lead. As soon as I explained the rotation of the earth and the origin of air currents, the follow-up question would be, right on cue—

But where does the air come from?

There are many ways to go with a query like this, but I like to bring it around to the oxygen cycle because it’s an invitation to converse about photosynthesis, my very favorite biological reaction. It happens also to be the world’s most complex biological reaction. No fewer than 100 proteins are required to spin sunlight, water, and carbon dioxide into molecules of sugar and oxygen.

At 3 billion years old, photosynthesis is an ancient process, and it explains many mysteries. The ripple-etched sidewalk in front of our house, for example, that was once the floor of a shallow sea: Its shale slabs are made up of the compressed bodies of photosynthesizing plankton and those who fed on them. And all those fossil fuels: The reason we call them nonrenewable resources is because the creatures whose bodies comprise them died before the world’s plants had filled the atmosphere with enough oxygen to decompose their own corpses. The undecayed dead were squashed into petroleum, gas, and coal. That doesn’t happen on the oxygen-rich planet we inhabit now.

And yet, in spite of the explanatory power of photosynthesis, the essence of the whole operation—the splitting of a water molecule—is an enigma. Biophysicists still don’t know exactly how chloroplasts manage it.

Elijah, the oxygen you are breathing in right now is a gift from green plants. Plants make their own food out of the sun. They breathe oxygen out. And then you breathe it in.

And then what?

And then you breathe carbon dioxide out. And the plants breathe your carbon dioxide in. That helps them make food . . . and make more oxygen for you.

So we’re nice to each other.