Will The New Air Pollution Science Choke City Planners?

Part One of A Two-Part Series

Not long ago, Michael Woo, a former Los Angeles city councilman and current member of the Los Angeles City Planning Commission, took up a case pending approval by that body: a mixed housing-retail development near the intersection of Cahuenga Boulevard and Riverside Drive. Like many of the remaining buildable sites in the city, the property is right next to a roaring motorway; the windows of some apartments would look right out onto the 134 Freeway. To Angelinos, who have grown up in a car culture, it was hardly a remarkable proposal. But Woo, perhaps one of the brainier members of the city’s political elite—after losing a mayoral race to Richard Riordan in the early 1990s he became a professor of public policy at University of Southern California—had a problem with it, and he couldn’t quite let it go.

Just a few weeks before, the Commission had witnessed a lengthy presentation by a scientist who’d been studying how living within 500 yards of high traffic corridors—freeways and some particularly busy streets—substantially raises the risk for a number of chronic diseases. “We were all sort of sitting there, looking at this proposal and discussing it through the conventional lens we normally use, when I said, `Wait a minute. Didn’t we just hear a pretty compelling argument about this the other day? Can we talk about that for a minute?’ It struck me that it was impossible to read those studies and then continue approving housing that sits that close to freeways.”

The Commission then asked for the developer’s point of view on the issue. “As I recall, the only real mitigation that they brought up was almost comic,” Woo says. “Their idea was, you know, we’ve got that covered: We’re going to make sure that residents can’t open the windows that face the freeway.” The project was approved.

Woo doesn’t particularly fault anyone in the exchange, because the implications of the new science of air pollution—much of it driven by pioneering work at USC, the University of California at Los Angeles, and California Institute of Technology—are utterly mind boggling. No one has quite calculated exactly how much buildable land would be excised from use for housing and schools if this growing body of work were to take hold in the policy realm, but, as Woo said, “We can’t hide from this issue anymore. The hard science on the subject is compelling. It makes you fundamentally rethink some pretty key parts of how, where and why we’re building housing in such locations.”

For decades, pretty much everyone “knew” that smog—usually measured as ozone, the gas that forms from sunlight’s ionizing effect on air particles—caused all kinds of health problems, principally those associated with the lungs, like asthma. But the truth of the matter is that, until ten years or so ago, no one knew how that happened; they didn’t know the “mechanism of action,” the intricate physiological processes that lead to chronic airway inflammation. Epidemiological data was confounding, because some high ozone communities showed lower rates of asthma than low ozone communities. Also, smog levels—measured as ozone—were going down, while asthma rates were going though the roof.

One suspect was what researchers called fresh emissions, comprised of ultrafine particles, or UFPs, which are so small that they can penetrate the furthest reaches of the lung’s bronchial branches and set off the systemic inflammation that causes respiratory disease. Thus, it was possible to have lower ozone levels and still have increased levels of inflammation, or as USC Professor Robert McConnell notes, “You could have cleaner horizons but still have increasing inflammation to people who live closer to where the particles are being produced.” McConnell has been leading the federally funded Children’s Health Study in Los Angeles for over a decade. “I tell people that I’m studying how pollution causes asthma, and people look at me and say, `I thought we already knew that,’” says McConnell. “The fact is that we assume risks that aren’t there, and we’re ignorant of risks that are there.”

What caused the sea change in pollution epidemiology—the ability to link exposure to tail pipe emissions and chronic diseases—is as much a story of ingenuity at the lab bench as it is one of persistence against conveniently indolent regulations. At USC, engineers over the past 20 years have invented ways to concentrate particles from the freeway, assess their specific toxicity in human doses, and then test various theses with lab animals genetically engineered to physiologically respond like humans. They have also developed ways to track real-time daily human exposures to ultrafine particles. On any given day in Los Angeles there are mobile smog units measuring how pollution ebbs and flows on a neighborhood-by-neighborhood basis. There are people wearing “personal ambient pollution” backpacks to track how individuals experience different loads of smog throughout their day, part of which may be spent in a low-pollution environment, part in a high. Through modern genomics, we also now know that several highly prevalent gene mutations make some people more susceptible to pollution, and that others make them less susceptible.

At all three universities, engineers in the aerosol sciences developed machines that could accurately measure not just ozone—a rather crude measure of air toxicity—but also specific toxins, known as ultrafine particulate matter, or UFPs, of less than 2.5 microns. It is stuff so small that it can reach the bottom of the airways; there, it can over-stimulate the so-called inflammatory cascade of the body’s native defense system and turn it into a disease called asthma. At UCLA, cell biologists, toxicologists and lung and heart specialists have even been able to image what happens to the human cell when it’s exposed to high levels of ultrafine particles. It is the kind of image that can make one utterly despairing, but one that also might clue modern physicians, medical researchers and environmental scientists on how to better focus on the issue and perhaps mitigate it.

A few examples of new directions within the science:

Ultrafine Particles, Diesel Exhaust And Asthma: A growing consensus holds that, infants, young children, and expectant women experience substantial elevations in risk for deficits in lung function growth when living near high volume motorways. There is less consensus on the recommended buffer zone, ranging from 75 meters to 500 meters.

Ultrafine Particles And Heart Disease: A growing body of laboratory experiments and human observational work links heart disease, especially the process leading to atherosclerosis and heart attack, to air pollution. Recent work at UCLA and USC on lab mice parked next to the 110 Freeway has suggested an alarming thesis of causality: That chronic exposure to high levels of ultrafine particles may make us more likely to get heart disease because it makes HDL—the so-called “good,” form of cholesterol that “cleans up” the bad form—dysfunctional.

Diesel, Ultrafine Particles And Alzheimer’s: Work coming out of Mexico City, increasingly LA’s sister city in the environmental sciences, documents how amyloid plaque, one of two suspect brain proteins associated with Alzheimer’s, increases with exposure to air particles, especially in children and young adults.

Diabetes, High Blood Pressure And Obesity: A small but growing body of research shows that being fat and breathing smog is really bad for you. Worse, high exposures may accentuate existing diabetes and metabolic syndrome, the perfect storm of high cholesterol, high blood sugar, and high blood pressure.

Air Pollution, Expectant Mothers, And Infants: UCLA researchers have repeatedly demonstrated a consistent, dose-dependent relationship between expectant mothers living in high traffic-emission-adjacent housing and premature births, low birth weights, birth defects and respiratory diseases. In a recent report, the UCLA Institute of the Environment concluded that the problems were of such magnitude as to “require drastic changes to motor vehicle and transportation systems” over the next decades.

In Part Two, Critser explores the politics of pollution.

Greg Critser is the author of Fat Land: How Americans Became the Fattest People in the World (Houghton Mifflin 2003), Generation Rx: How Prescription Drugs Are Altering American Lives, Minds, and Bodies (Houghton 2005), and Eternity Soup: Inside the Quest to End Aging (Random/Harmony 2009).