Why Is Air Pollution So Harmful? DNA May Hold the Answer


The threat of air pollution grabs our attention when we see it — for example, the tendrils of smoke of Australian brush fires, now visible from space, or the poisonous soup of smog that descends on cities like New Delhi in the winter.

But polluted air also harms billions of people on a continuing basis. Outdoors, we breathe in toxins delivered by car traffic, coal-fired plants and oil refineries. Indoor fires for heat and cooking taint the air for billions of people in poor countries. Over a billion people add toxins to their lungs by smoking cigarettes — and more recently, by vaping.

Ninety-two percent of the world’s people live in places where fine particulate matter — the very small particles most dangerous to human tissues — exceeds the World Health Organization’s guideline for healthy air. Air pollution and tobacco together are responsible for up to 20 million premature deaths each year.

Airborne toxins damage us in a staggering number of ways. Along with well-established links to lung cancer and heart disease, researchers are now finding new connections to disorders such as diabetes and Alzheimer’s disease.

Scientists are still figuring out how air pollution causes these ailments. They are also puzzling over the apparent resilience that some people have to this modern onslaught.

Some researchers now argue that the answers to these questions lie in our distant evolutionary past, millions of years before the first cigarette was lit and the first car hit the road.

Our ancestors were bedeviled by airborne toxins even as bipedal apes walking the African savanna, argued Benjamin Trumble, a biologist at Arizona State University, and Caleb Finch of the University of Southern California, in the December issue of the Quarterly Review of Biology.

Our forebears evolved defenses against these pollutants, the scientists propose. Today, those adaptations may provide protection, albeit limited, against tobacco smoke and other airborne threats.

The dense foliage of tropical forests gave chimpanzees and gorillas a refuge from dust. But the earliest humans, wandering the open grasslands, had nowhere to hide.

Dust was not the only hazard. The lungs of early humans also may have been irritated by the high levels of pollen and particles of fecal matter produced by the savanna’s vast herds of grazing animals.

Dr. Finch and Dr. Trumble maintain that scientists should consider whether these new challenges altered our biology through natural selection. Is it possible, for instance, that people who are resilient to cigarette smoke have inherited genetic variants that protected their distant ancestors from cave fires?

One way to answer these questions is to look at genes that have evolved significantly since our ancestors moved out of the forests.

One of them is MARCO, which provides the blueprint for production of a molecular hook used by immune cells in our lungs. The cells use this hook to clear away both bacteria and particles, including silica dust.

Later, our ancestors added to airborne threats by mastering fire. As they lingered near hearths to cook food, stay warm or keep away from insects, they breathed in smoke. Once early humans began building shelters, the environment became more harmful to their lungs.

“Most traditional people live in a highly smoky environment,” Dr. Finch said. “I think it has been a fact of human living for us even before our species.”

Smoke created a new evolutionary pressure, he and Dr. Trumble believe. Humans evolved powerful liver enzymes, for example, to break down toxins passing into the bloodstream from the lungs.

Gary Perdew, a molecular toxicologist at Penn State University, and his colleagues have found evidence of smoke-driven evolution in another gene, AHR.

This gene makes a protein found on cells in the gut, lungs and skin. When toxins get snagged on the protein, cells release enzymes that break down the poisons.

Other mammals use AHR to detoxify their food. But the protein is also effective against some of the compounds in wood smoke.

Compared to other species, the human version produces a weaker response to toxins, perhaps because AHR protein is not the perfect protector — the fragments it leaves behind can cause tissue damage.

Our species arrived at the Industrial Revolution two centuries ago with bodies that had been shaped for millions of years by this highly imperfect process.

Clean water, improved medicines and other innovations drastically reduced deaths from infectious diseases. The average life expectancy shot up. But our exposure to airborne toxins also increased.

“If we compressed the last five million years into a single year, it wouldn’t be until Dec. 31, 11:40 p.m., that the Industrial Revolution begins,” Dr. Trumble said. “We are living in just the tiniest little blip of human existence, yet we think everything around us is what’s normal.”

The Industrial Revolution was powered largely by coal, and people began breathing the fumes. Cars became ubiquitous; power plants and oil refineries spread. Tobacco companies made cigarettes on an industrial scale. Today, they sell 6.5 trillion cigarettes every year.

Our bodies responded with defenses honed over hundreds of thousands of years. One of their most potent responses was inflammation. But instead of brief bursts of inflammation, many people began to experience it constantly.

Many studies now suggest that chronic inflammation represents an important link between airborne toxins and disease. In the brain, for example, chronic inflammation may impair our ability to clear up defective proteins. As those proteins accumulate, they may lead to dementia.

Pathogens can hitch a ride on particles of pollutants. When they get in our noses, they can make contact with nerve endings. There, they can trigger even more inflammation.

“They provide this highway that’s a direct route to the brain,” Dr. Fox, of the University of California, Los Angeles, said. “I think that’s what makes this a particularly scary story.”



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