Mary Poppins was a fraud: The life of your average English chimney sweep was pretty crappy. Practically from the time they could walk, sweeps spent hours each day scrambling up into claustrophobic brick chimneys—some just 9 inches deep by 14 inches wide—in order to clean out grime and even put out the odd fire. At best, they emerged filthy with coal soot, their knees scraped raw from the climb. At worst, the sweeps got stuck, especially in crooked chimneys and chimneys narrowed by years of atherosclerotic soot buildup. If they got really stuck, a bricklayer would have to be found to cut them out, but not infrequently the poor lads suffocated in the meantime.
On top of all that, in later life, even if they’d squirmed up their last chimney decades earlier, the sweeps became susceptible to scrotal cancer. It started as scrotum warts. Many sweeps dispatched these warts by squeezing them between a split piece of wood and popping them off with knives or razors. Eventually, though, a sort of mesa of raised red skin appeared and turned into a smelly sore, which might spread to the thighs or anus. Doctors would either prescribe arsenic paste to slough the sores off, or operate and remove swaths of scrotum. Often, though, the sweep waited too long to seek care, and he would die. (If curious, you can see pictures of a similar scrotal cancer here, but be warned: they’re not for the squeamish. Then again, you have read this far ...)
The famous London doctor Percivall Pott first noticed the connection between chimney sweeping and scrotal cancer in a brief report in 1775. (Until then, many doctors mistook the sores for the French pox or other venereal diseases.) Pott and later doctors traced the source of the cancer to sending boys up still-hot chimneys (a common practice), which made them sweat and allowed soot to adhere to their wet skin. The scrotum’s many wrinkles provided an especially fine home for grime, especially when (another common practice) boys climbed naked and their thighs rubbed against their junk in the tight spaces, grinding the soot in. Chimney sweeps also had a well-earned reputation (even by 1700s standards) as being pretty indifferent to bathing, which meant the scrotum soot never got washed away. After years of such abuse, in Pott’s memorable summary, the cancer awakens and “seizes the testicle, which it enlarges, hardens, and renders truly and thoroughly distempered.”
Scientists have since proved Pott’s basic outline correct, and his remarkable medical detective work more or less inaugurated the field of occupational medicine. Still, Pott lacked the tools to work out every detail. He couldn’t have known, for instance, what exactly made the soot a carcinogen. Nor could he have explained the lag between the exposure as an urchin and the cancer as a man. Solving those two mysteries would in fact take centuries of work, but both answers would eventually trace back to a small bit of DNA on chromosome 17.
Despite an incredible variety of forms and presentations, all cancer basically traces back to mutated DNA inside cells. Most cells want to proliferate and copy themselves over and over, but for the good of the body at large, we have a system of watchdog genes that prevent them from doing so. This system is robust and redundant—multiple genes must fail for it to break down. But when it does fail, greedy cells multiply beyond control and hurt other tissue.
Many different chemicals can damage DNA and disrupt those cancer-prevention genes. Coal soot contains a chemical called benzo[a]pyrene, which itself doesn’t do much harm, but which our bodies metabolize into another chemical that isn’t so benign, BPDE. BPDE has a rude habit of butting in between the strands of the DNA double helix and bonding with one of the bases, G. This disrupts DNA replication and induces G mutations.
But BPDE doesn’t seek out just any old G. It seems to target Gs in one of the most important genes we have, p53, on chromosome 17. This gene makes a multitalented protein that helps determine the fate of a cell if it suffers any sort of DNA damage, including damage that can lead to cancer. If the damaged DNA strands look fixable, the p53 protein binds to certain handyman genes and activates them, enabling them to mend the damage before any potential cancer can get going. If the DNA has been frayed or mutilated beyond repair, the p53 protein arrests cell division and basically instructs the cell to commit suicide, stopping any cancer cold. In other words, p53 acts as a guardian, helping to fix any mutations it can, and ensuring that really dangerous cells get executed. But p53 cannot fix itself after BPDE damage, and if p53 goes down, malignant cancer-causing mutations can accumulate.
Over half of all human cancers involve p53 damage, including the scrotal cancer of Pott’s poor sweeps. Again, because cancer requires multiple genes to fail, not all of the sweeps came down with it. Many got lucky, apparently, and never accumulated additional mutations. (The need for multiple genes to fail also explains why the scrotal tumors took years to surface.) But in general, after BPDE paralyzed the p53 in their scrotal cells, chimney sweeps were vastly more vulnerable to cancer down there than gravediggers, butchers, coopers, cobblers, or other lower-class Londoners.
Despite Pott’s prescient work, English chimney sweeps continued to suffer for decades, in ways that sweeps in other countries did not. Pott scared the Danish sweepers guild, for instance, into urging daily baths on its members, and sweeps in other countries adopted acrobat-tight clothing with gaiters and hoods to keep soot off their skin. Cockney sweeps, meanwhile, when they weren’t scrambling up chimneys starkers, wore loose shirts and baggy pants whose folds actually collected soot. The English government tried to replace boy sweeps with mechanical contraptions in 1817, but special interests killed the movement. Not until 1840 did reform legislation pass, and even then some homeowners kept sending the urchins up the chimneys for decades more, slowly strangling, ash by ash, that crucial little bit of chromosome 17.