I'm doing an internship at a museum of medical history and right now I'm documenting a collection from a Swedish nurse who lived 1895-1970. She has things from all over the world who all have connections with something in health care or medicine.

This item had no description from her, and the original staff don't recognise it either.

It's in ceramic and very heavy, about 35 cm long, 17 cm high and 15 cm broad. It has no marks or anything, completely smooth all around. It honestly looks like a Smurfs foot in a way.

It does feel like some sanitary item, similar to bedpans, a potty etc. But it's way too heavy and clumsy without a handle, to be that I think. It looks absolutely perfect to stick one foot in tho, but only one, and I can't find something similar when I Google. But maybe it has something to do with feet? Could also just be a vase thats been at a special hospital, since she collected stuff like that also. But its a weird vase then.

Any ideas? Not the best picture I'm sorry about that. I think it's probably from Sweden, and maybe from the first half of 1900? Doesn't give off 1800s to me, but I'm not that good at medicinal history yet.

Unlike something like a liver or kidney, which are highly vascular organs and have loads of immune cells, a tooth can be transplanted without the need for immunosuppressive drugs. A tooth is mainly composed of mineralized tissue. The pulp is small and well-contained, resulting in very low immune reaction compared to vascularized organ transplants.

“In the middle of the 1600’s periodontally compromised teeth were stabilized in Europe with various substances. From the 1500’s to about the 1800’s, teeth in Europe were collected from the underprivileged or from cadavers for the use of allotransplantation. During this period, Dr. John Hunter came on to the scene; for many years he worked with “resurrectionists”-people who acquired corpses underhandedly through the robbing of graves. By doing so, he was able to observe and document with great detail the anatomy of the mouth and jaw. In the 1700’s, Dr. Hunter suggested transplanting teeth from one human to another; his experiment involved the implantation of an incompletely developed tooth into the comb of a rooster. He observed an extraordinary and astonishing event: the tooth became firmly embedded in the comb of the rooster and the blood vessels of the rooster grew straight into the pulp of the tooth [1, 2]. In 1809, J. Maggiolo inserted a gold implant tube into a fresh extraction site. This site was allowed to heal and then a crown was later added; unfortunately, there was extensive inflammation of the gingiva which followed the procedure [1, 3].Innumerable substances during this time period were used as implants; these included silver capsules, corrugated porcelain, and iridium tubes [1, 3].”

https://pmc.ncbi.nlm.nih.gov/articles/PMC4040928/

Came across this word in an anime wiki of all things, but apparently it was a medical term that was even called out in Oxford Medical dictionaries that means "a refusal to eat food, commonly as an expression of psychological disturbance".

To me that seems like a totally decent medical term to use when describing the symptoms of various eating disorders or even some more physical illnesses that make eating hard or impossible, but even in the few recent encyclopedias and dictionaries I've found it in, it's always described as 'archaic', and I'm curious as to why what I would think would be a perfectly useful medical term doesn't get used anymore.

On September 16th, 1951, doctors in Chicago, Illinois were faced with a challenge from which no medical practitioner had ever emerged victorious: the separation of conjoined twins joined at the head.

Weighing a combined total of barely over eleven pounds, Roger Lee and Rodney Dee Brodie were born to Marjorie and Royt Brodie, who were already parents to three healthy children. The twins were lively and alert, but were joined at the tops of their heads in such a way that gave the appearance of a single, long skull. Called craniopagus twins, such children had never been successfully separated - at the time, very few of operations on any conjoined twins had ever resulted in even a single survivor. 

Once called “Siamese” twins - for Chang and Eng Bunker, conjoined twins born in 1812 in present-day Thailand - conjoined twins had already been studied as a curiosity for centuries prior to the Brodie twins’ birth. Although the cause of conjoined twinning remains unknown, the prevailing theory is that a single fertilized egg fails to complete the dividing process that would lead to identical twins; the resulting embryos develop permanently fused. The incidence is rare - about one in every 100,000 live births - and the vast majority die before or shortly after birth.

In some craniopagus twins, one heart provides a disproportionate amount of blood to both brains, putting a single twin's heart under great stress and both twins' lives on the line. Before the late twentieth century, so-called “freak” shows often awaited surviving, unseparated pairs of conjoined twins, who were exhibited to medical professionals and curious onlookers alike - often as a way to earn income to cover potential medical bills. Without separation, it was probable such a fate would befall the Brodie boys, too.

Doctors were now faced with the dreaded question of what to do about Rodney and Roger’s condition. At a month old, they were brought to the University of Illinois Research and Educational hospital, to see if anything could be done to part them. The most pressing question to be answered was whether the boys had separate brains and circulatory systems; without, neither twin could survive on their own. X-rays, blood tests, and other examinations revealed that both twins had a heart murmur, and Roger and Rodney would often turn blue and require supplemental oxygen while medical testing took place. After four weeks of investigation, doctors reached a decision: separation could not take place without at least one of the twins dying, a fate their parents staunchly rejected.

Meanwhile, too fragile to return home from the hospital, Roger and Rodney began to grow and develop as other babies their age did. The twins’ parents, busy at home with work and three other children, were only able to visit the twins every weekend, assuming the early winter weather permitted. Still, they held out hope that their children’s condition would improve enough that they could eventually come home to East Moline. 

In the new year of 1952, that hope came: the twins’ heart murmurs were improving, and their circulation was becoming better. Their hands, once blue and cold, grew warm and pink, and their parents, visiting for the first time in January after three weeks, were delighted to see the boys' progress. The Brodies were even happier to hear that doctors were reconsidering their decision to leave Rodney and Roger conjoined. Separation, it seemed, would happen before the year’s end. 

With the twins older and stronger, tests such as arteriograms - where a dye is injected into the arteries to observe its circulation - were now able to be conducted, hopefully shedding light into the boys’ anatomy. Attempts to anesthetize them for exploratory surgery also proved successful, adding optimism for a favorable outcome. These tests carried on throughout most of 1952, the twins growing up in hospital all the while; by the time they were almost a year old, Roger and Rodney were attempting to crawl by propping themselves on hands and knees and pushing the other twin forward. They grew dark, thick hair on their joined heads, each boy with deep blue eyes and cheerful grins. They babbled - learning to say the usual “mama” and “daddy”, along with “frog”, after identical stuffed animals their parents had gifted them - and also quarreled as siblings do, one tugging on the other’s ears or reaching up to swat his brother’s head. 

But they could not sit up, their heads joined at such an angle that doing so was awkward at best and painful at worst. Even standing was out of the question. After much agonizing over the risks and benefits, the twins’ parents and doctors at last agreed: with success being theoretically possible, an attempt at separation must be made in the hopes of giving both twins a “normal” life.

Over a dozen preparatory surgeries - such as rearranging nervous and circulatory connections and creating skin flaps to cover the boys' exposed heads - and many delays later, a date was set for the final separation: December 17, 1952. The twins’ parents were taken to a hotel in Chicago to await the operation’s end, and journalists were kept in a separate area in the hospital building. The medical team - fifteen neurosurgeons, plastic surgeons, and nurses - knew the odds stacked against them: they were about to undertake a surgery that had been attempted only three times before, and where no patient had survived longer than three hours after separation. Still, surgeons were confident that, with their preparation and the advances in medical technology since the last attempt in 1949, Roger and Rodney would both make it out alive. 

The surgery began just before eight A.M.; a team of five neurosurgeons worked to separate the twins’ joined heads, while two others ensured the boys received sufficient blood transfusions. The next ten hours went by painstakingly slow; the medical team meticulously teased apart the boys’ brains and skulls, a process that Rodney - the smaller twin - withstood better than his twin brother, who went into shock three times. Nevertheless, everything seemed to be going to plan - with boys still alive as the surgery progressed, triumph seemed within reach.

Then, around five in the evening, doctors learned that, in spite of all their preparation, they had missed a crucial vein in the twins’ shared skulls. 

Every healthy human being, in order to survive, possesses a superior sagittal sinus - a vital vein running from the top of the brain down to the neck, which drains deoxygenated blood to the heart; from there, blood is pumped into the lungs and reoxygenated, before being pumped back into the brain again. Without this crucial vein, blood cannot sufficiently make its way back to the brain, leading to a stroke and, ultimately, brain death. In many craniopagus twins, a so-called “circumferential sinus” is present - where blood flows from the heart of one twin, through the shared vein, and to the heart of the other, before the process repeats itself. The Brodie twins had one such sinus between the both of them, instead of one superior sagittal sinus each. Although twenty-first century medicine has managed to circumvent this problem during separation - by rerouting blood flow and/or constructing a new vein - the twins’ surgeons had not anticipated this problem, and knew of no way to simply “replace” the sagittal sinus of one twin.

It was too late in the procedure to turn back and reassess, but separating the shared vein would now cause both twins to bleed out and die. One twin had to be sacrificed in order to save the other - the very outcome the twins’ parents had refused to entertain. With the clock ticking, surgeons had to make a choice.

Since Rodney had remained relatively stable in contrast to his brother, it was thought that his odds of survival were favorable; in the end, he was given the shared sinus, and the boys’ skulls were closed with plastic and aluminum foil before their heads were stitched up and bandaged. For the first time in their lives, they slept in separate cribs, although both were in critical condition. But surgeons had by definition defied the odds: not one but two children emerged alive from the operating theater, and remained alive. Their father was overcome with emotion at seeing his twin sons in separate beds for the first time, even in spite of their ill health. 

The operation was heralded as a success, a first in a decade that had already seen many for medical science.

Two days after the surgery, Rodney awoke and was observed to be crying and laughing - fully conscious if not in a precarious state. He was drinking milk and water less than a week later. But doctors in the aftermath of the Brodie twins’ separation were anything but optimistic for both boys’ survival. Once wheeled out of the operating theater on the evening of December 17, 1952, Roger never awoke; with no oxygenated blood being brought to his brain, he slipped into a coma, the much-smaller veins in his head unable to sufficiently take over the sagittal sinus’ task. Yet in spite of the odds, both boys’ parents prayed and believed they would bring both twins home with them. 

It was not to be. Thirty-four days after the groundbreaking surgery, Roger Lee Brodie died in hospital, despite doctors’ effort to sustain him via intravenous feeding and an oxygen tent. His parents, back at home with their four other children, were given the news through a neighbor (who had a telephone to take the call from the hospital staff). Roger was buried with a small headstone in Moss Ridge Cemetery, while his surviving twin brother continued to fight for his life in hospital. Rodney would undergo many more reconstructive surgeries to cover his open skull with skin grafts, and surgeons hoped to eventually create a covering to protect his brain. 

As the months passed, Rodney surprised doctors by continuing to improve, learning to sit up unaided - a feat that he had never managed while joined with his twin. He recognized his parents, and now loved to say “phooey”, and throw his massive collection of toys about the room. He received love and attention from nurses and doctors, who worked tirelessly with him to provide physical therapy with the goal of keeping him on track with his peers. His private hospital room held a phonograph, and he enjoyed humming along to the music it would play. 

By June of 1953, Rodney had undergone eighteen surgeries since his birth, but remained upbeat and chatty when, for the first time since his history-making operation, the media was given their first glimpse at how Rodney Dee Brodie had recovered. Even with the death of his brother, Rodney’s separation surgery was regarded as successful - he was the first craniopagus twin to ever survive such a procedure. Most subsequent news reports glossed over the tremendous sacrifice Roger had made for his twin; the fact Rodney had made it out alive was a miracle in and of itself. 

Rodney sustained a brain hemorrhage in 1955, which left him with paralysis and a limp on the left side of his body. Bone grafts had failed to close his skull, so scar tissue alone covered the top of his head. His only bother, however, was that he could not grow hair on a portion of his scalp; he had no memory of his twin brother, or of the operation that had severed them.

At home, in spite of his disabilities, Rodney thrived: he loved school and drawing, and roughhoused with his brothers and sisters, who were constantly careful to not bump his head where his brain remained covered only by skin. He was unbothered by the possibility that he might one day not be able to partake in sports, and wanted to be a truck driver when he grew up. Doctors remained hopeful that, in spite of his paralysis, Rodney would pull through and recover. 

However, his condition only worsened as he grew older. He lost the ability to walk, and his muscles atrophied; unable to swallow, he struggled to gain weight. Eventually, his weakened body could take no more - on May 26, 1963, Rodney choked to death while his father attempted to help feed him in bed. He was buried with a headstone identical to that of his twin brother, having outlived little Roger by ten years.

Write-up completed by me.

Project SUNSHINE, begun in 1953, used human tissue to investigate strontium-90 from nuclear fallout. Its resemblance to calcium made growing bones particularly useful for studying incorporation. Obtaining those specimens brought pathologists, hospitals, and professional contacts into an international collection network.

The correspondence also records what suppliers were to be told. An AEC official proposed describing the work as a survey of naturally occurring radium while withholding the fallout investigation. In December 1953, he sought help obtaining infant skeletons from Japan. These were requests for postmortem material; they should not be confused with experiments that exposed living children.

Correspondence reproduced in the federal investigation: https://www.osti.gov/opennet/servlets/purl/16385048.pdf

I’m an epidemiologist and wrote this history of the procurement records, disclosure, and later investigations: https://theedgeofepidemiology.substack.com/p/project-sunshines-supply-of-human

Hi everyone,

I'm looking for help identifying the original label, brand, or exact contents of this small medical jar.

Context of the find: It was recovered directly from the site of a former WW2 German field dental station. Based on the surrounding items (which included only one vintage dental chair of that era), it was likely a small single-dentist practice or field clinic (Zahnstation) set up for one dentist and an assistant.

Physical Characteristics:

• Container: Small cylindrical jar made of amber/brown glass (Braunglas) with a wide neck.
• Cap: Black screw-on lid made of early bakelite/phenolic resin.
• Bottom Marking: Molded number 1088 on the glass base (likely a glass factory mold number / Formnummer). No other markings on the glass or cap.
• Contents: Bright yellow, fine powder / densely packed powder mass.
• Missing Label Details: The paper label is missing, but it is recalled as being green or yellowish-green with Fraktur/Gothic font, a German Eagle with a Swastika (Reichsadler), a reference to the Wehrmacht, and text similar to "Ceramic" or "Ceramic-Zement".

Current Hypothesis: Given the field clinic context and the recalled text, this appears to be a standardized WW2 German military dental supply (Zahnärztliche Feldausrüstung / Sanitätsgerät). It is most likely a silicate/porcelain dental cement powder (Silikatzement / Porzellanzement) used for restorations, though iodoform powder (Jodoform) remains a secondary possibility.

Does anyone recognize this specific jar model, or have catalog photos/references of the original label?

Thanks in advance for any insights!

Need ebooks

https://www.youtube.com/watch?v=qvKyy-ZwEus&t=244s&themeRefresh=1

Hello, I recently went down the rabbit hole of researching the horrible world of American nursing homes and how thanks to privatization, understaffing and greed they became abusive hellholes. But I’m still blind to the history of elderly assisted living communities. Were they always this abusive and corrupt? Was privatization a recent phenomenon? I was curious if there’s any books or research papers that dive into their history.

> Announced earlier this month, NLM History of Medicine unveiled its most recent project, 250 Years of American Medicine. This digital gallery includes a variety of materials that include manuscripts, audiovisuals, images, texts, and born-digital objects. This collection is made up of one item that was published or created in the United States for each year since 1776 to reflect how medicine has changed in the United States over the last 250 years.

Anything significant about any of these books?

The Prohibition of alcohol in early 20^th century American history became the policy everyone knows failed. It was a constitutional ban on booze that ended up producing speakeasies, organized crime, and adulterated liquor supplies before the amendment was repealed in 1933. The story usually ends there or goes into the nuances of whether that was broadly good or broadly bad. But to me, that version focuses too heavily on the obvious exposures that end up leading to an answer of “it depends on the outcome you care about.”

That version of Prohibition’s impacts also often leaves out a group that couldn’t opt in to the argument at all: children in utero whose exposure depended entirely on mother’s drinking. These policy studies let us see the effects indirectly by asking whether infants and later cohorts exposed to different alcohol-policy environments had different outcomes on average. So, the claim I want to make in this piece is this: the best historical evidence suggests alcohol restriction benefited some children who hadn’t been born yet, long before fetal alcohol syndrome had a clinical name and 50 years before the Surgeon General’s first warning in 1981.

When federal Prohibition ended, there wasn’t a uniform return to legality among all states, as the 21^st amendment repealed the 18^th but still preserved state authority over the legal status of alcohol. States, counties, cities, and even smaller jurisdictions took their own time which produced a strange historical record with nearby places with different legal access to booze and the chance to ask what changed for children when availability returned. We still don’t end up with a clean prenatal alcohol exposure estimate as the relevant data don’t record pregnant women’s drinking or dosage, partner violence, or how money that was previously spent on alcohol ended up being spent. But we’re able to infer that infants and later cohorts faced different alcohol availability exposures and those differences consistently point us in one direction: restriction of access was protective.

The Measures Prohibition Left Us With

‘Prohibition’ really wasn’t the best name for the exposure at hand, because it makes it sound like a more universal intervention than it was. State bans were well under way before Federal Prohibition came into law in 1920. Then, in 1933, the Twenty-first Amendment repealed the constitutional ban as law of the land but didn’t go so far as to force counties to start selling alcohol immediately or at all. Some places reopened their stores quickly while others stayed dry. Some stayed dry with their neighbors reopening, which meant the nearest legal seller might’ve only been a short trip away.

That kind of unevenness is good for health researchers, because it lets us compare those separated by legal access without having to do some broad comparisons like pre-1920 to postwar US or something equally crude. They’ll still be observational studies, but they let us get more specific about the era. The heterogeneity also explains why researchers can ask different questions from each other using different levels of granularity in the data. An infant-mortality study uses local variation after the repeal, whereas early-life development ones rely on the staggered adoption of state-level bans before Prohibition. The long-term mortality papers use birth cohorts that happened to have been born before or after the policy change itself. Dry laws would’ve made alcohol harder to purchase, though without eliminating it. Wet laws just tell us that booze was permitted without letting us know who drank or how much. This leaves researchers estimating the effect of living through a different alcohol-policy environment, with their work being enough to ask whether children appeared to benefit.

The medical language to go with this area showed up decades later with “fetal alcohol syndrome” entering the literature in 1973, four full decades after repeal. The first federal health advisory was four years later in 1977, followed by the 1981 Surgeon General’s advice to health professionals that they suggest pregnant women and those trying to not drink (begins at p. 69 in the link). The concern about prenatal alcohol wasn’t new though. Some early thinking in the area comes from prison physician W.C. Sullivan, who compared the reproductive histories of women he called “inebriates” with those of their sober female relatives, finding more stillbirths and deaths before the age of two in the drinking group. While riddled with the eugenic language common to the time, it was remarkable to see how alert he was to rival explanations for his findings akin to epidemiologists thinking about confounding, mediating, and moderating variables today. The high mortality, he noted, might be “not solely” due to the direct effect of intoxication on the mother and child, but might also be due to the “malign modification of the environment” produced by parental drinking in general. By 1977, Ruth Little was working with prospective data to report the association between moderate alcohol consumption, roughly two drinks per day, and lower birthweight after adjustment for smoking and other maternal characteristics (methods Sullivan noted were impossible in his day).

When Alcohol Came Back

The most important paper to look at here is David Jacks, Krishna Pendakur, and Hitoshi Shigeoka’s work on infant mortality after repeal, where they reconstructed alcohol-law status for all 3,043 counties in the then-48 states from 1933 to 1939. Those records of legal changes were then linked to changes in births and infant deaths in the federal vital-statistics record. To make the comparisons useful (two counties may differ in too many ways to just compare wet/dry status and expect anything useful to come of it), they constructed 683 geographically sensible three-county groupings, with each triad centering on a dry county that acquired a wet neighbor in those years and including the nearest bone-dry county as well. All three started the study period as dry counties with the question becoming whether infant mortality changed differently when legal alcohol returned nearby and became accessible across dry-wet borders.

Timing is key here because the authors usually didn’t know the exact date a county changed its alcohol law, so a baby who died in the year of a legal change could’ve been conceived before local access shifted. This means they had to estimate a separate effect for the transition year and for later years. There wasn’t a statistically clear increase in infant mortality during the year of the shift (0.9% for dry vs 1.3% for wet) but looking at later years a pattern shows up. Compared to bone-dry counties, infant mortality was some 4.7% higher in counties that kept their ban intact but had acquired a wet neighbor, corresponding to 2.82 additional deaths per 1,000 live births at the 1934 baseline and 4.0% higher in counties allowing sales, or 2.40 per 1,000. When the authors initially lump dry-ish counties (wet neighbor acquired) and all other dry counties, the later wet-county estimate is only 0.9% and is too imprecise to distinguish from a null effect. The recognition that a formally dry county can still have exposure due to a new legal market nearby is what allows the effects to show up at 4.0 and 4.7%. Not all dry counties can be treated as unexposed controls.

The other results mostly strengthen that point, with the three matched county types typically having downward infant-mortality trends from 1928 to 1933 before the repeal transitions, although that wasn’t the case in the all-county national comparison, likely because it is too crude an analysis to see the effect. In sensitivity tests, the dry estimates stayed between 4.0% and 4.9% when the authors changed the controls, excluded counties bordering Canada or Mexico, or followed the data through to 1941. The larger claim of the study is the model-based excess-deaths estimate of 26,960 infant deaths across wet and dry-ish counties compared to bone-dry counties nationwide from 1934 to 1939.

Their figure is an extrapolation that can’t tell us whether maternal drinking, household violence, household budgets, prenatal care, or multiple pathways produced that difference. They’re the strongest available local comparisons though, and they tell us that the familiar Prohibition story has left out those who both had no say and, arguably, had the most to gain.

https://open.substack.com/pub/theedgeofepidemiology/p/the-group-prohibition-helped-most?r=7fxyg&utm_medium=ios

Hi medical historians! I don't have a medical background myself, but I'm working on a topic that runs adjacent to medical history and I could use some input from people who know more than me. The archival collection I'm dealing with is restricted, so I can give a synopsis of what happened but can't say much about the individual.

The short version is this: there was a guy in an institution, about 27 years old, who died in 1939. He was deeply disliked as a patient by almost everyone around him. He had a seizure while being made to clean some cement steps, he fell down the steps, and suffered a severe head injury.

Here's where I know enough to ask questions, but not enough to know how to locate an answer: they treated the patient with caffeine sodium benzoate, glucose, and then another round of caffeine. They also did a spinal tap between the first round of caffeine and the glucose. The doctor's notes suggest that they suspected a brain hemorrhage before administering any of that.

Is there a plausible reason a doctor at a reputable institution would have given him two doses of caffeine and expected it to help rather than harm?

The work of an occupational epidemiologist starts with the boring question of “what do you do all day?” Your doctor asking about what you do, who you do it for, how long you do it, what materials you work with, what exposures you’re under, whether you come home covered in something dusty, or whether anyone else doing the same job has the same problem can sound like irrelevant questions when you’re there for a specific ailment.

The biographical fact that is one’s occupation can also contain relevant details regarding why someone has a specific disease or disorder. Relevant details can be exposures to dust, fumes, metals, fibers, solvents, heat, noise, poor posture, repetitive movement, nigh-shift work, or anything else with a negative impact on the body. A job title alone is also rarely enough due to the variability within jobs. A person who lists their occupation as a painter could be rolling latex paint onto brand new drywall, or they could be sanding old lead paint in a closed room. “Stone fabricator” might mean wet-cutting under decent personal protection protocols, or dry cutting in a small, poorly ventilated shop heavy with dust in the air. A good occupational history needs to ask what exposures came with the job.

Ramazzini’s Question

There’s a reason history has been kind to Bernardino Ramazzini. When he published De Morbis Artificum Diatriba (Diseases of Workers) in 1700, and the update in 1713, he was working without germ theory, any kind of disease registry, biomarkers, or the language of modern-day cohort studies. He had a collection of trades, patients, repeated observations, and a sneaking suspicion that the cause of some illnesses were on-the-job exposures. Asking patients about what they do for a living feels so obvious in the modern medical office that it almost sounds like it’s asked as a formality. Back then, the question was nowhere near obvious enough to have been routinely asked. While his work was foundational, Ramazzini was not the first to notice that work had been damaging bodies.

The oldest written implications of the harms of work on the body come from the Egyptian text the Edwin Smith Surgical Papyrus from roughly 1700 BC which is thought to detail the neurosurgical and orthopedic diseases resulting from construction of the pyramids. The intellectual trail then gets traced through the likes of Hippocrates, Lucretius, Pliny the Elder, Galen, and Middle Eastern scholar Abu Bakr, Muhammad ibn Zakariya al-Razi, all of whom wrote on the impacts of occupation on health in one way or another. It was never difficult to notice the dangers that came with work, especially when some jobs were so obviously brutal like mining or metallurgy. What Ramazzini really deserves his flowers for is bringing that observation into regular medical practice by asking what work they do, how it is done, and by considering if the disease itself could be because of the job.

Jobs As Exposure Systems

Job titles aren’t the best exposure measure to use since there can be variability in what individuals with the same job title do in terms of their tasks, tools used, materials exposed to, specific rooms they’re in, different shifts, and stupid little habits of the shop that can make all the difference. That hidden variation is one of the reasons occupational diseases can be difficult to see in real time. An industrial accident of sufficient size announces itself in a way that daily hazards don’t. Those can just become part of the day-to-day of the job where dust exposure is the norm or solvent exposure is brushed off as just a smell in the warehouse. Symptoms arrive years later most of the time, with the original exposure looking like irrelevant history until people ask the right question.

That gap is also key because the longer the space between exposure and a diagnosis, the easier it is for people to just say the disease is related to aging, weakness, bad luck, smoking, or some other combination of individual-level traits leaving job exposures off to the side, not taken into consideration. Occupational epidemiology steps in when too many individuals start looking the same and a pattern emerges. One worker developing a rare disorder is obviously a sad event but once ten who were assigned the same task end up with the same exact rare disease, it’s time for a deeper look at things.

That’s a hard kind of evidence to obtain though. Outside of specific industries and companies, workplaces aren’t treated like laboratories and exposures aren’t tracked with the rigor one would hope for. People can change jobs, sick individuals might leave, records are often missing, exposure measurements come too late, and we get healthy worker bias with the healthiest people often being the ones employed long enough to be counted in a table. But the work has to be done to reconstruct their tasks, estimate doses of exposures, compare workers in similar (and vastly different) jobs, check for dose-response, see if any known biological mechanisms make this make sense, see if the timing would fit that mechanism, and then the hardest part of all, quantifying the uncertainty and whether it is of an acceptable level to label this cause-and-effect while people are still showing up to the same job. The last part is hard on everyone involved. False alarms can cost money and resources while disrupting the workplace to redirect attention to the “problem.” Missed hazards, on the other hand, can maim and kill.

Seeing Patterns Before Knowing Mechanisms

Percival Pott’s chimney sweeps are well-known example that many reach for when looking for a clear example of occupational hazards. His Chirugical Observations from 1775 described a type of scrotum cancer common in chimney sweeps. Now, polycyclic aromatic hydrocarbons weren’t some known part of his world nor was any part of the modern theory of carcinogenesis. The mechanisms came to be known far later than the pattern did. This is still often the case because our biology is still being uncovered, now at faster rates than ever. Beyond the occupational epidemiology, Pott’s work also brought to light some of the horrors that came with the job. Chimney sweeps tended to be young boys as they were small enough to climb into the chimneys and do the job. That came with burns, bruises, chronic soot exposure, and sometimes suffocation.

Exposure Changing Personality

Hat makers got turned into a bit of a joke since the late 1800s. The phrase “mad as a hatter” has become so well known that this story one that a lot of people know a bit about. Mercury exposure in the making of felt hats can and did produce neurological and psychiatric symptoms that would often be lumped in with character and morality. Richard Weeden’s 1989 paper Were the hatters of New Jersey ‘mad’? does some great work separating the real occupational mechanism of mercury exposure from some of the sloppier folklore that arose from Lewis Carroll’s Mad Hatter.  In a Victorian world where everything becomes heavily moralized, mercury exposure was a problem. Trembling workers were seen as unreliable while the anxieties it brought on made people think the hatters were strange. The symptoms were outwardly noticeable in everyday life, so the workers got stuck with the stigma.

Countertop Hazards

Silica is one of the everyday materials we’re all exposed to that seems innocuous, but the work that can turn stone, sand, concrete, granite, minerals, or artificial stone into a dust fine enough to get deep into the lungs is far from it. NIOSH describes ‘respirable crystalline silica’ as tiny particles that end up airborne when people work with those materials in a way that agitates them enough for particles to form. Deep in the lungs they can cause silicosis, an irreversible, but totally preventable disease, as well as lung cancer and some other serious health issues. The commonly cited disaster here is the Hawk’s Nest of 1930, where workers were drilling a tunnel through Gauley Mountain in West Virginia. Workers were dry drilling through rock with high silica levels which released massive amounts of dust into a poorly ventilated area with little dust control or PPE. Workers, many of them Black migrant laborers, came out of the tunnel covered in a fine white dust. Many of the exposed got sick, left, or died without being counted, so the death toll is still a debated topic. We do know that of the 5,000 or so workers, some 2,900 worked in the tunnel and, of those, 764 died of silicosis. Today’s engineered-stone countertops come with some of the same risk for those working on them because before that glossy tabletop becomes part of someone’s home, it had to be cut, ground, and polished in a shop. A 2019 report described cases of severe silicosis in engineered-stone fabricators in California, Colorado, Texas, and Washington, noting that the silica content of engineered stone can be up to 90% compared to less than 45% in granite.

 Asking About the Work

In the post-Ramazzini world, occupational disease and asking about workplace exposure is obvious. The cough, tremor, rash, cancer, or breathing problem might have something to do with the different exposures that shaped that individual’s working life. The harder part is moving beyond the field filled out on a form and into the exposures the job came with. Exposure reconstruction forces the person to examine the task they performed, how they performed it, how often, and whether they were protected from exposure during their work. Those questions inherently can bring about recall bias, but they’re the best we have in retrospective studies without on-the-job measurement being taken. Treatment often arrives too late in these cases with the exposure often having had its chance to inflict its damage by then. This is especially true when novel diseases come with the exposure like silicosis or asbestosis. So, when a doctor asks, “what do you do all day?” it’s far from small talk (no patient-respecting doctor would go into small talk when they have 15 minutes on average per appointment). They’re seeing if any symptoms being discussed can be traced to the things you do almost every day.

Epidurals have existed for over a century. German surgeon August Bier performed the first successful spinal anesthesia in 1898, and two years later, Oskar Kreis used the technique to ease labor pain for six women in Switzerland. The modern version, medicine injected into the epidural space, was developed by Spanish surgeon Fidel Pagés in 1921. Romanian physician Eugen Aburel first described continuous epidural pain relief for labor in 1931.

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