Woolsorters’ Disease: Arsenic, Not Anthrax

An Essay

Preface

This essay draws on What Really Makes You Ill? Why Everything You Thought You Knew About Disease Is Wrong by Dawn Lester and David Parker. Their work presents a comprehensive challenge to germ theory and reexamines numerous diseases conventionally attributed to bacterial or viral causes. I support their thesis. What follows is a focused examination of one case study from their broader argument: the disease that afflicted Yorkshire textile workers in the nineteenth century, known as woolsorters’ disease, and conventionally attributed to anthrax bacteria. The evidence suggests a different cause.

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I. The Arsenic Century

In 1848, hunters in Hampshire discovered coveys of partridges dead in the fields. The birds sat upright, eyes open, arranged in what one observer called a “macabre vigil.” Death does not usually leave birds looking so composed. Dr. Fuller, investigating the deaths, performed autopsies on two specimens and found inflamed oesophagi and clean intestines—a pattern suggesting an irritant poison rather than disease. To confirm his suspicion, he fed the meat to his cat. The cat vomited for twelve hours and survived. The birds had pecked wheat seeds soaked in arsenic, a common agricultural treatment intended to ward off parasites.

This incident appears in James C. Whorton’s The Arsenic Century: How Victorian Britain Was Poisoned at Home, Work, and Play, a comprehensive account of arsenic’s infiltration into every domain of nineteenth-century British life. Whorton’s title is not metaphorical. A London physician in 1849 called arsenic “the greatest blot upon the civilization of the nineteenth century”—a civilisation that prided itself on progress, on empire and industry and scientific advancement, yet could not keep a cheap toxin from seeping into every corner of daily existence. Barristers died as readily as barrow boys. Elegant homes held the same hazards as tenement flats.

The scale of arsenic production defies comprehension. By the 1870s, a single warehouse in Cornwall held enough white arsenic to exterminate every living creature on earth within a month. Arsenic was a byproduct of mining—copper, tin, gold, zinc, lead—and the expansion of British mining produced a flood of the substance that required commercial outlets. Manufacturers found them. Where did all that arsenic go? Some into the ocean. Some into rat poison and agricultural treatments. The rest infiltrated daily life with a thoroughness that seems almost systematic in retrospect.

Arsenic coloured wallpapers, the famous Scheele’s green and its variants producing the vibrant emerald hues beloved by Victorian decorators. These papers released arsenical fumes, particularly in damp conditions, poisoning families as they slept in their own bedrooms. Arsenic brightened candles. It dyed clothing—green gowns caused rashes and systemic illness in the women who wore them and the servants who handled them. It appeared in children’s toys and artificial flowers. Workers manufacturing these products suffered corroded fingers, ulcerated skin, and respiratory inflammation, their health sacrificed for consumer goods that would poison their eventual owners.

Food and drink offered no refuge. Arsenic contaminated beer during production, leading to epidemics like the 1900 Manchester outbreak where thousands fell ill from tainted pints and over seventy died. Investigation traced the poison to sulfuric acid contaminated with arsenic, used in glucose production for brewing. The 1858 Bradford sweets incident killed twenty-one and poisoned hundreds more when arsenic was mistaken for daft—a common adulterant—and mixed into peppermint lozenges. Accidental poisonings occurred regularly when arsenic, stored alongside baking ingredients, found its way into family meals. White powder looked like white powder. Servants and cooks, often illiterate and untrained in distinguishing toxic substances, stirred arsenic into dumplings and puddings with fatal results.

Arsenic was also medicine. Physicians prescribed it in Fowler’s solution for malaria, chorea, asthma, and skin conditions. The medical establishment called it a “wholesome poison,” believing that small doses restored vigour, enhanced complexion, and promoted general health. Styrian peasants in Austria ingested arsenic habitually, claiming it boosted vitality—and indeed, gradual exposure could build tolerance, allowing some individuals to consume quantities that would kill others. This tolerance became a legal defense in poisoning trials, muddying the question of intent and dosage. Meanwhile, patients prescribed arsenical tonics traded one affliction for another: neuropathy, numbness in extremities, blackened skin, and cancers that emerged years or decades later. The therapeutic use of arsenic created a paradox in which the same substance was simultaneously recognised as deadly and dispensed as treatment.

The occupational hazards were equally severe. Miners extracting arsenic-laden ores suffered respiratory illness from dust inhalation, coughing blood and wasting away from what was called “miner’s phthisis.” Smelters released fumes that devastated local vegetation and waterways, creating barren landscapes around Cornish works. Wallpaper makers mixing arsenic greens developed ulcers on their hands and faces, their skin sometimes turning green or black from chronic absorption. Factories filled with arsenical fumes left workers dizzy and nauseated. Artificial flower makers, dipping petals in arsenic dyes, suffered what was termed “flower-maker’s disease”—corroded fingers, inflamed lungs, vomiting, and diarrhoea. The Lancet carried numerous reports throughout the century about workers sickened by their trades, though the connections were often made piecemeal and without systematic investigation.

Agriculture presented particular risks. Farmers soaked seeds in arsenic solutions to protect crops from parasites, contaminating soil and poisoning wildlife. The partridge deaths were not anomalous; they were predictable consequences of widespread seed treatment. Livestock grazing on contaminated land ingested arsenic with their food. The poison accumulated in the food chain, affecting predators that ate poisoned prey.

Most significantly for the present inquiry, farmers immersed sheep in arsenic baths to kill ticks and lice. An effective arsenic-based sheep dip was developed in 1830. The practice became widespread, protecting flocks from infestation and improving wool quality. But the consequences extended far beyond the animals being treated. An article titled “Arsenic and Old Wool” documents that The Lancet carried many reports during the nineteenth century about shepherds who suffered from the effects of toxic sheep dip. The pervasiveness of this contamination is evidenced by a striking modern fact: old sheep dip sites in Australia contaminated by arsenic are now considered a threat to public health. Arsenic is a persistent toxin. It does not break down. It remains in soil, in water, in wool, in the bodies of those exposed.

Shepherds were not the only people affected. As the “Arsenic and Old Wool” article states: “In addition to shepherds and woolsorters, anyone who handled wool from sheep dipped in arsenic-based compounds would have been affected by this highly toxic substance.” The chain of exposure extended from the sheep farmer applying the dip, through the shearer handling the treated animal, to the woolsorter working with the raw fleece, to the spinner, the weaver, and ultimately the consumer of the finished product. Each link in this chain encountered arsenic residues.

This was the environment in which woolsorters’ disease emerged: a society saturated with arsenic, failing to recognise the scope of its own poisoning. Forensic science was developing tests to detect arsenic in murder victims—the Marsh test, introduced in the 1830s, revolutionised poisoning trials—but the broader pattern of occupational and environmental exposure went largely unexamined. The medical establishment was increasingly captivated by a new theory that would redirect attention away from toxicological explanations entirely.

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II. The Emergence of Woolsorters’ Disease

In the early nineteenth century, wool was a major industry in England, and woolsorting was not considered a particularly hazardous occupation. Workers sorted fleeces by quality and type, separating grades for different manufacturing purposes. The task required skill and experience but posed no obvious physical danger. Workers handled raw wool with their bare hands, breathed air filled with wool fibres and dust, and spent their days in close contact with the material. Through the 1820s, this work proceeded without notable health consequences.

This changed in the late 1830s. According to a 2004 article titled “The History of Woolsorters’ Disease: A Yorkshire Beginning with an International Future,” the national introduction of alpaca, mohair, and various Eastern wools in the 1830s “quickly increased cases of bronchitis, pneumonia and deadly blood poisoning within the woolsorters group.” The first cases were reported in 1838. The death toll began to rise significantly. The disease became known as woolsorters’ disease, also called splenic fever—a name that noted the involvement of the spleen, the organ responsible for filtering blood.

The timing demands examination. Arsenic-based sheep dip was developed in 1830. Within a few years, it became the standard treatment for protecting flocks from parasites. The first cases of woolsorters’ disease appeared in 1838, shortly after new types of imported wool entered the British market—wool from regions that had adopted the new arsenic dip technology, wool treated with compounds containing one of the most toxic substances known to medicine.

Workers handling these fleeces—fleeces from sheep treated with arsenic compounds—began developing respiratory illness, pneumonia, and blood poisoning. The sequence is straightforward: arsenic sheep dip introduced, treated wool enters the market, workers handling that wool fall ill with symptoms consistent with arsenic poisoning. The correlation is direct and temporal.

The symptom profile of woolsorters’ disease aligns precisely with the known effects of arsenic exposure. Acute arsenic poisoning causes violent vomiting, difficulty swallowing, burning pain in the stomach and throat, difficulty breathing, cold and clammy skin, convulsions, and circulatory collapse. The victim may die within hours, or may endure days of torment as organs become inflamed and corroded. Chronic and sub-acute poisoning unfold more insidiously: fatigue, loss of appetite, numbness in extremities, skin eruptions, respiratory problems, and gradual systemic deterioration.

The “deadly blood poisoning” reported among woolsorters describes sepsis—systemic infection of the blood. The medical establishment acknowledges that sepsis is caused by toxins. The conventional view attributes these toxins to bacteria. The alternative view attributes them to arsenic and other poisons that produce identical effects through direct chemical action on body tissues and organ systems.

The persistence of arsenic compounds meant that anyone handling treated fleeces would be exposed repeatedly. Woolsorters worked directly with raw wool, manipulating fibres with their hands, shaking out fleeces, breathing air thick with wool dust. The particles they inhaled, the residues that settled on their skin and were absorbed through dermal contact, carried arsenic into their bodies day after day. Unlike acute poisoning from a single large dose, this occupational exposure was chronic—smaller amounts accumulated over time, building up in tissues, gradually overwhelming the body’s capacity to cope.

The spleen’s involvement in woolsorters’ disease is significant. The spleen filters blood, removing damaged cells, pathogens, and toxins from circulation. An organ tasked with clearing poisons from the bloodstream would be among the first to show damage from chronic toxic exposure. “Splenic fever” describes exactly what one would expect from systemic poisoning affecting blood-filtering organs.

Little progress was made in the ensuing decades to discover the cause of the problem. The disease remained mysterious, its victims mounting, its mechanism unexplained. The investigation that did eventually occur was shaped by a development in Germany that would redirect the entire trajectory of medical thinking: the rise of bacteriology and the identification of microscopic organisms as the cause of disease.

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III. The Bacteriological Capture

In 1876, Robert Koch announced his discovery of Bacillus anthracis, the bacterium he claimed caused anthrax. Koch’s work established the methodology that would come to define germ theory: isolate the organism from diseased tissue, grow it in pure culture, introduce it into a healthy animal, and demonstrate that the same disease results. This framework proved enormously influential, reshaping medical thought within a generation.

The timing proved decisive for the investigation of woolsorters’ disease. Reports about Koch’s discovery encouraged researchers to ascertain whether the Yorkshire illness and anthrax were related. The possibility that a bacterial cause might explain the mysterious deaths among textile workers attracted scientific attention that decades of unexplained fatalities had failed to generate.

Experiments were conducted. According to the historical record, animals inoculated with blood from fatal cases of woolsorters’ disease died of anthrax. The conclusion drawn at the time: the blood contained anthrax bacteria, the same organism Koch had identified, which infected and killed the test animals. This experimental result was presented as proof that woolsorters’ disease was anthrax in a different occupational setting.

The link was considered “finally confirmed” when cattle in Bradford died of anthrax after drinking water that had been used to wash imported wool. Here was the complete picture, or so it seemed: infected animals were shorn, their contaminated fleeces shipped to Yorkshire, spores from those fleeces released into wash water, cattle drinking that water becoming infected and dying from the same disease afflicting woolsorters. The chain of transmission appeared clear. The bacterial theory was established.

These experiments became the foundation for the bacterial interpretation of woolsorters’ disease. The investigation effectively ended. A cause had been identified—B. anthracis—and the medical establishment moved forward on that basis. Louis Pasteur developed an anthrax vaccine for livestock in 1881, though its effectiveness proved questionable. In Pasteur: Plagiarist, Imposter, R.B. Pearson documents the use of the Pasteur vaccine in Russia, where 4,564 sheep were vaccinated, after which 3,696 sheep died—a catastrophic failure rate that was quietly set aside as the bacterial paradigm consolidated its hold on medical thinking.

The World Health Organization’s 2008 report on anthrax reflects the current consensus, describing anthrax as a disease caused by bacterial toxins that produce sepsis and septic shock. The report acknowledges that toxins are the causal agents of anthrax symptoms. It attributes those toxins to bacterial production. But the report also admits significant gaps in understanding—gaps that are inexplicable if the bacterial theory is correct.

One question the WHO poses remains unanswered: “How precisely do grazing and browsing animals acquire it?” This question is remarkable. If anthrax is a bacterial disease spread by spores that persist in soil, the mechanism of transmission should be straightforward: animals graze, ingest spores, become infected. Yet after more than a century of research, the precise mechanism remains unclear. The WHO admits the poor level of knowledge about anthrax leaves many unanswered questions.

This persistent uncertainty suggests the framework itself is inadequate. The rise of bacteriology ensured that “little, if any, attention was paid to a toxicological investigation of the disease.” This is the critical historical fact. The arsenic hypothesis was not tested and found wanting. It was not disproved through careful experimentation. It was simply not considered. The new paradigm of bacterial causation captured medical attention completely, and alternative explanations were abandoned without examination.

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IV. Reinterpreting the Evidence

The experiments that “confirmed” the bacterial theory of woolsorters’ disease warrant closer examination. Each can be explained through toxic causation without recourse to bacterial infection.

The inoculation experiments. Animals were injected with blood from fatal cases of woolsorters’ disease and subsequently died. The investigators concluded that the blood contained anthrax bacteria, which infected and killed the test animals. But consider the alternative: the blood of workers who had been chronically exposed to arsenic—who had inhaled arsenic-laden wool dust daily, absorbed it through their skin, accumulated it in their tissues over months or years of occupational exposure—would contain arsenic. The poison accumulates in blood and organs. Injecting that blood into animals would introduce arsenic directly into their systems. The animals died of poisoning, not infection.

The symptoms produced would be consistent with arsenic toxicity: rapid decline, organ failure, death. These symptoms are also consistent with the conventional description of anthrax. The experiments did not distinguish between the two mechanisms. They simply assumed bacterial causation because that was the hypothesis being tested. No controls were performed to measure arsenic content in the blood. No comparison was made between blood from arsenic-exposed workers and blood from unexposed individuals. The experiment proved that something in the blood caused death; it did not prove that the cause was bacterial.

The Bradford cattle deaths. Cattle in Bradford died after drinking water that had been used to wash imported wool. This was presented as confirmation that anthrax spores from infected sheep contaminated the water and transmitted the disease. But wool from sheep treated with arsenic-based dip would release arsenic residues when washed. The water used for washing would become contaminated—not with bacteria, but with a known poison. Cattle drinking that water would ingest arsenic. They died of poisoning, not infection.

The partridge deaths documented by Whorton provide a direct parallel. Birds ate arsenic-treated seeds and died. Dr. Fuller’s cat ate poisoned partridge meat and vomited for twelve hours. No bacterial theory was invoked because the toxic cause was evident. The Bradford cattle present the same pattern: animals ingesting a substance contaminated by arsenic treatment, dying as a result. The only difference is the interpretation imposed by investigators already committed to a bacterial framework. The assumption of bacterial causation preceded the evidence; the evidence was then read through that assumption.

The WHO’s unanswered question. The World Health Organization’s inability to explain how grazing animals acquire anthrax becomes fully comprehensible under a toxicological interpretation. Animals grazing on land contaminated by arsenic from sheep dip, from mining runoff, from tannery effluent, from industrial pollution, ingest the poison with their food and water. They sicken and die from toxic exposure. The mechanism requires no bacterial spores, no chain of infection, no invisible microorganisms persisting in soil for decades. It requires only what the historical record abundantly documents: widespread environmental contamination with a known poison.

The toxin question. Consider the symptom profile carefully. The medical establishment acknowledges that anthrax produces its effects through toxins that cause sepsis and septic shock. Sepsis is systemic poisoning. The symptoms—fever, respiratory distress, circulatory collapse, organ failure, shock—are the symptoms of acute toxic exposure. The establishment attributes the toxins to bacterial production. The alternative interpretation attributes them to the arsenic compounds that saturated the Victorian environment and accumulated in the bodies of those who worked within it. Both explanations invoke toxins. The question is their source.

The pathology attributed to anthrax is consistent with arsenic poisoning. Inflamed capillaries in the digestive tract, heart, and lungs. Reddened stomach lining, described in historical accounts as resembling “boiled lobster” or spotted with purple. Damage to blood-filtering organs. These are the effects of a corrosive poison acting on living tissue. They can be produced by arsenic without any bacterial involvement.

The experiments of the 1870s and 1880s did not prove bacterial causation. They proved that something in the blood of woolsorters’ disease victims, and something in water used to wash treated wool, could kill animals. The assumption that this something was bacterial preceded the evidence and determined its interpretation. A toxicological investigation would have tested for arsenic content. That investigation was never performed.

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V. The Wider Exposure Pattern

Woolsorters were not the only workers associated with anthrax outbreaks. The pattern of the disease follows the pattern of arsenic exposure across multiple industries, a correlation that becomes visible only when the bacterial assumption is set aside.

Tanneries. The tanning industry has been historically associated with anthrax. The WHO document notes that “the main enzootic livestock areas traditionally lay ‘downstream’ from tanneries and the implication has been that watercourses have carried contaminated tannery effluent.” The conventional interpretation holds that hides from infected animals contaminated the water with bacterial spores, spreading disease to livestock and workers.

But tanneries used arsenic extensively. The “Arsenic and Old Wool” article confirms: “White arsenic was further used as a preservative of hides, skins and furs.” Tanning processes involved multiple toxic chemicals, but arsenic was prominent among them. Tannery effluent discharged into waterways would carry arsenic residues. Livestock drinking downstream water would ingest the poison. The alleged “contamination” of watercourses was real—but the contaminant was arsenic, not bacteria. Tannery workers were routinely vaccinated against anthrax, a practice that has since been discontinued. They were workers in an industry that handled arsenic-treated materials and discharged arsenic-laden waste, vaccinated against a “disease” whose symptoms match arsenic poisoning.

Mining. Mining is another industry associated with the release of toxic substances that contaminate the environment. Tin mining was one of the industries in nineteenth-century Yorkshire, the same county where woolsorters’ disease arose. Tin ore is typically found in association with sulphur and arsenic. Mining and smelting processes release arsenic into the air, soil, and water—into the environment that workers breathe, that livestock graze, that communities inhabit.

The convergence in Yorkshire is striking. Textile workers handled arsenic-treated wool. Mining operations released arsenic into the local environment. Tanneries used arsenic as a preservative and discharged effluent into waterways. A population exposed to arsenic through multiple simultaneous pathways developed a disease characterised by blood poisoning and respiratory failure—symptoms entirely consistent with arsenic toxicity. To attribute this pattern to bacteria requires ignoring the documented presence of a known poison in favor of an invisible microorganism whose mechanism of transmission remains unexplained.

Agricultural contamination. Whorton documents that arsenic from sheep dip contaminated agricultural land throughout Britain. The dip was applied, residues dripped onto the ground, and arsenic accumulated in soil over years of repeated treatment. Livestock grazing on that land ingested arsenic. Wildlife eating treated seeds died in the fields—the partridges of Hampshire, and countless other animals whose deaths went unrecorded or unexplained. The contamination was systemic, affecting the entire food chain.

When farm animals sickened and died, the deaths were attributed to anthrax—a bacterial disease whose mechanism of transmission the WHO still cannot explain, but which becomes immediately comprehensible as environmental poisoning. The animals were not infected by invisible spores persisting in soil. They were poisoned by arsenic that had been deliberately applied to the land and that accumulated over time.

The geographic pattern. The distribution of anthrax outbreaks correlates with arsenic exposure, not bacterial presence. Wherever arsenic-based sheep dip was used, wherever mining released arsenic into the environment, wherever tanneries processed hides with arsenical preservatives, wherever industrial processes deposited arsenic into air and water—these were the locations where anthrax appeared. The disease mapped onto industrial and agricultural poisoning, not onto any pattern explicable by bacterial transmission.

The persistence of arsenic compounds ensured that contamination accumulated over time. Unlike organisms that die and decompose, arsenic remains. It builds up in soil. It leaches into groundwater. It enters plants and animals and passes through the food chain. The “Arsenic Century” did not end when the century ended. Its residues persist, and old sheep dip sites remain hazardous today.

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VI. What Was Never Investigated

The arsenic hypothesis for woolsorters’ disease was not disproven. It was never tested. The rise of bacteriology in the latter part of the nineteenth century captured medical attention so completely that toxicological investigation ceased. Koch’s discovery of B. anthracis provided an explanation that fit the new paradigm, and the investigation stopped there. The framework determined what questions were asked, and questions about arsenic were not among them.

This represents a fundamental failure of scientific method. A hypothesis was accepted not because alternatives were excluded through rigorous testing, but because the prevailing intellectual framework made alternatives invisible. The temporal correlation between arsenic sheep dip and the emergence of woolsorters’ disease—the development of the dip in 1830, the first cases in 1838—was not examined as a potential causal relationship. The occupational exposure of woolsorters to arsenic-treated fleeces was not quantified. The arsenic content of wool from treated sheep, of blood and tissue from affected workers, of water used to wash imported fleeces, was not measured. The experiments that “confirmed” bacterial causation were not designed to detect or exclude arsenic poisoning.

The questions that would test the arsenic hypothesis remain unanswered because they were never asked. Did the emergence of woolsorters’ disease correlate with the introduction of arsenic-treated wool into British markets? What were the arsenic levels in the working environments of affected woolsorters? Did the blood and tissues of woolsorters’ disease victims contain elevated arsenic? Did the Bradford cattle that died after drinking wool-washing water show pathology consistent with arsenic poisoning? Were arsenic levels measured in that water? Did regions with more intensive sheep dip use show higher rates of both animal and human “anthrax”?

None of these investigations were performed. The bacterial explanation was accepted, and the matter was considered closed. Subsequent generations of researchers inherited the assumption and built upon it, never returning to question the foundation. The anthrax vaccine—never comprehensively tested in human trials, according to the WHO, because it would be “unethical” to expose humans to such a deadly pathogen—has been administered to military personnel and others deemed “at risk,” despite documented adverse effects including symptoms resembling Gulf War Syndrome.

The persistence of arsenic in the environment means some evidence may still be recoverable. Old sheep dip sites remain contaminated, their soil containing arsenic levels dangerous to human health. Historical wool samples, if preserved, might retain measurable residues. Archived tissue samples from woolsorters’ disease victims, if they exist, could be tested with modern analytical techniques. The tools of contemporary toxicology far exceed what was available in the nineteenth century. A retrospective investigation is theoretically possible.

But such investigation would require a willingness to question the bacterial consensus—a willingness that the medical establishment has not demonstrated. The paradigm established in the 1870s and 1880s continues to shape research questions, funding decisions, and clinical practice. Challenging it requires not merely presenting alternative evidence, but confronting institutional commitments that have accumulated over a century and a half.

What remains is a historical record that shows: a society saturated with arsenic at every level; an occupational disease that emerged in precise temporal correlation with arsenic sheep dip; experiments that demonstrated poisoning while being interpreted as demonstrating infection; a pattern of “anthrax” outbreaks that mapped onto arsenic exposure across multiple industries; and a question the World Health Organization still cannot answer about how grazing animals acquire the disease.

The evidence points toward toxic causation. The investigation that would confirm or refute that hypothesis was abandoned over a century ago, when the excitement surrounding germ theory swept aside all competing explanations. It has never been resumed.

Woolsorters’ disease was not a mystery solved by the discovery of B. anthracis. It was a mystery obscured by it. The Yorkshire textile workers who sickened and died in the nineteenth century deserve a better accounting than they received. The evidence for what killed them has been available all along, buried under a paradigm that made it invisible. Arsenic saturated their world, contaminated their wool, accumulated in their bodies—and when they died, their deaths were attributed to an invisible bacterium while the visible poison was ignored.

The question is not whether the arsenic hypothesis is correct. The question is why it was never investigated. The answer lies in the capture of medical thinking by a single explanatory framework—germ theory—that displaced all alternatives before they could be tested. That capture persists today. Reopening the investigation would require acknowledging that a century of consensus might be built on an untested assumption. Until that acknowledgment occurs, woolsorters’ disease will remain what it has been since the 1880s: a case study in how prevailing paradigms determine not only what answers are accepted, but what questions are permitted to be asked.

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References

Lester, Dawn, and David Parker. What Really Makes You Ill? Why Everything You Thought You Knew About Disease Is Wrong. 2019.

Whorton, James C. The Arsenic Century: How Victorian Britain Was Poisoned at Home, Work, and Play. Oxford University Press, 2010.

“The History of Woolsorters’ Disease: A Yorkshire Beginning with an International Future?” Occupational Medicine 54, no. 7 (2004): 489–493.

“Arsenic and Old Wool.” Alliance for Cancer Prevention. http://allianceforcancerprevention.org.uk

Nass, Meryl. “The Anthrax Vaccine Program: An Analysis of the CDC’s Recommendations for Vaccine Use.” American Journal of Public Health 92, no. 5 (2002): 715–721.

World Health Organization. Anthrax in Humans and Animals. 4th ed. WHO Press, 2008.

Pearson, R.B. Pasteur: Plagiarist, Imposter. 1942.

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