And then came homogenization.? Milk manufacturers worked out that if they squeezed the milk at very high pressure through very tiny tubes, they could break up the fat globules and reduce their diameter by about a factor of five. That reduces the mass of each one by a factor of 125. Now the weedy upward buoyant push on each globule provided by gravity is completely overwhelmed by viscous forces. The homogenized fat globules rise so slowly that they might as well not bother.§ Just making them smaller shifts the battle into different terrain where viscosity can score a clear victory. Cream won’t rise to the top anymore. The blue tits had to find another source of breakfast.
So the forces are the same, but the hierarchy is different.? Both gases and liquids have viscosity—even though gas molecules don’t stick to each other like the ones in liquids, they jostle each other a lot, and the giant game of bumper cars has the same effect. This is why an insect and a cannon ball don’t fall at the same speed unless you take all the air away and drop them in a vacuum. Air viscosity matters a lot for the insect, and hardly at all for the cannon ball. If you take the air away, gravity is the only force that matters in both cases. And a tiny insect trying to fly in air uses the same techniques that we use to swim in water. Viscosity dominates their surroundings, just as it does ours in the pool. The smallest insects are swimming through air much more than they’re flying through it.
Homogenized milk demonstrates the principle, but its application goes far beyond the doorstep. Next time you sneeze, you might want to think about the size of the droplets you’re spraying around the room. What stops cream going up also stops disease coming down.
Tuberculosis has been with humans for millennia. The earliest record of it is in ancient Egyptian mummies from 2400 BCE; Hippocrates knew it as “phthisis” in 240 BCE, and European royalty were called upon to cure the “king’s evil” in medieval times. As the Industrial Revolution drove people to live in towns, “consumption,” the disease of the urban poor, was responsible for a quarter of all deaths in England and Wales in the 1840s. But it wasn’t until 1882 that the culprit was found, a tiny bacterium called mycobacterium tuberculosis. Charles Dickens described the common sight of consumptives coughing, but he couldn’t write about one of the most important aspects of the malady, because he couldn’t see it. Tuberculosis is an airborne disease. Carried out of the lungs with each cough are thousands of fluid droplets, plumes of minuscule crusaders. Some of them will contain the tiny rod-shaped TB bacteria, each only one ten-thousandth of an inch long. The fluid droplets themselves start off fairly big, perhaps one hundredth of an inch. These droplets are being pulled downward by gravity and once they hit the floor, at least they’re not going anywhere else. But it doesn’t happen quickly, because it’s not just liquids that are viscous. Air is too—it has to be pushed out of the way as things move through it. As the droplets drift downward, they are bumped and jostled by air molecules that slow their descent. Just as the cream rises slowly through viscous milk to the top of the bottle, these droplets are on course to slide through the viscous air to reach the floor.
Except they don’t. Most of that droplet is water, and in the first few seconds in the outside air, that water evaporates. What was a droplet big enough for gravity to pull it through the viscous air now becomes a mere speck, a shadow of its former self. If it was originally a droplet of spit with a tuberculosis bacterium floating about in it, it’s now a tuberculosis bacterium neatly packaged up in some leftover organic crud. The gravitational pull on this new parcel is no match for the buffeting of the air. Wherever the air goes, the bacterium goes. Like the miniaturized fat droplets in today’s homogenized milk, it’s just a passenger. And if it lands in a person with a weak immune system, it might start a new colony, growing slowly until new bacteria are ready to be coughed out all over again.
Tuberculosis is treatable if the right drugs are available. That’s why it has mostly disappeared from the western world. But at the time of writing, TB is still the second greatest killer of our species after HIV/AIDS, and it’s a gigantic problem in the developing world. Nine million people developed TB in 2013, and 1.5 million of them died. The bacterium has changed in response to antibiotics, becoming resistant to so many waves of drugs that it’s obvious it can’t be eradicated using medicine alone. The number of multi-drug-resistant strains of TB is on the increase. Outbreaks are popping up in hospitals and schools. So recently the focus has shifted to those tiny droplets. Rather than cure TB once you have it, how about changing your buildings to prevent the spread of those disease-laden plumes so it never gets to you in the first place?
Professor Cath Noakes works in civil engineering at the University of Leeds, and she is one of the researchers chipping away at this particular coalface. Cath is very enthusiastic about the potential for relatively simple solutions to emerge from a sophisticated understanding of tiny floating particles. Engineers like her are now learning how these tiny vehicles for disease travel, and it turns out this has very little to do with what’s in them and how long they’ve been there. It has everything to do with the battle of forces on the particle, and the battle lines are drawn by the particle size. It’s been discovered that even the larger droplets can travel farther than anyone had thought, because turbulence in the air can keep them aloft.# The tiniest ones can stay in the air for days, although ultraviolet and blue light damage them. If you know where your particle sits on the size scale, you can work out where it’s going to go. So, if you are designing a ventilation system for a hospital, it’s becoming possible to plan to remove or contain specific particle sizes, and therefore control the spread of disease. Cath tells me that each airborne disease may require a different plan of attack, depending on how much of it you need to get sick (in the case of measles, very little) and where in your body the disease settles (the TB bacterium has different effects in your lungs and your windpipe). These studies are still in their early days, but they’re advancing very quickly.
Humans have been at the mercy of TB for generations, but now we can visualize its spread, and that gives us the chance to control it. Where our ancestors saw only a foul room of sickness, awash with mysterious miasmas, we now understand the subtle swirling of the air around each patient, the sorting and shunting of disease particles, and how the consequences take effect. The outcomes of this research will be incorporated into the hospital designs of the future, and many lives will be saved by engineering on the macro scale to influence particles on the micro scale.