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Almost every afternoon my friend Carl and I go for a walk usually on the Apollo section of the Roaring Run hiking trail. We’ve agreed on a few restrictions on our walks: the temperature can’t be below 24 degrees or above 90, it can’t be raining too hard (a light drizzle is OK, though, and snow is very acceptable), and there can’t be an on-going Code Orange (or higher) air quality alert.
The Pennsylvania Department of Environmental Protection (PA-DEPA) issues the color coded air quality alerts (Green (good), Yellow (moderate), Orange (unhealthy for select groups), Red (unhealthy), Maroon (very unhealthy) and Purple (hazardous)) based on their measured levels of ozone, particulates, sulfur dioxide, carbon monoxide and nitrogen dioxide in ground-level air. These pollutants come from a variety of sources including cars, power plants, factories, construction sites, incinerators and other types of fires. Ozone is especially formed in the summer when high temperatures and sunlight drive the conversion of some of these gaseous pollutants into ozone-rich soup of smog, but most of the other pollutants (especially the particulates) are present all year round.
When these continually generated pollutants become trapped in a ground level volume of air they can quickly build up to unhealthy levels. Stagnant winds and temperature inversions, a phenomenon where a layer of warm air forms over a lower layer of cold air and prevents its movement or mixing, can lead to the local accumulation of pollutants. The river valleys of Western Pennsylvania are common places where temperature inversions can occur, and the frequent Orange alerts that are posted in our area throughout the year reflects this landscape influence on our air circulation.
We try to avoid exposure to these unhealthy air days, but, apparently, according to a paper recently published in the Quarterly Review of Biology (December, 2019) humans and their bipedal, pre-human ancestors have been walking about and living in various types of polluted air for many millions of years, and the evidence for this is written into our genes!
Seven million years ago Africa became warmer and drier. One of the consequences of this climatological change is that the extensive forests of the African continent began to fragment and shrink leaving behind the great African grasslands called savannas. Primates, including some of our hominid ancestors, were very abundant in the African forests and were well adapted to arboreal life. The opening of the new, grassland habitats with their new resources and new sets of limiting factors, though, required a new set of anatomical features and specializations in order for a species to survive and succeed. Some of these features were anatomical (upright body posture, bipedal locomotion, etc.) and are well represented in the fossils of Australopithecus, one of our first, savanna dwelling ancestors. Other adaptations were physiological and are only just being revealed by the exploration of our living DNA and the preserved DNA in fossilized bones.
For example, drying Africa was a dusty place especially near the expanding Sahara Desert. The new savanna was also filled with grass pollen and microscopic spores and particles from the breakdown of the carcasses and the fecal remains of the evolving, great herds of grazing mammals. The primate species that stayed in the forests (the future gorillas and chimpanzees) were shielded from these airborne pollutants, but the pre-human, primate species that moved out into the savannas breathed great quantities of these into their lungs. One of the adaptations to this environmental stress was the development of a gene called the MARCO gene.
The MARCO gene enables macrophages throughout the body to grab on to bacteria or other irritant particles (like silica in the lungs) and remove them from contact with other, more sensitive cells. The version of MARCO seen in modern humans is quite different from the MARCO seen in present day apes. This modern human version has been dated to have finished forming about a half a million years ago and is found not only in Homo sapiens but also Homo neanderthalensis. It is hypothesized that the initial selection for this gene began many millions of years ago in the dusty savannas of Africa.
Homo erectus (the ancestor of both H. sapiens and H. neanderthalensis) domesticated fire possibly a million years ago. From that point on humans were extensively exposed to high levels of smoke and all of its associated toxins and irritants around campfires or in fire-heated dwellings. There is a gene in many mammals that produces a protein found in the skin, intestines and lungs. This protein breaks down many types of food, water and air-borne toxins. The gene is called “AHR.”
AHR, though, is not meant to function continuously or at high levels. The action of its protein generates some very damaging molecular fragments from the toxin. In organisms occasionally exposed to a toxin, these damaging by-products are tolerated, but, in organism continuously exposed to some toxin, these breakdown products can do a great deal of harm. Modern humans, according to paper published a few years ago in Molecular Biology and Evolution (October, 2016) have a very weak version of the AHR protein, possibly because of their million years or so of continuous exposure to smoke.
Another gene that might be at least peripherally related to the developing adaptation of humans to savanna existence is the ApoE4 gene. This gene functions to help modulate the inflammatory responses to pathogenic and also parasitic infections. It is also affected by air pollutants. If an individual has a sequence of diseases and parasitic infections throughout their lives, the ApoE4 gene and its proteins apparently can help that individual focus the inflammatory components of their immune response to control or destroy the disease causing pathogen or parasite. If, however, an individual does not have a robust infection/parasite history, the ApoE4 gene can trigger unacceptable inflammation in many systems of the body including some sections of the brain. This inflammation is one of the causes of Alzheimer’s Disease, and the ApoE4 gene is a genetic marker for individual’s with high chance of developing early onset Alzheimer’s and also Alzheimer’s that is triggered by air pollution. (see Signs of Summer 13, August 17, 2017)
A recent paper in BMC Medicine (20 March, 2019) outlines the extensive mechanisms of influence of the ApoE4 proteins and their relationship to Alzheimer’s, cerebrovascular disease, vascular dementia, dementia with Lewy Bodies, and Multiple Sclerosis. The functioning of this gene also illustrate a broader consideration of our evolutionary history and present day, post-industrial environment.
Humans have many genes designed to control and eliminate disease-causing agents from our bodies. The abundance of these genes reflects the impact that pathogens and parasites have had on human mortality and, therefore, human evolution throughout our long pre-industrial existence. With the development of sanitation and scientific medicine, death, particularly early, pre-reproductive death, due to infectious diseases has greatly declined. We still, though, have our full genetic arsenal that can trigger inflammation and immune system activity when stimulated by a wide range of environmental molecules that include many air pollutants. This has led to an increase in the chronic inflammation of many of the organs systems of our bodies. Alzheimer’s Disease, atherosclerosis (and its associated coronary and vascular diseases), chronic obstructive pulmonary disease, etc. are some of the great medical maladies besetting modern humans, and they may be the result of collateral damage from the inflammation that is triggered by our genetic adaptations to evolutionary and survival problems that we have so recently “solved” via our cultural and technological evolution.