The threat of air pollution catches our attention when we see it, for example, the tendrils of smoke from Australian forest fires, now visible from space, or the poisonous smog soup that descends in cities like New Delhi in the winter.
But polluted air also hurts billions of people continuously. Outdoors, we inhale toxins delivered by car traffic, coal plants and oil refineries. Indoor fires for heating and cooking pollute the air of billions of people in poor countries. More than a billion people add toxins to their lungs by smoking cigarettes, and more recently, vaping.
Ninety-two percent of the world's people live in places where fine particles, the very small particles most dangerous to human tissues, exceed the guidelines of the World Health Organization for healthy air. Air pollution and tobacco together are responsible for up to 20 million premature deaths each year.
Airborne toxins harm us in many ways. Along with the well-established links with lung cancer and heart disease, researchers are now finding new connections with disorders such as diabetes and Alzheimer's disease.
Scientists are still discovering how air pollution causes these ailments. They are also baffling about the apparent resistance some people have to this modern attack.
Some researchers now argue that the answers to these questions are in our distant evolutionary past, millions of years before the first cigarette was lit and the first car hit the road.
Our ancestors were enchanted by toxins in the air even while the biped apes walked through the African savannah, 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 ancestors developed defenses against these pollutants, scientists propose. Today, these adaptations can provide protection, although limited, against tobacco smoke and other threats in the air.
But our evolutionary legacy can also be a burden, Dr. Trumble and Dr. Finch speculated. Some genetic adaptations may have increased our vulnerability to diseases related to air pollution.
It is "a truly creative and interesting contribution to evolutionary medicine," said Molly Fox, an anthropologist at the University of California, Los Angeles, who was not involved in the new study.
The story begins about seven million years ago. Africa at that time was gradually becoming more arid. The Sahara emerged in North Africa, while the grasslands opened in eastern and southern Africa.
The ancestors of chimpanzees and gorillas remained in the retreat forests, but our former relatives adapted to the new environments. They evolved in a tall and thin frame, suitable for walking and running long distances.
Dr. Finch and Dr. Trumble believe that the first humans faced another challenge that has been largely overlooked: the air.
Periodically, the savanna would have experienced severe dust storms from the Sahara, and our distant ancestors could have run the risk of damaging their lungs by inhaling silica-rich particles.
"When there is dust, we will see more lung problems," said Dr. Finch. Even today, Greek researchers have discovered that when the Sahara winds reach their country, patients arise in hospitals with respiratory problems.
The dense foliage of tropical forests gave chimpanzees and gorillas a refuge from dust. But the first humans, wandering the open grasslands, had nowhere to hide.
Dust was not the only danger. The lungs of early humans may also have been irritated by the high levels of pollen and fecal matter particles produced by the vast herds of grazing animals in the savanna.
Dr. Finch and Dr. Trumble argue that scientists should consider whether these new challenges altered our biology through natural selection. Is it possible, for example, that people who are resistant to cigarette smoke have inherited genetic variants that protected their distant ancestors from cave fires?
One way to answer these questions is to observe the genes that have evolved significantly since our ancestors moved from the forests.
One of them is MARCO, which provides the plan for the production of a molecular hook used by immune cells in our lungs. Cells use this hook to remove bacteria and particles, including silica dust.
The human version of the MARCO gene It is distinctly different from that of other apes. That transformation occurred at least half a million years ago. (Neanderthals also carried the variant). Breathing dusty air drove MARCO's evolution in our ancestors who walk through the savannah, Dr. Finch and Dr. Trumble raise the hypothesis.
Later, our ancestors joined the airborne threats by dominating the fire. While they stopped near homes to cook, keep warm or away from insects, they inhaled smoke. Once the first humans began building shelters, the environment became more harmful to their lungs.
"Most traditional people live in a highly smoking environment," said Dr. Finch. "I think it has been a fact of human life for us even before our species."
The smoke created a new evolutionary pressure, he and Dr. Trumble believe. Humans developed potent liver enzymes, for example, to break down toxins that pass 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 produces a protein found in the cells of the intestine, lungs and skin. When toxins get caught in the protein, cells release enzymes that break down poisons.
Other mammals use AHR to detoxify their food. But 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 the AHR protein is not the perfect protector: the fragments it leaves can cause tissue damage.
Before the fire, our ancestors did not need to use AHR very often; in theory, their bodies could tolerate the limited damage caused by the protein.
But when we start breathing smoke regularly and we need the AHR protein constantly, the gene It could have become dangerous to our health.
Dr. Perdew believes that humans developed a weaker AHR response as a way to find "a sweet spot," a compromise that minimized the damage of airborne contaminants without causing too many side effects.
These adaptations were never perfect, as evidenced by the fact that millions of people still die today from indoor air pollution. But evolution does not seek perfect health.
"All that matters from an evolutionary point of view is that it be reproduced," said Dr. Perdew. “If you die at age forty, so what? It's a cold and ruthless way of thinking about it, but it is what it is. "
A changed environment
Our species arrived at the Industrial Revolution two centuries ago with bodies that had been molded over millions of years by this highly imperfect process.
Clean water, improved medications and other innovations dramatically reduced deaths from infectious diseases. The average life expectancy skyrocketed. But our exposure to toxins in the air also increased.
"If we compress the last five million years in a single year, it will not be until December 31 at 11:40 p.m. that the Industrial Revolution will begin," said Dr. Trumble. "We are living in the smallest detail of human existence, but we believe that everything around us is normal."
The industrial revolution was largely driven by coal, and people began to breathe the fumes. The cars became ubiquitous; propagation of power plants and oil refineries. Tobacco companies manufactured cigarettes on an industrial scale. Today they sell 6.5 trillion cigarettes a year.
Our bodies responded with perfected defenses for hundreds of thousands of years. One of his most powerful 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 can affect our ability to eliminate defective proteins. As these proteins accumulate, they can lead to dementia.
Pathogens can get caught in contaminant particles. When they enter our noses, they can make contact with nerve endings. There, they can trigger even more inflammation.
"They provide this road that is a direct route to the brain," said Dr. Fox of the University of California, Los Angeles. "I think that's what makes this a particularly scary story."
Some genetic variants that emerged in our smoky past may offer some help now. They could allow some people to live a long time despite smoking, Dr. Finch and Dr. Trumble suggest.
But researchers have studied another gene for which the opposite seems to be true: a variant that was once useful has become harmful in an era of increasing air pollution.
The variant, ApoE4, came to light for the first time because it dramatically increases the risk of developing Alzheimer's disease. More recently, researchers also discovered that ApoE4 increases the risk that exposure to air pollution will lead to dementia.
But these studies were restricted to industrialized countries. When researchers searched other societies, such as farmers in poor villages in Ghana or indigenous people in the forests of Bolivia, ApoE4 had a very different effect.
In these societies, infectious diseases remain an important cause of death, especially in children. Researchers have discovered that in these places, ApoE4 increases the chances of people surviving to adulthood and having children.
Natural selection may have favored ApoE4 for hundreds of thousands of years due to this ability to increase survival. But this gene and others may have had harmful side effects that remained invisible until the modern sooty and smoking age.