WHY air pollution causes lung disease is obvious. Why it also causes heart disease is, though, a conundrum. One suggestion is that tiny particles of soot migrate through the lungs, into the bloodstream and thence to the walls of blood vessels, where they cause damage. Until now, this has remained hypothetical. But a study published in ACS Nano, by Mark Miller of Edinburgh University, suggests not only that it is correct, but also that those particles are specifically carried to parts of blood vessels where they will do maximum damage—the arterial plaques associated with cardiovascular disease.
One reason the particle-migration hypothesis has proved hard to confirm is that it is tricky to follow soot around the body. Soot is made of carbon, and that element, when finely divided and at low concentration, is difficult to isolate in biological material. Instead, Dr Miller and his colleagues used soot-sized particles of gold for their experiments. These are easy to detect, even at low concentrations, by means such as mass spectroscopy and Raman spectroscopy. Also, gold is chemically inert and therefore unlikely to be toxic. This is important, because some of Dr Miller’s experimental animals were people.
The first group of these human guinea pigs were 14 healthy men. Each was asked to exercise for two hours while inhaling air containing particles of gold. Dr Miller and his colleagues then monitored the volunteers’ blood and urine for 24 hours, and again three months later.
As expected, none of the volunteers showed signs of gold in their blood or urine before their exposure to the particles. All but two, however, did so 24 hours later. This proved that tiny particles can indeed migrate from the lungs into the circulation. Moreover, at the three-month recheck, the concentrations of gold in their bodily fluids remained more or less unchanged. Gold, once breathed in, is retained.
This experiment did not, however, tell Dr Miller where the particles were going and how they (or, rather, their carbon equivalents) can cause heart problems. He and his colleagues suspected that the culprits were immune-system cells called macrophages. These exist to engulf foreign bodies, such as bacteria, and would thus be quite capable of swallowing small particles of carbon or gold. They are also involved in inflammatory responses, which are helpful when short-lived (such as in reaction to a wound) but threatening when chronic (as in the inflammation associated with arterial plaques). Dr Miller and his colleagues thus wondered if their particles were being carried specifically to those plaques by macrophages.
Preliminary experiments on mice genetically engineered to be prone to vascular disease suggested they were. Dr Miller made these animals breathe in gold particles twice a week for five weeks. Then, a day after the final exposure, he killed and dissected them. He found that a given mouse’s diseased arteries contained five times as much gold as its healthy ones did.
To see if something similar is true in people, the team then recruited three further volunteers. In this case, those signed up were the opposite of healthy. They were patients with plaque-clogged arteries, who were at risk of suffering a stroke. This particular trio were asked to breathe in the gold dust 24 hours before they underwent surgery intended to clear their plaques and unblock their constricted vessels. Dr Miller and his colleagues were thus able to examine the extracted plaques for the presence of gold—which they found, as by now they expected to, in abundance.
It remains to be determined whether particles of carbon behave in the same way as particles of gold. But, given carbon’s high chemical reactivity compared with gold’s, it is a fair bet that macrophages will be even more likely to notice and swallow it. So, though Dr Miller’s work does not point towards a better treatment for pollution-induced cardiovascular disease, it does add weight to the arguments of those who worry about levels of air pollution.
Source: Fatal attraction: The link between pollution and heart disease | The Economist
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