Breathless
Want to know what toxin has been killing workers since Paleolithic times—and is hiding in modern kitchens? The ancient Romans called it a widow-maker… because husbands died so quickly, some women had as many as seven.
This is the Pick Your Poison Podcast. I’m Dr JP. ER doctor. Toxicologist, and unapologetic lover of all things poison.
“Want to know what toxin has been killing workers since Paleolithic times—and is hiding in modern kitchens?
The ancient Romans called it a widow-maker… because husbands died so quickly, some women had as many as seven.
Stay right here to find out.
This is an interactive story.
Survival isn't guaranteed.
What happens next depends on you. Will our patient live or die?
It's up to you and the choices you make.
Grab your stethoscope and let's go.
Today’s episode starts with a phone call.
You’re in the emergency department when your phone rings. It’s a colleague—a friend—who volunteers at a free clinic for uninsured patients.
“I’m sending someone your way. One of my patients just walked in complaining of shortness of breath. His oxygen saturation? 88% on room air.”
Low. Hypoxia.
“You called an ambulance?” you ask.
A pause.
“I wanted to. He refused—he’s worried about the cost. His wife is driving him in.”
The clinic is 30 minutes away. Without traffic.
“Look out for him. Please.” she says. “He doesn’t look good.”
You keep one eye on the ED tracking board, waiting for his name to appear—ready to pull him straight back the second he walks through the door.
The triage nurse rooms him directly into room 7. You grab the intern and head straight in.
He’s sitting upright on the stretcher—a thin, thirty-year-old man. He’s working hard to breathe. A dry, persistent cough interrupts him every few seconds.
“I’ve had the cough for about six months,” he says between breaths. “Started off mild, I thought it was just a cold. He stops to catch his breath.
His wife continues, “He went to the free clinic. The doctor ordered an xray. It was negative. She gave him this inhaler. It helped some, but not much.” She holds up an albuterol inhaler.
“I kept getting worse so I went back. She said maybe it was an atypical infection, or something that didn't show up on the X-ray and gave me some antibiotics. Still didn’t help. Before I was in good shape, I played soccer every weekend. Now—” he stops again breathing heavily.
“He can barely walk across the house,” his wife says.
He says No fever. No congestion or runny nose. No chest pain or leg swelling. No coughing up blood. Just the cough—dry, no sputum.
He denies any past medical history, including no prior history of asthma. Other than the albuterol, he's not taking any medicines. He doesn't smoke or vape. No marijuana or other illicit drugs.
His vital signs are as follows: Temperature 98.6 F or 37 C, blood pressure 120 over 80, Heart rate is 97 beats per minute, Respiratory rate is 30 breaths per minute with oxygen saturation 88% on room air and 92% on 2 L of oxygen via nasal cannula the nurse put on.
On physical exam the first thing you notice is the hollows at his temples, temporal wasting, indicating significant weight loss. He is awake and alert with a normal mental status. His lungs are clear to auscultation; his heart sounds are normal. No abdominal tenderness and normal muscle exam. He still has his pants on. The waistband is at least 4 inches too big, it’s gaping around his waist.
How much weight have you lost? You ask.
“20 pounds, without trying.” Nine kilos.
“How long?”
“Six months,” he says.
Question number one: Which part of the history and physical exam raises the most concern?
Hypoxia, low oxygen.
Six months of cough.
20 lb weight loss
Failure of antibiotics
The answer is, see, the 20 lb weight loss is pretty concerning at this point, though if you answered A or B, I certainly wouldn't disagree with you. Sometimes low oxygen is something as simple as asthma or bronchitis and not everything responds to antibiotics like viruses. The 20 lb weight loss, though, certainly raises concern for things like lung cancer, undiagnosed HIV, tuberculosis.
You and the intern step out to discuss the case. You both agree with your friend's management as an outpatient, treating him for an upper respiratory infection, perhaps an atypical pneumonia or bronchitis. The intern orders basic lab work and another chest X-ray.
An hour later his basic labs come back unremarkable. He doesn't have an elevated white blood cell count. He's not anemic, his electrolytes and kidney function are normal.
The radiologist has this to say about the patient's chest X-ray.
“Possible ill-defined opacity over the right lung field which may represent overlapping structures, atelectasis, developing infectious or inflammatory changes, or artifact. No definite focal consolidation is identified though this cannot be entirely excluded. Correlate clinically.”
Great this is a classic radiology hedge. Let me translate for you. In medical terms the chest X-ray read is could be something there. Could be nothing. Also could be just about anything.
You tell the intern, "Let's get a CAT scan of his chest. We can rule out pulmonary embolus or blood clots and try to get a better understanding of what's in his lungs on the chest X-ray." An hour later you scan through the images together.
She says, "Wow his lungs don't look good at all. What is all that stuff ?"
She's voiced exactly what you were thinking: his lung fields are definitely not normal. Normal lungs are black because they are filled with air but in this case much of his lungs are white, meaning they are filled with something else. What else?
“No idea you say. Let's read on in the radiology read.”
The radiology report comes back as diffuse paving stone appearance in the lungs and right upper field infiltrate.
What does this mean? First the right upper lobe infiltrate is a classic location for tuberculosis. The patient has noted he's losing weight and he has a chronic cough. He denied coughing up blood but this certainly doesn't exclude tuberculosis. The intern says he's originally from Mexico. You can get tuberculosis anywhere, including the U.S., but the risks are higher in some less developed countries.
Is this tuberculosis? It could be and we have to seriously consider it. She says, "Let me call ID."
I've seen lots of cases of tuberculosis, both mild and serious, even including cases of tuberculosis in the spine called Pott's disease. People of course can and do die from TB. They certainly will get low oxygen levels eventually but this usually happens in the end stages of the disease. And he's had symptoms for months not years. It needs to be ruled out but I'm not entirely convinced it's the cause of his rapidly progressing symptoms.
After a few minutes on the phone with I.D., the interns says they agree with ruling it out via sputum cultures to check for Mycobacterium tuberculosis and other types of atypical mycobacterium. She says Infectious Disease also thinks it doesn't completely fit.
The CT scan was negative for pulmonary embolus. They didn't see any masses to suggest lung cancer. What about the paving stone appearance that radiology reported on the CT scan? Does this go with tuberculosis? It doesn't. In medicine we love to apply Occam's Razor, meaning we like to have a single diagnosis that unifies all the complaints rather than multiple different diagnoses. I think this is a case where Occam's Razor may fail us and we have to consider two problems.
We know that this is a toxicology podcast not a pulmonary one so the intern says she'll go back to get more history. The patient moved here from Mexico six years ago. He's been working in a warehouse that manufactures parts for kitchens. He's not been taking any over-the-counter medicines or supplements. And no medicines from Mexico. He has a cat and two pet turtles. There's a family history of heart attack and colon cancer.
Question number two. Which of these elements is most concerning?
A, being originally from Mexico.
B. his family history.
C. the pet turtles.
D. his job.
The answer, is D it's the occupational history (i.e. his job here) that concerns me. Being from Mexico isn't particularly relevant. Nor is his family history. Turtles carry a lot of diseases, specifically Salmonella but that causes a food poisoning-like infection, clearly not the issue here.
You pull up the CAT scan again, scrolling through and thinking about the paving stone appearance as well as a recent news article you just read a few days ago. What kind of things for kitchens, you ask her?
Question number 3: it's time to pick your poison. Is this disease?
Asbestosis
Popcorn Workers' Lung
Metal fume fever
Silicosis
Answer: D. This is silicosis. Asbestosis is from asbestos exposure, like in shipyards or old buildings, it doesn't cause a paving stone appearance and you wouldn't expect making parts for new kitchens to involve asbestos. Popcorn workers' lung causes boop, or Bronchiolitis obliterans related to toxins in artificial butter. Metal Fume Fever occurs after welding due to zinc or other heavy metals it causes a fever and flu-like symptoms. You ask the intern if he works with fake quartz countertops.
Her eyes widen and she says, "How did you know?"
A recent news article you say. Synthetic countertops, particularly synthetic quartz, have become popular in modern kitchens. Ironically, tragically, workers are contracting one of the most ancient occupational diseases as a result.
First, what is silicosis? It's technically a pneumoconiosis, meaning lung disease caused by inhalation and retention of particulate matter. After the Greek pneumo, meaning lung, and konis, meaning dust. It's caused by small particles getting into the lungs. Interestingly the size of the dust matters because large particles can’t get down deep into the lungs. Pneumoconiosis is usually caused by particles less than 5 microns in diameter, small enough to fit all the way down into the very ends of the airways.
A classic pneumoconiosis I'm sure everyone's heard of is black lung in coal miners. But there's a very large number of different kinds of pneumoconiosis, including: asbestosis from asbestos, talcosis from exposure to talc, Berylliosis caused by Beryllium exposure, seen in aerospace and electronics manufacturing industries. In modern times currently silicosis is the most common worldwide cause of pneumoconiosis.
What is silica anyway? That's question number 4. Is it?
Breathing in microscopic particles from stone and sand
B. Exposure to toxic fumes from melting metals
C. Contact with liquid chemicals used in manufacturing
D. Inhalation of synthetic plastic particles
The answer is A: it's breathing in microscopic particles, like sand but specifically made of silicon dioxide or SiO2. Not a gas, not a chemical, just dust.
Silica occurs naturally. It can occur in either crystalline or amorphous forms. It's the crystalline form that causes disease. Okay tox fellows, this non-fascinating fact is for you, it may be on the toxicology boards. The specific crystalline forms that cause silicosis are quartz, tridymite, and cristobalite forms. Amorphous forms are found in things like glass, fiberglass, and diatomaceous earth. These don’t cause silicosis.
It's tragic people are getting silicosis in modern times because it's actually one of the most ancient occupational diseases. It's probably been around since the Paleolithic era.
Yes you heard me right.
In those days, it resulted from shaping flint into arrows and spearheads. The dust would get into your lungs, causing silicosis and lung disease. It's been found in the lungs of ancient Egyptian mummies. I love this description from 1649 from a Dutch physician describing the lungs of a stone cutter on autopsy. “In his lungs, I found a large quantity of stone dust, drawn in with the air during inhalation, and filling almost all the air vesicles, so much so that during the dissection of the lung (which was extremely hard), I seemed to cut through a heap of sand or a sandy mass with my knife. Because the vesicles were filled with this dust, they could not admit the inspired air, and thus the patient had died. Another autopsy description from a few years later in Italy described Stonecutter's lungs as "stuffed with small stones."
The toxicity of silicosis itself as well as its association with certain jobs has long been recognized. Silicosis exposure risk is high in Mining, Quarrying, Stone cutting, and Working in a foundry or ceramic manufacturing.
Even in ancient times, Carpathian mines located in Poland, Czechoslovakia, and Romania, were called "widow makers" and Pliny wrote some women had as many as seven husbands because the men kept dying from lung disease. In the 1800s, The life expectancy of British sandstone quarry workers was documented at less than forty years old.
It's extremely tragic, as I said, that one of the world's most well-known occupational diseases causing severe lung disease continues to be an issue in modern workers. Most recently. silicosis has been in the news after causing significant respiratory disease in workers making synthetic quartz countertops. In California there have been more than 500 cases of silicosis associated with engineered stone since 2019, including tragically 30 deaths and 55 lung transplants. It is also a reportable disease in California, meaning if you make the diagnosis, you have to report it to the Health Department so that they can monitor the cases. Australia has completely banned the importation and sale of engineered stone containing silica.
Why synthetic? Silica is naturally occurring in marble and quartz they have about 30-40% silica. However in engineered stone, as it's called (i.e. fake quartz countertops), the concentration of silica is often times greater than 90%. The synthetic countertops are made by taking silica, mixing it with binders and coloring agents, and then molding it into a slab shape. Those who are most at risk are those who cut and shape the countertops.
Back to our patient. What happens to the lung lungs when you breathe in silica dust? The mechanism is pretty simple. The tiny particles get down into your lungs where they don't belong. This leads to inflammation. Inflammation leads to fluid accumulation. Think of a sprained ankle that swells up thanks to the inflammation around the ankle. Inflammation in the lungs, though, can cause a lot more trouble. If there is enough fluid, oxygen can't diffuse across from the air into the bloodstream because it is essentially blocked by the fluid. With chronic inflammation, fibrosis begins to form. Fibrosis you can think of like a scar. If the inside of the lungs become scarred, you can't absorb oxygen across it because it's inert. Ultimately the lungs scar down, becoming stiff and preventing oxygen from crossing into the bloodstream.
The classic type of silicosis is chronic silicosis. It usually develops ten years or more after exposure to relatively low concentrations of silica. A lot of the symptoms are due to fibrosis that we mentioned above. Sometimes patients are asymptomatic with only abnormal chest X-ray findings. Other times they have progressive cough and shortness of breath.
Accelerated silicosis is sort of a medium type occurring 5 to 10 years after initial exposure to relatively medium concentrations of silica.
Acute silicosis is a rapidly fatal form and it occurs after exposure to extremely high concentrations, happening after a few weeks to years of exposure. It's the kind you often see in sandblasters and engineered stone countertop workers. More on this in a minute. Patients develop cough, shortness of breath, fatigue, weight loss, fever.
Which one does our patient have? Question 5.
Chronic silicosis.
Accelerated silicosis.
Acute silicosis
Answer: C. Acute silicosis. Given that his symptoms started within six months and have been rapidly progressive. Unfortunately acute silicosis can be fatal within months.
You go back to talk to him more about his work and his potential exposure. He confirms that he works with engineered stone countertops, and that he is responsible for cutting the slabs and rounding the edges. This is definitely high-risk work. He is not very forthcoming about where he works. In fact he won't tell you the name or the address, simply saying it's a few hours away from here. He's vague about personal protective equipment, saying he often wears a mask but doesn't give any further specifics as to whether it's something like a paper surgical mask or a true respirator.
Why is he protecting the job that put him at risk? He confirms he doesn't have insurance but clearly this would fall under an occupational exposure and his medical care should be covered by work. There's a number of reasons why: First he may be undocumented. Unfortunately undocumented people often work in high-risk jobs in warehouses not certified by OSHA and not following strict regulations about safe levels of exposure and PPE, etc. Second he may be worried about in getting trouble with work and having a job to go back to. Of course we're thinking, "Why would he want this job?" but if the factory gets in trouble for OSHA violations, it could shut down and he may be out of work altogether.
You explain your concern that this could be silicosis. His wife starts crying but the patient doesn't react, and you get the impression that he's not surprised and has already figured this out. Since his oxygen level is low, you admit him to the hospital for oxygen as well as for further workup, with pulmonary and infectious disease consults.
A week later your intern tells you his sputum cultures came back positive and he's been diagnosed with both silicosis and tuberculosis. Is this a strange coincidence or extremely bad luck? Well it's bad luck for sure but not a coincidence because silicosis and tuberculosis go together. Patients who have silicosis have about three times the risk of developing tuberculosis as an average person because their lungs are damaged, making it easy for the bacteria to get in and take hold. People with silicosis are also at risk for lung cancer because it's considered a carcinogen. There is also an increased risk of autoimmune disease, including connective tissue disease and vasculitis. Scleroderma is particularly associated with silicosis.
How exactly do you diagnose it? There's actually tons of different criteria, some of which are radiographic, some are clinical. The bottom line is a history of exposure along with clinical symptoms that fit is ultimately enough. A lung biopsy isn't necessary to make the diagnosis but if you do you can see the silica crystals sparkling under the microscope with the right dye. If you look at the slides, it's a sort of dangerous beauty of sparkling particles in the lung tissue.
Silicosis dramatically reduces life expectancy. It has to do with what we mentioned above first, whether you get acute or chronic silicosis. It's been recognized for a long time that certain jobs carry higher risks. Essentially a higher burden of exposure to silicosis causes acute disease and dramatically shortens life expectancy.
A lot of the modern understanding of silicosis started during the Industrial Revolution particularly 1800s in Sheffield, England. At this time the utensil industry was located here so they made knives, forks, and spoons. It was known that grinders, responsible for shaping the utensils, died at an early age, many in their 20s and 30s, and most before 50. They often used their grindstone as a tombstone, reflecting a grim understanding of the nature of their death
I said it before and I can't help saying it again. It’s really astonishing to me that this disease is so well known and so understood but still tragically outbreaks happen with pretty regular frequency around the world. You may remember back in the 2000s workers in Turkey were in the news. They developed silicosis from sandblasting, not in a mine but from making sandblasted denim. One study of 20- and 30-year-olds who worked in this industry reported a 5-year survival rate of only 69% with silicosis. In 2009 sandblasting of denim was outlawed in Turkey but unfortunately it still persists in other places around the world. In California. Since 2019 Almost all have occurred in Latino males and the median age of diagnosis is 46. The median age of death - 51.
Occupational interventions can and do significantly reduce silicosis. Occupational exposure limits work. Silicosis dropped dramatically in the US and Western Europe in the 18th and 19th centuries after implementation of safety measures. Recent studies from the 90s in China and the UK confirmed a reduction in cases with strict implementation of dust control measures. One important step is to avoid what's called dry cutting if the silica is cut under water. As you can imagine there's much less dust and the risk of silicosis is much less. PPE is important for reducing exposure so even if there is dust, you don't breathe it into the lungs.
That said there is still some debate about permissible exposure limits. For example according to OSHA, who oversees occupational health in the U.S., allows a permissible exposure limit of 0.1 mg/m3, resulting in an approximate lifetime silicosis risk of about 25%. Some argue the permissible exposure limit should be reduced to 0.05,g/m3 because it's believed this reduces the risk of silocosis to less than 5%.
Back to our patient. He's treated with a multi-drug cocktail for tuberculosis. He continues to get oxygen. What's the treatment for silicosis? Unfortunately supportive care. Albuterol and breathing treatments if that helps, oxygen if necessary. The main and most important treatment is removing the silica exposure. Smoking sensation can also help for obvious reasons.
Ultimately many patients require lung transplants. The three-year survival rate after lung transplant for silicosis is 76%. Steroids have been tried but haven't shown a benefit. Physicians have even tried lung lavage, where they actually try to wash the silica out of the lung but no benefit has been shown from this either.
Evidence from China suggests utility with Pirfenidone, an anti-inflammatory and anti-fibrotic agent, and tetrandrine an anti-inflammatory and immunosuppressive agent may be useful but this has not yet been proven definitively.
I wanted to tell you about a really interesting source of exposure, one related to climate change, which we may be seeing more and more of. In the Himalayas, where several women were diagnosed with silicosis. They were all homemakers, meaning none worked outside the house. None of them smoked. Ultimately a large amount of silica was found inside their houses thought to be due to dust storms carrying silica in the air. Imagine getting silicosis because you've been chronically exposed to dust storms. Yikes.
Back to our patient. He's discharged home without oxygen. The pulmonologist thinks that treating tuberculosis has improved his lung function in the short term but his overall outlook is pretty grim. He's advised not to go back to work. He follows up again with your friend in the free clinic. A year later she tells you he's dependent on oxygen and can barely walk due to shortness of breath. He’s listed on the transplant list, hoping for a double lung transplant. This is a fictional case, as are all our cases, to protect the innocent. But it is based on real poisonings.
Which utensil in 1800s England was associated with the highest mortality rate amongst workers?
Forks
Spoons
Knives
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While I’m a real doctor this podcast is fictional, meant for entertainment and educational purposes, not medical advice. If you have a medical problem, please see your primary care practitioner. Until next time, take care and stay safe.