THE SMOKING GUN, OR WHAT CERTAINTY LOOKS LIKE
This blog is about cigarettes, Spanish ribbed newts, exploding batteries, teeth, and xeroderma pigmentosum.
You probably know that smoking is bad for you, because your parents told you so. But how did they know? Probably because the surgeon general of the United States told them so in 1964. But how did Luther Terry know?
Not how you think.
The clearest way to demonstrate that smoking is bad for your health is to do a randomized controlled trial, much like we talked about in blog one: take a bunch of people who don’t already smoke, divide them up into two pretty much equal groups (on separate deserted islands), prevent one group from smoking, make the other group smoke, and check in on both groups yearly for the next fifty years.
This study has never been done. Why? Because it would be wildly expensive and a gigantic pain in the ass. But then again, they built the Burj Khalifa. The real reason this trial hasn’t been done is ethics. Even back in the 1950s, people strongly suspected that smoking was bad for you, so no ethical researcher would have enrolled a nonsmoking patient in a trial that might require the patient to start smoking. Plus, most nonsmokers don’t want to smoke. So it’s hard to imagine them volunteering for a trial in which they might be required to do The One Thing They’ve Consciously Chosen Not to Do. For those reasons, a randomized controlled trial on smoking was never performed, and never will be.*
So how does science know that smoking is bad for you? Let us count the ways. First, we know that cigarette smoke contains at least seventy different molecules that can each cause cancer on their own. Remember formaldehyde, that super-promiscuous small molecule that will pretty much react with any biological molecule ? Turns out, formaldehyde causes cancer in humans and is in cigarette smoke. So is benzene. And arsenic, which, in addition to being the poison of choice for a few hundred years back in the Middle Ages, is also a carcinogen at lower, not immediately deadly doses.
You might reasonably ask how we know that each of those seventy molecules causes cancer. For many of them, it’s because a particular trade (e.g., chimney sweeps in nineteenth-century London) was exposed to very high levels of a chemical (e.g., soot) and people in that trade developed absurdly high rates of cancer (e.g., scrotal cancer). Other chemicals, like arsenic, occur naturally in drinking water in certain parts of the world, and you end up seeing lots of cases of cancer there. Then there’s animal experimentation. Every one of the seventy-plus chemicals in cigarette smoke has been independently given to almost every imaginable species of animal in the course of thousands of individual experiments by hundreds of scientists over the past fifty-plus years. All of those chemicals reliably cause cancer in at least one species.
Let’s zoom in briefly and talk about one specific class of chemical in tobacco smoke called N-nitrosamines. These molecular mafiosi cause cancer in rainbow trout, zebrafish, medakas, guppies, platyfish-swordtail hybrids, Spanish ribbed newts, palmate newts, African clawed frogs, northern clawed frogs, grass frogs, ducks, chickens, grass parakeets, opossums, Algerian hedgehogs, tree shrews, European hamsters, Syrian golden hamsters, Chinese hamsters, migratory hamsters,* Dzungarian dwarf hamsters, gerbils, white-tailed rats, regular rats, mice, guinea pigs, minks, dogs, cats, rabbits, pigs, thick-tailed bush babies, capuchin monkeys, grass monkeys, patas monkeys, rhesus monkeys, and cynomolgus monkeys.
That’s thirty-seven different species.
In addition to giving one chemical to a bunch of different species of animal, scientists also administered that chemical to one species in different ways. For example, let’s look at one chemical in the N-nitrosamine family called NNK.
Scientists put NNK into rats’ drinking water.
Result: lung cancer.
They injected it under rats’ skin.
Result: lung cancer.
They inserted it into rats’ stomachs via feeding tubes.
Result: lung cancer.
They swabbed it in the insides of rats’ mouths.
Result: lung cancer.
They inserted it directly into rats’ bladders via catheters.
Result: still lung cancer!
Not only did scientists test different species and routes of administration, they also tried varying the dose. That’s kind of intuitive: if you increase the dose of a toxin and the symptoms get worse, that’s a decent clue that the toxin might have something to do with those symptoms. A series of ten experiments done by scientists in at least three different institutions established what’s called a “dose-response curve” but which I like to call a “how far up shit’s creek you are” curve. Essentially, the scientists gave different groups of rats different doses of NNK and recorded what percentage of them developed lung cancer at each dose. For example, roughly 5 percent of rats given 0.034 milligrams per kilogram of body weight three times weekly for twenty weeks developed lung cancer, but when the dose was increased to .3 milligrams per kilogram of body weight, 50 percent of rats got lung cancer. At 10 milligrams per kilogram, roughly 90 percent did. (For reference, the dose of cyanide that kills roughly 50 percent of rats is about 5 milligrams per kilogram.)
As you can imagine, these experiments are a lot of work for scientists and a lot of cancer for rodents. In the roughly twenty-year period between 1978 and 1997, scientists published eighty-eight studies in which thousands of unlucky mice, rats, and hamsters were given NNK (and lucky ones were not). Animals given NNK developed markedly more cancer than the animals not given NNK. All these studies—and many more—show pretty convincingly that NNK and other N-nitrosamines are potent carcinogens in lots of different animals.
But hang on. Showing that there are known animal and human carcinogens in cigarette smoke—no matter how convincingly—doesn’t actually prove that smoking cigarettes is bad for you. You could imagine Big Tobacco saying, Sure, smoke has some chemicals in it, but it’s only in contact with your lungs for half a second before you exhale. None of those chemicals actually stay inside the human body.
Except they do, and we know they do in at least three different ways. First: the infamous black lung. Remember in high school when your teacher showed you that jet-black diseased-looking lung and told you it came from a smoker? It turns out that those “demonstration” lungs come from pigs, and since barnyard animals don’t usually go through two packs a day for twenty years, those lungs are artificially stained brown or black.* So if you had X-ray vision and could see into a smoker’s chest, it would not look like a coal mine. But if you were to compare an actual smoker’s lung with a nonsmoker’s lung under the microscope, you would see lots of cells called macrophages in both lungs. These cells are part of your immune system and basically gobble up any foreign material—including smoke particles—to try and prevent it from doing damage. But in the smoker’s lung, depending on how long the person had been smoking, the macrophages would look yellow, brown, or even black. This is because smoke particles are chemically difficult to break down, so macrophages store them in little compartments within themselves. Imagine your parents’ basement: trash bags full of useless and dangerous crap that they can’t throw away. Same idea. When enough of these particles accumulate, they become visible as little yellow or brown dots. The more you smoke, the more speckled your lungs become.
The second way we know cigarette chemicals get inside you is thanks to radioactive tracer studies, in which scientists use radioactive atoms to label certain molecules and then use a fancy Geiger counter to figure out how much radioactivity (which means how much of the labeled molecule) is in whatever organ they’re looking at. There have been a ton of radioactive tracer studies done over the years, but one in particular stands out: in 2010, scientists published a study in which they radiolabeled nicotine in cigarettes, put some people in a radiation body scanner, and asked them to smoke one single puff of a cigarette containing radioactively labeled nicotine. Roughly twelve seconds after the puff, radioactivity was detectable in the subject’s lungs; roughly twenty-two seconds post-puff, it was detectable in blood at the subject’s wrist; and roughly fifty seconds post-puff, it was detectable in the subject’s brain. This is pretty damn remarkable: it’s probably the closest we’ll get (for a while, anyway) to seeing a chemical spread out throughout the body as time passes.
The third way we know that chemicals in cigarettes get inside you is: pee. There have been tens, probably even hundreds, of what are called urinary metabolite biomarker studies, which is science-speak for “measuring specific chemicals in pee.” But let’s back up. You’ve heard the word metabolism, probably in the context of something like Bruh, it’s cold outside, my metabolism is slooooooow today. But metabolism is much more than how quickly you burn your food; it’s a spiderweb of chemical reactions that determine the fate of every molecule that gets into your body—food, drink, drug, or cigarette smoke. Your metabolism changes the molecules in cigarette smoke to make them dissolve better in water. This helps your body pee them out. Once they’re in your pee, scientists can measure them. The tricky part is that there are so many chemicals in cigarette smoke and so many metabolic reactions that it can be tough to figure out which chemicals came from cigarettes and which ones came from food, drink, other drugs, or the environment around you. There have been hundreds of studies comparing smokers with nonsmokers to try to clear up this mystery. Eventually scientists zeroed in on a hit list of eight possible biomarkers that were all chemically related to carcinogens in cigarette smoke. Then, in 2009, a group of scientists published a study in which they:
found seventeen smokers.
measured levels of those eight chemicals in their blood.
required the smokers to quit smoking.
kept measuring the eight chemicals every couple of weeks for two months.
Within three days of quitting, levels of five of the eight biomarkers went down by 80 percent or more. Levels of another went down by roughly 50 percent. And the seventh biomarker took about twelve days to reach 80 percent reduction. Only one of the eight didn’t show any reduction after quitting. This experiment is particularly convincing because you’re not comparing two different people; you’re comparing the same person as a smoker and then as a nonsmoker.
So scientists have established beyond a reasonable doubt that cigarette smoke contains carcinogens and that smoking brings those carcinogens into your body. This might seem like a lot of evidence—and it is—but it’s not enough to prove that smoking cigarettes causes lung cancer. All we’ve shown so far is that smoking cigarettes brings carcinogens into your body. What happens once they’re inside you?
Answering this question requires figuring out exactly what happens to each of the seventy-plus carcinogens in cigarette smoke once they get inside you: their “metabolic fate.” It turns out that carcinogens are not usually carcinogenic in their initial form. But as they pass through our metabolic machinery (specifically a protein with the Terminator-like name of cytochrome P450) they are converted—for an infinitesimally short time—to an activated form, meaning their chemical reactivity is turned up to an 11. Most of the time, they’re safely deactivated and peed out, but occasionally an activated molecule can slip away and form a chemical bond with something else in the cell, which, even more occasionally, is our old friend DNA. This general pathway—carcinogen gets into cells, gets activated by cytochrome P450, and then binds to DNA—has been tested in repeated experiments for hundreds of carcinogens over the past seventy-plus years, both with carcinogens found in cigarettes and those found outside of cigarettes.
Thus we have another link in the chain: carcinogens in cigarette smoke bind to DNA. But, believe it or not, chemicals binding to DNA still doesn’t prove that they cause cancer. We have to figure out what happens to that chemically altered DNA.
When chemicals bind to DNA in ways your body doesn’t expect (the way cigarette smoke carcinogens do), your body deals with the damaged DNA the way you try to deal with a damaged computer: by trying to fix the damn thing. In the best-case scenario, a cell successfully repairs its DNA, and you go on with life as if nothing happened. Occasionally, though, the damage is unfixable or the repair effort fails. In that case, the cell goes, I’M OUT, and kills itself.* This might seem bad, but it’s not the worst thing that could happen. There are a couple scenarios that are worse. The cell could fix the damage but do a bad job. Or it could fail to detect the damage before starting to copy its DNA . . . and copy it wrong. Either way, the result is a mutation.
You’ve probably heard of DNA mutations. A mutation is a change in the genetic code, the blueprint the cell uses to live its life. If our logical chain of reasoning so far is correct, we would expect smokers to have more mutations in their DNA than nonsmokers, because they’ve had more chemicals bind to their DNA than nonsmokers. And they do. There haven’t been quite as many studies done to support this part of the logical chain, because large-scale DNA sequencing has only recently gotten cheap enough to do routinely. But in one striking example, researchers surgically removed a lung tumor from a fifty-one-year-old man who had been smoking twenty-five cigarettes per day for fifteen years and found more than 50,000 mutations compared to a nonsmoker’s genome. Other studies haven’t shown quite as dramatic a difference, but they consistently show that smokers have many more mutations than nonsmokers.
We’re still not done. Scientists have shown pretty convincingly that smokers have more mutations in their DNA, but how do we know that mutations cause cancer?
Between 1938 and 2017, the U.S. government appropriated almost $130 billion to the National Cancer Institute. Today, NCI spends roughly $5 billion per year on cancer research, making cancer the number one destination of our research dollars. A lot of this money goes toward figuring out what causes cancer, and the consensus answer is that DNA mutations cause, or help drive the growth of, lots of different cancers.* Let’s look at two pieces of evidence (out of many) that support this idea.
One comes from a completely different field. There’s a rare human disease called xeroderma pigmentosum, or XP, which sounds like a Harry Potter spell but is actually a devastating disease. People with XP are extremely sensitive to the sun. They get badly sunburned within a few minutes of being in full sun, develop freckles pretty much everywhere they don’t cover up, their eyes go red, and those under twenty have rates of skin cancer about 1,000,000 percent higher than normal. That’s not a typo. One million percent higher. In 1968 scientists discovered that XP is caused by inherited mutations in a few key genes your body needs to repair its DNA. This fits in very nicely with the theory that DNA mutations can cause cancer: if your body is bad at fixing its DNA, DNA damage would become mutations much more frequently, and that would explain the incredibly high rates of cancer among people with XP.
Another piece of evidence is more related to smoking. Scientists recently sequenced thousands of genes from 188 lung tumors and found that the two most commonly mutated genes were KRAS and TP53, both of which we know—thanks to the $130 billion NCI has spent on cancer research—are involved in pushing cells to grow faster (KRAS) and preventing them from shutting themselves down if they get out of control (TP53). Both of these behaviors are classic markers of cancer cells. So that’s an excellent clue, but to really prove that mutations in those genes cause cancer, you have to actually mutate them and see what happens. Amazingly, we have the technology to insert mutant copies of KRAS and TP53 into human egg cells and see if the resulting humans get lung cancer . . . but that might be one of the cruelest studies ever conceived. Instead, scientists mutated both those genes in fifty-six mice. Every single mouse got lung cancer. In nineteen mice (34 percent), the cancer metastasized. By comparison, only 5 percent of mice with just KRAS mutated had metastatic cancer.
That’s one way to explain the wrench. We could also revisit the penultimate link in the chain: DNA damage, if not properly fixed, can lead to mutations. What if certain people are just better at fixing their own DNA than others? We’ve already seen that certain people who are particularly bad at fixing their DNA (those with xeroderma pigmentosum) end up with insanely high rates of skin cancer if they aren’t super-careful to avoid ultraviolet light their entire lives. It’s conceivable that certain other people are particularly good at fixing their DNA. In this group, you’d guess that smoking would cause just as much DNA damage as in anyone else, but it would be repaired more quickly and with fewer mistakes. So most DNA damage would not lead to mutations, and these people could smoke their whole lives and never get lung cancer.
There’s a third way to explain the wrench. In addition to lung cancer, smoking also causes a smorgasbord of other diseases, including cardiovascular disease and stroke. So you could die of a heart attack way before smoking would have given you lung cancer.
All the experiments we’ve looked at in the previous pages were done after the surgeon general issued the 1964 report. And yet, knowing very little about the exact chemical mechanism of how smoking causes cancer, the authors of the report wrote: “Cigarette smoking is causally related to lung cancer in men” (emphasis mine) and “The risk of developing lung cancer increases with duration of smoking and the number of cigarettes smoked per day, and is diminished by discontinuing smoking.”
They did not write “seems to be related to” or “may cause” or “might influence” or “could potentially be a contributing factor to the genesis of the existence of” lung cancer. They just came right out and told the nation that smoking is a cause of lung cancer.
How could they have been so sure? Remember, there had never been one single solitary randomized controlled trial on the long-term health effects of smoking.
First, you should know three pieces of background information.
Piece one: In the early 1960s, about 40 percent of Americans smoked, and each smoker blew through over 4,000 cigarettes per year, on average. That’s roughly half a pack per day.
Piece two: Before the early 1900s, lung cancer was an incredibly rare disease—so rare that, in 1898, one single solitary PhD student wrote one article that reviewed all the lung cancer cases in the world: 140 cases. Throughout the twentieth century, there was an incredible rise in lung cancer cases, which paralleled—with a three-decade delay—the rise in cigarette sales.
Piece three: About 60 percent of Americans didn’t smoke, so there were plenty of nonsmokers available to compare against the smokers. Lots of people were ready and waiting to become science.
These three things frame what may well be the most ambitious knowledge-gathering exercise humanity has ever performed. In the late 1950s and early 1960s, well over a million people were enrolled in studies on smoking: their every ailment, condition, disease, morbidity, and dysfunction observed, classified, verified, and recorded, from the moment they were enrolled to the moment they died (or didn’t). Some studies were relatively small and short; others included half a million people and are still underway to this day, more than fifty years later. All of them were “prospective cohort” studies.
As we saw in previous blogs, in these studies, you recruit a bunch of people, put them through a medical exam, get them to tell you whether they smoke and how much, and then follow everyone for years and see which group has more lung cancer (or heart disease, or death, or whatever outcome you’re interested in). The concept is similar to a randomized controlled trial, except that you don’t require people to smoke (or not smoke). You just find people and record whether they are already smoking (or not).
The authors of the surgeon general’s report relied on data from seven cohort studies to investigate whether there was a link between smoking and lung cancer. In one British study, every participant was a doctor. (Back in 1964, a lot of doctors smoked.) In another, every participant was a veteran. The largest study—448,000 participants—was of American men in twenty-five states. Some studies had been operational for just five years. Some had been running for over twelve. All told, the studies had enrolled over a million people in England, Canada, and the United States.
The results were stunning. On average across all studies, smokers were about eleven times as likely to die of lung cancer than nonsmokers. “Eleven times as likely” means 1,100 percent—one thousand one hundred percent—as likely. If you took a nonsmoker’s risk of dying from lung cancer, doubled it, doubled it again, and doubled it a third time, it would still be lower than a smoker’s risk of dying from lung cancer.
Let’s take the evidence train to the next logical station. If cigarettes kill you, you would expect more cigarettes to kill you more.* Four of the seven cohort studies tracked how many cigarettes participants smoked. In every single study, the risk of dying from lung cancer increased steeply with increasing numbers of cigarettes smoked. Likewise, you’d expect that people who inhaled more deeply would get a higher lifetime dose of cigarette smoke. And indeed, people who inhaled “deeply” had a 120 percent greater risk of dying than nonsmokers.
No matter how the authors sliced and diced the numbers, the conclusion from all the cohort studies was the same: people who smoked were much, much more likely to die from lung cancer than people who didn’t smoke; and they were also more likely to die from other diseases than people who didn’t smoke.
But did that mean that cigarette smoking caused lung cancer?
The tobacco industry had been insisting for years that the answer was “not necessarily,” using arguments like this: Yes, there is a parallel between the sale of cigarettes and lung cancer, but there is also a parallel between the sale of silk stockings and cancer of the lung and also that simply because one finds bullfrogs after a rain does not mean that it rained bullfrogs. Allow me to add my own metaphor to the mix: just because a warm pie is sitting on your kitchen counter doesn’t mean your mom came over unannounced and baked it. The point of all these metaphors is this: just because two things are associated doesn’t necessarily mean that one thing caused the other. There may very well be alternate explanations. Silk got more fashionable. Bullfrogs converge after a rain to eat worms. Little Red Riding Hood could have brought the pie over from her place, you could have ordered it off Seamless, it could have been reheated from two days ago, or aliens could have baked it and teleported it inside your house. Now there will silk-clad bullfrogs eating a pie baked by aliens in your dreams. You’re welcome.
Anyway, lots of people debated alternate explanations other than smoking for the incredible rise in lung cancer: Were doctors simply better at diagnosing it? Could it be car exhaust or the paving of roads, both of which rapidly increased alongside cigarette smoking? What about industrial pollution? Or maybe it wasn’t related to chemicals in the environment at all; maybe there was some gene that caused both a craving for cigarettes and lung cancer. So we come back to our original question: How were the authors of the surgeon general’s report so sure that smoking was causing lung cancer?
It wasn’t because they understood the how. Yes, there had been some animal experiments, the most notable of which involved condensing cigarette smoke and painting it on mouse skin, which resulted in skin cancer.* And scientists had also identified a small number of likely or known carcinogens in cigarette smoke. But the crux of the authors’ reasoning was mostly based on the large prospective cohort studies that showed four things:
Lung cancer happened after—not before—smoking.
The vast majority of lung cancers happened in smokers.
This link was found in a variety of different populations.
The increase in risk was huge and got higher the more you smoked or the deeper you inhaled.
And there’s one other thing to consider: the day-to-day experience of someone with lung cancer. It’s not an easy cancer. You don’t just get to chill out in a hospital, have a minor procedure, joke around with the nurses, and then go home to your cancer-free life. Even today, with all the advances of modern medicine, your chance of still being alive five years after a lung cancer diagnosis is about 19 percent. So, as the committee was considering whether to definitively say that smoking caused lung cancer, they must have had these considerations in the backs of their minds—and they knew that lung cancer deaths were skyrocketing. In 1898, it was a medical oddity. By 1964, it was killing more than 50,000 Americans every year. Today, that number is over 140,000. (Globally, lung cancer killed almost 1.8 million people in 2018.) So even though there wasn’t the incredible breadth of mechanistic evidence linking smoking to lung cancer that we have today, there was a large body of observational evidence, no plausible alternative explanation, and a catastrophic potential downside to not speaking out. This was enough for the committee and the surgeon general to put a stake in the ground and announce definitively that smoking causes lung cancer.
CIGARETTES CONTAIN CARCINOGENS
THOSE CARCINOGENS GET INSIDE YOUR BODY
ONCE THERE, THEY CHEMICALLY REACT WITH DNA
THIS SCREWS WITH IMPORTANT PROCESSES LIKE COPYING DNA, SO YOUR BODY TRIES TO FIX THE DAMAGE
OCCASIONALLY THIS RESULTS IN A MUTATION
MUTATIONS ACCUMULATE IN YOUR DNA
ENOUGH MUTATIONS IN GENES THAT CONTROL CELL GROWTH CAN PUT CELLS ON THE PATH TO CANCER*
Plus, more than a million people were enrolled in multiple long-term observational studies, and no matter where the study was done or who the participants were, the increase in lung cancer risk among smokers was stratospherically high and increased the more they smoked.
All the people involved—the participants in all these studies, the surgeon general’s committee members, the scientists puzzling out the mechanism—and all the animals who died in service of the cause did something pretty frickin’ incredible. They built a bridge from the Land of Not Knowing, shrouded in mist and shadow, to the Land of Almost Certainly Knowing. This bridge is built from thousands of experiments and studies, each a dense brick, supporting and being supported by others, without holes between them, together spanning the full width of the Gulf of Ignorance. We haven’t talked about every single brick—not by a long shot. But hopefully all the bricks we have talked about, and the logical mortar that binds them together, give you a reasonable idea of what it looks like when a group of scientists well and truly know something.
Unfortunately, as we’ve seen before, scientists are really bad at naming things, and this is no exception. Instead of something cool like BRIDGE OF TRUTH, scientists decided to name these bridges “theories.” As you might already know, the word theory means something very different in science than it does in English.
In English, a theory is usually a flimsy explanatory thought generated by an observation or two. For example: you wear a red shirt and win a golf tournament. Theory: red shirts make you better at golf.
In science, a theory is a solid and well-constructed Bridge of Truth. Gravity. Atoms. Evolution. All these are scientific theories: unlikely to collapse if you wear a red shirt and lose.
I’m not a fan of the word theory, for two reasons:
It has two exactly opposing meanings in science vs. English (solid vs. flimsy), and
the English definition has already won.
Let’s not sugarcoat this last point. To most people, the word theory means “crazy idea that I just pulled out of my butt.” And that’s why a sentence like “scientists have developed a theory that smoking causes lung cancer” sounds so . . . unimpressive. We’ve all got that stubborn English definition kicking around in our stubborn brains.
But in the also-stubborn real world, scientists know that smoking causes lung cancer.
Despite the now utterly overwhelming evidence that smoking causes cancer—as well as heart disease and other things you definitely don’t want—the tobacco industry is doing spectacularly well. Why? Basically, because it managed to export cigarettes from England and the U.S. to the rest of the world.* But as any good Stock Photo Businessperson will tell you, diversifying your integrations will synergize your corpuscles. In other words, it’s better to not have all your eggs in one basket. For a long time Big Tobacco’s one basket was the cigarette. And even though the cigarette is generating loads of cash outside the U.S., it sure would be nice (for Big Tobacco) if there were an alternate nicotine delivery device to help diversify the corpuscles here at home.
Enter the electronic cigarette, also known as the e-cigarette. We know a lot less about the chemistry and health effects of e-cigarette smoke (also called vapor) than we do about regular cigarette smoke, but let’s wade out into the evidence and see what we can see. The most dramatic difference between regular cigarettes and e-cigarettes actually has nothing to do with smoke. Regular cigarettes are powered by the energy released when tobacco burns. E-cigarettes, on the other hand, are powered by lithium ion batteries, which means that they sometimes decide to catch fire or explode, seemingly by themselves. This produces some truly horrific injuries.
In one case, an e-cigarette exploded while in the mouth of an eighteen-year-old, breaking one of his front teeth at the gum line, smashing another all the way up into his gum, and blowing a third clean out of its socket. In another case, a twenty-year-old man’s e-cigarette suddenly exploded, shooting the mouthpiece into his face with so much force that it broke the right bridge of his nose, splintering the bone into pieces. And because apparently that wasn’t enough, the battery shot out in the other direction and started a fire—adding arson to injury. In a third case, a twenty-six-year-old man was testing an experimental model when it failed catastrophically, spraying shrapnel into the man’s chest and left shoulder. Remember that time Dick Cheney “accidentally” shot his hunting partner in the face? Yeah, this looked like that. (The doctors treating him called his skin injuries “shotgun-like.”) Finally, there have been many cases of e-cigarettes exploding in people’s pockets, causing burns and other havoc to their thighs. I’ve read at least two cases in which people ended up with second-degree burns or other damage to their woo-hoo parts. E-cig explosions are, of course, incredibly rare. But the damage shows just how much energy is packed into those little batteries.
The less dramatic but more obvious difference between regular cigarettes and e-cigs is that regular cigarettes have many more chemicals in them than e-cigarette liquid (a.k.a. e-liquid or e-juice). At first blush, this is counterintuitive: after all, regular cigarettes are basically just dried-up tobacco leaves rolled up in a piece of paper with a filter stuck at one end. If you count only the ingredients that get used up during smoking, that’s a grand total of . . . two. In the opposite corner, a recent analysis of e-cigarette liquid suggests that despite having just three or four ingredients listed on the label, there could be sixty or more different chemicals floating around in there. But before you fall off your chair, remember that “tobacco” is not a single ingredient: each leaf was once a living thing made of countless cells, each carrying DNA, proteins, sugars, and a cacophony of other chemicals the plant made before it was picked, washed, cured, cut, and stuffed into a rolled piece of paper. So what looks like just two ingredients is actually many more: at last count, there were about 5,700 different chemicals identified in tobacco (not including additives), and the scientists who wrote the book on tobacco chemicals estimate that there are “literally tens of thousands” more yet to be identified.
But there’s one chemical that looms large. You could say there’s
One chemical to rule them all, one chemical to find them.
One chemical to bring them all, and in the smoker bind them.
Nicotine.
Nicotine is the main reason smokers keep smoking; it’s what makes cigarettes addictive. It’s also the whole point of e-cigarettes: they were invented to deliver nicotine without the side dose of cancer. In addition to being addictive, nicotine is also poisonous the old-fashioned way: if you get too much of it inside you, you’ll die. If it makes you feel any better, we’re not nicotine’s intended target; tobacco plants make it to kill insects that would otherwise eat them. In other words, nicotine is a natural pesticide; in fact, it was extracted from tobacco and used as a pesticide as far back as the seventeenth century. And tobacco plants evolved a pretty potent poison: even the most conservative estimates put the lethal oral dose at around 10 milligrams per kilogram of body weight. That means that a 30-milliter bottle of high-nicotine e-liquid contains enough nicotine to kill a fully grown adult, and more than enough to kill a toddler. You would have to eat 83 cigarettes—or smoke 603—to get the same amount of nicotine that’s in that 30-milliliter bottle. Also, while cigarettes taste like . . . cigarettes, e-liquid can taste like “Birthday Cake,” “Fruit Loops,” or any of thousands of other flavors designed to make kids want to eat them.* So if you vape, please keep your e-juice away from kids: some of those bottles are literally candy-flavored poison.
Finally, we arrive at the least obvious—and most important—difference between regular and e-cigarettes: the smoke.
To understand the difference between “vape” and “smoke,” we have to go back to the first difference. A regular cigarette is powered by a combustion reaction, which means smoking it is somewhat like sucking on the tip of a tiny campfire. If you took high school chemistry, you were probably taught that combustion looks like this:
A NICE SIMPLE HYDROCARBON (LIKE METHANE) | + | OXYGEN | → | CARBON DIOXIDE | + | WATER |
But there was also this thing called incomplete combustion, which looked like this:
A NICE SIMPLE HYDROCARBON (LIKE METHANE) | + | NOT ENOUGH OXYGEN | → | CARBON MONOXIDE | + | WATER | + | CARBON |
If a cigarette was (a) a simple hydrocarbon and (b) combusted completely, the only two products of the reaction would be carbon dioxide (a gas) and water (also a gas, since the burning happens at high temperatures). Cigarettes would disappear into thin air as you smoked them. Obviously, this does not happen. Cigarettes are chemically incredibly complex mixtures, and they do not combust completely. So instead of a nice simple reaction, the best we can do is something like this:
BURNING THING MADE UP OF THOUSANDS OF CHEMICALS | + | NOT ENOUGH OXYGEN | → | GIGANTIC CHEMICAL CLUSTERWHOOPS OF THOUSANDS OF CHEMICALS |
Cigarette smoke is a wildly complex chemical cocktail. What about e-cigs?
If lighting up a regular cigarette is like sucking on the tip of a tiny campfire, then vaping is like a cross between huffing a can of hairspray and a Glade PlugIn. An e-cigarette is not powered by a combustion reaction; instead, a metal coil heats up the e-liquid to about 302°F to 662°F (150°C to 350°C—kind of like a plug-in air freshener), which generates a mist (kind of like what comes out of a can of hairspray). Regular cigarettes burn much hotter: 1,472°F (800°C) or higher. Because the temperature is much lower in an e-cigarette, and because e-liquid is chemically much simpler than tobacco, the number of chemicals in e-cig vape is almost certainly much lower than in regular cigarette smoke. Why almost certainly? Because e-cigarettes haven’t been around for that long, and it can take a while to try and figure out what’s in something. In 1960, fewer than five hundred chemicals had been identified in tobacco and cigarette smoke. (Those numbers have risen fairly steadily to more than 10 times the number today.) My point is: there is probably more to discover in e-cigarette mist—and we’re starting to do exactly that.
Speaking of “mist,” I have to hand it to whoever came up with that term (and “vaping”), because those words make it sound like you’re sipping on a harmless fluffy cloud of water vapor . . . which you’re not. Even though there’s no combustion reaction as in a regular cigarette, the vaporizer gets hot enough to do some chemistry. For example, the heat can break down two of the most commonly used chemicals in e-liquid, propylene glycol and glycerin (a.k.a. glycerol), forming formaldehyde, acetaldehyde, and acrolein. You definitely don’t want to be breathing in buckets of formaldehyde , and the same goes for the other two musketeers in this particular trio. All three of these guys have been reliably detected in many different brands of e-cigarette mist (though all at lower levels than in cigarette smoke), along with roughly eighty other chemicals along for the ride in the e-liquid or produced by its vaporization.
Let’s pause here and take a quick detour into the world of chemical accounting.
As many people have already noted, 80 chemicals is a lot fewer than 5,700 chemicals. And if you’re a vaper, you’ve probably seen a sentence in an ad that goes something like: “E-cigarettes don’t have nearly as many chemicals as cigarettes do, so they’re not as bad for you.” And you’ve definitely seen at least one anti-smoking ad that says something like: “There’s a toxic mix of more than 7,000 chemicals in every puff.” The implication is clear: the more chemicals something contains, the worse for you it is.
This is, in my opinion, wildly illogical.
You know what else has thousands of chemicals in it? Iceberg lettuce. So does chicken. And lima beans. By contrast, cyanide has exactly one chemical in it. It is one chemical, and a very simple one at that—and it’s deadly. The number of chemicals in something is the least useful piece of information you could be given. It is, like that Instagram post of your friend in the gym, marketing bullshit. It tells you nothing about what those chemicals do in your body, or even how much of each chemical is in the thing. Cigarettes cause lung cancer, but it’s not because there is some chemical accountant who decided long ago that anything with more than thirty-seven chemicals in it must be toxic. Cigarettes cause lung cancer because of which chemicals are in smoke and how much of them there are, not how many.
So, for the chemicals we know are toxic, what’s the difference between regular cigarettes and e-cigarettes?
From the handful or so experiments that have been done so far, it seems like e-cigarette mist has fewer known toxins than regular cigarette smoke, and the ones it does have are present at lower levels. For example, the amount of formaldehyde in e-cigarette mist is roughly one-tenth the amount in regular cigarette smoke, and the amount of NNK (the potent lung carcinogen) in e-cigarette mist is roughly one-fortieth the amount in regular cigarette smoke.
So let’s break out the champagne-flavored e-juice, amirite?
Not quite yet.
Here’s where we get into the two sides of the vape debate.
The Optimists: E-cigs have way less toxic shit in them than regular cigs, so they’re better for you!
The Cautious Folk: Just because they’re better for you doesn’t mean they’re not bad for you. You’re still inhaling an aerosol with a bunch of known toxins in it.
I have to say that I find the Cautious Folk’s argument slightly more convincing. Getting shot with a .22 is certainly healthier than getting shot with a .357, but that doesn’t mean the .22 is healthy. Comparing e-cigarettes to regular cigarettes makes the e-cigarettes look pretty damn good, but that’s mostly because regular cigarettes are so bad. It’s entirely possible that e-cigs are much healthier for you than regular cigarettes and also increase your risk of lung cancer or other diseases. The more informative comparison is exactly the same one that was done for regular cigarettes: How bad are e-cigarettes for you compared to . . . nothing? We can reasonably guess that they’re worse for you than nothing, but as for how much worse—we don’t really know the answer to that yet. A few studies are starting to emerge, like early spring flowers poking through the snow, but e-cigs haven’t been around that long, so the type of large long-term prospective cohort studies (like the ones scientists did on regular cigarettes) are still under way.
But there’s yet another thing to consider: the ramp theory. Let me explain. If you want to quit smoking but keep the nicotine, there are a few different options available: the patch, gum, lozenges, inhalers, etc. But none of these replicate everything that goes along with smoking: lighting up, inhaling, the quick nicotine hit, pairing cigarettes with coffee, smoke breaks—in other words, the whole ritual. The pharmacist who invented the modern e-cigarette, Hon Lik, wanted to develop something that both delivered nicotine and also preserved the ritual, because he felt that was the best way to switch from regular cigarettes to something less harmful. And I don’t blame him: this makes perfect sense. If you want smokers to quit, it’s easier to guide them down a ramp than throw them off a cliff. But the problem with ramps is they can work both ways: you can imagine a scenario in which people who have never smoked in their lives might take up vaping, adopt all the smoking rituals, and eventually start smoking regular cigarettes.
This type of theorizing gets complicated fast, but the basic point is that the health impact of e-cigarettes doesn’t just depend on how bad they are for you; it also depends on how vaping influences smoking—both starting and quitting.
So, tl;dr.
Smoking: we absolutely know it’s terrible for you, and we know how terrible it is for you.
Vaping: we don’t know exactly how bad it is for you, but we do know it’s not good for you. That said, if you have to choose between smoking and vaping, all available evidence points strongly to vaping. It may help you quit, and it seems like it’s not as bad for you as smoking. But if you’re choosing between vaping and nothing, all available evidence points strongly to nothing, for three reasons. Reason one: vaping is almost certainly worse than good ol’ plain air. Reason two: vaping can be an on-ramp to the thing we know is terrible for you—smoking. Reason three: the vape liquid could be contaminated.
If the tl;dr was tl and you dr, just remember this:
And if you do vape, keep that e-cig far away from your junk.
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