Phossy Jaw as an Occupational Disease

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Phossy jaw is a type of necrosis that historically belongs to occupational diseases. This health condition was first observed in 1839. At that time, scientists described lesions of the tissues and jawbone as well as complete necrosis of the jaws of workers in the match manufacturing industry. It was found that white and yellow phosphorus in the vapor state had the strongest damaging properties, attacking the bone tissue through caries and the sockets of extracted teeth.

However, further studies confirmed that, apart from the local action on the jaw, toxic effects were exerted on the entire human skeleton (Pollock, Brown, & Rubin, 2014). Researchers found that the pathogenesis of the phossy jaw was complex because the period of partial excretion of phosphorus from the body was up to several years. The purpose of this research paper is to examine this severe disease and discuss its implications.

Background Information About the Disease

The phossy jaw has been described as necrosis of tissues and bones in the mouth cavity. This condition was accompanied by severe back pain, abscesses, and a generally weakened health condition. This disease was first noted at the beginning of the 20th century in workers who produced matches. They had to work in conditions that caused them to endure high phosphorus exposure and to have direct contact with its vapor.

As a result, individuals developed facial disfiguration due to irreversible processes to their jaws. Often either one or both of their jaws had to be removed. Apart from complex surgical interventions, diseased individuals experienced neurological disturbances that affected their lives. In 1888, frequent trade union speeches led to the prohibition of the use of white phosphorus in match production. Later, this decision was consolidated at the Berne Convention.

The Chemical Causing Toxicity

To understand the pathogenesis of the disease, it is necessary to dwell upon the allotropes of phosphorous. Phosphorous (P4) can form several allotropic modifications; however, only white (sometimes yellow) and red phosphorus have been used for production purposes. The white (yellow) modification has a tetrahedral structure, and it is the poisonous form of phosphorus (Gordon, 2017). During evaporation, this element forms a fog that contains phosphoric anhydride, phosphorous anhydride, and other oxides, all of which cause poisoning if inhaled. It is important that this element takes oxygen from many compounds, and when it comes into contact with different metals. In addition, phosphorus readily dissolves in body fluids and, when absorbed, starts to poison the body.

Poisoning occurs during the production of this element by electrothermal distillation from a mixture of Ca3(PO4)2 (Gordon, 2017). Additionally, workers exposed to this element can be poisoned by phosphorous during the production of synthetic paints, phosphorous fertilizers, fireworks, and some phosphorus compounds in the pharmaceutical industry. In addition, poisoning can happen during the processing of yellow phosphorus to red for the production of matches.

Environmental Occurrence and Fate

Phosphorus is one of the common elements of the earth’s crust and makes up 0.08–0.09% of its mass. Seawater contains approximately 0.07 mg/l of phosphorus. However, this element does not occur in the free form due to high chemical activity. This element can form about 190 different minerals. In addition, phosphorus can be found in all parts of green plants. It is also located in animal tissues and is a part of such compounds as DNA (Gordon, 2017).

Phosphorus cannot be subjected to complete biological destruction. It is a biocide and is destructive for all forms of life. Nevertheless, in the oxidized state, this element is an integral part of any living form (Gordon, 2017). For this reason, it should be subjected to complete detoxification. At present, there are no ways to neutralize this element and turn it into a safe form (when phosphoric acid remains instead of phosphorus).

Phosphorus Exposure

As stated earlier, the main toxic element causing phossy jaw is phosphorus. It is extremely toxic due to its high chemical activity. The lethal dose of this substance is 0.05–0.1 g. The maximum allowable concentration of phosphorus vapor in the air during operation is 0.03 mg/m3 (Gordon, 2017). The permissible concentration of this element in the atmospheric air is 0.0005 mg/m3, while in drinking water, no more than 0.0001 mg/l of this substance is allowed.

History of Phossy Jaw

The phossy jaw was determined to be a type of osteoporosis that arose from chronic phosphorus poisoning. In the body of the affected person, a perturbation of calcium-phosphorus metabolism was observed. Due to systematic exposure to the toxic form of phosphorus, individuals experienced a decrease in strength and elasticity of bone tissue, as well as increasing back pain. In addition, these processes were accompanied by hyperphosphatemia in which the excretion of phosphates from the body with urine was impaired (Moss, 1994). When the disease progressed to a more severe form, osteonecrosis occurred, bone tissue started to degenerate, and abscess sore appeared in that area. Gradually, the lower jaw of a person would be destroyed.

Famous Tragedy

The history of this disease can be traced to the invention of matches that would ignite from friction. The first successful creation of such matches belonged to John Walker, who, in 1826, added antimony sulfide, salt, and gum to their composition so that the match would ignite by friction. After that, Charles Soria replaced antimony sulfide with white phosphorus. These matches burned well, and up to the beginning of the 20th century, the composition of matches did not change.

However, as the production of matches grew, so did the number of diseased workers, which resulted in a famous tragedy related to matchmaking (Marx, 2008). It turned out that phosphorus was extremely poisonous and led to serious diseases.

Despite the fact that phosphorus was highly toxic, starting from the 1900s, people continued to work in hazardous settings. The existing regulations did not set strict rules related to occupational safety; therefore, workers had to operate in poorly ventilated rooms with no access to clean air (Marx, 2008). This was accompanied by the fact that employees had to handle materials with which contact was dangerous; workers were directly exposed to chemicals that could undermine their well-being, leading to a significant deterioration of their health state (Moss, 1994). Because workers had a severe need for money, they had to work in any setting where work might be available.

In the case of the tragedy at the matchstick factory, many of the workers were children whose health was less strong than that of adults. According to Marx (2008), in 1862, almost 61 cases of the phossy jaw were recorded, but no drastic measures were taken to prevent further instances of this disease. The London matchgirls’ strike of 1888 drew public attention to the fact that white phosphorus damaged the health of workers; nonetheless, this did not result in any significant improvements to safety regulations (Moss, 1994). In 1899, the cases of this illness were numerous, causing increased awareness of phossy jaw disease.

Society was highly concerned since many people were already suffering from health complications, and many of these sufferers died. Nevertheless, it is worth noting that it was difficult to establish an official link between phossy jaw and matchmaking factories, and it was declared that it was an occupational disease only in 1900 (Marx, 2008). As mentioned earlier, since 1888, frequent strikes showed the need to employ new safety regulations, and the production of strike-anywhere matches was banned only in 1906 by the Berne Convention.

Routes of Exposure and Effects of Toxicity

This element entered workers’ bodies in various ways. It depended on their physical well-being and conditions of contact with phosphorus. Most often, the element penetrated the body through the respiratory tract. In addition, there were cases when phosphorus entered the body through the gastrointestinal tract when workers swallowed or accidentally ingested dust. In the case of the tragedy at a match factory, many workers were children who neglected elementary safety techniques such as hand washing and mouth sanitation, and phosphorus penetrated their bodies through both the respiratory and gastrointestinal tracts (Moss, 1994). In some cases, phosphorus was sucked in through burned or damaged skin, but these cases were rare. In general, poisoning occurred via inhaling the phosphorus vapor.

When contact with this toxic element occurred, it instantly entered the blood and tissues of an individual. Phosphorus belongs to the category of enzyme poisons; therefore, it has extremely high toxicity and begins to damage the body even at low concentrations in the blood (Moss, 1994). After the element entered the bloodstream, it split into the tissues of the body and consistently affected the entire skeleton of a person. These processes began as a result of disturbances in intracellular oxidation processes. After phosphorus penetrated different systems of the body, it was released via exhaled air, feces, and sweat.

The pathogenesis of phosphorus damage centers on the disturbance of mineral metabolism in bones. In particular, the normal relationship between the main components of the bone (Ca/P) was disrupted, and the amount of calcium increased (Moss, 1994). The more that workers were exposed to phosphorus, the higher the level of calcium became. The bones became more fragile and brittle, with suppuration and necrosis of the tissues. Pathological changes began with damage to the jaws and spread to other bones of the skeleton (Gordon, 2017). Along with these processes, workers experienced weakness, headache, lack of appetite, emphysema, gastritis, and other symptoms that significantly lowered their quality of life.

Pathogenesis

Scientists claimed that phosphorus acted on the parenchymal organs in the first place, in particular, on the liver, heart, and nervous system. In the human body, enzymes conducted protein breakdown with the increased formation of the derivatives such as fat, leucine, tyrosine, and lactic acid. As a result of the intoxication process, nitrogenous products (such as creatinine and so on) began to be excreted at an increased rate, together with urine.

In a situation of minor poisoning, the symptoms appeared within half an hour or several hours after the element entered the body. The diseased individuals experienced symptoms such as burning in the stomach, headache and weakness, thirst, and more. In a severer stage, the symptoms became more pronounced, and individuals showed signs of severe damage to the central nervous system (Rasmusson & Abtahi, 2014). Sometimes, the affected person could develop acute parenchymal hepatitis; however, this symptom was not often observed. In severe cases of poisoning, workers developed acute dystrophy of the liver with diffuse toxic kidney damage.

In cases of chronic intoxication, pathological changes appeared in the jaws. These occurred in three stages. In the first stage, patients felt pain in one or several teeth, which intensified at night. The pain became permanent, leading to the removal of the affected tooth.

However, this procedure did not relieve the victims of pain. During this period of the disease, it was impossible to observe any changes in the bone, but only the atrophy of the alveolar bone was observed (Rasmusson & Abtahi, 2014). In the second stage, the phenomenon of bone osteoporosis was observed, and the jawbone area was red and swollen. The third stage involved pathological changes in the bone and its necrosis. This was accompanied by pus, which occurred in connection with the attachment of a secondary infection. Gradually, the bone became more fragile, and necrosis processes became irreversible.

Latest Research

At present, the phossy jaw is recognized as bisphosphonate-induced osteonecrosis of the jaw (BIONJ) (Pollock et al., 2015). It can appear not only due to exposure to toxic fumes but also as a consequence of specific treatment or drug intake. The link between these two conditions was established in 2003. Since then, specialists have been engaged in the development of a treatment for this condition.

It has been proved that the course of treatment should depend on the nature of the clinical manifestations. General restorative and symptomatic therapies are available to cure this illness. In the first stage of the disease, it is necessary to exclude contact with phosphorus without further treatment (Gordon, 2017). In the second and third stages, it is crucial to resort to surgical intervention (Hellstein & Marek, 2005). Together with surgical treatment, antibiotic and vitamin therapies are carried out. Timely cessation of contact with the poison and early surgical intervention will ensure healing, and other manifestations of BIONJ will be eliminated.

Future Research

Notably, at present, there is no information on how to degrade white phosphorus without the artificial introduction of chemical reagents, which is a significant issue since phosphorus is one of the most dangerous of the toxic elements (Hellstein & Marek, 2005). There are no studies on the metabolism of this element in the presence of microbiota, as well as on the toxicity of phosphorus for prokaryotes. Therefore, it is necessary to find biogenic methods for white phosphorus detoxification.

Conclusion

It can be concluded that white phosphorus turned out to be extremely dangerous and led to severe poisoning of the body. The most frequently described symptoms of chronic phosphorus poisoning were osteoporosis, which arose in workers as a result of a calcium-phosphorus metabolism disorder. In severe cases, osteoporosis led to complete necrosis of bone tissue and the formation of abscess sore in that area. At present, the phossy jaw is recognized as bisphosphonate-induced osteonecrosis of the jaw. The evidence suggests that contemporary treatment regimens are quite effective and can help affected individuals to recuperate fully.

References

Gordon, B. (2017). Phossy jaw and the French match workers: Occupational health and women in the third republic. London, UK: Routledge.

Hellstein, J. W., & Marek, C. L. (2005). Bisphosphonate osteochemonecrosis (bis-phossy jaw): Is this phossy jaw of the 21st century? Journal of Oral and Maxillofacial Surgery, 63(5), 682-689.

Marx, R. E. (2008). Uncovering the cause of “phossy jaw” circa 1858 to 1906: Oral and maxillofacial surgery closed case files-case closed. Journal of Oral and Maxillofacial Surgery, 66(11), 2356-2363.

Moss, D. A. (1994). Kindling a flame under federalism: Progressive reformers, corporate elites, and the phosphorous match campaign of 1909-1912. Business History Review, 68(2), 244-275.

Pollock, R. A., Brown, T. W., & Rubin, D. M. (2015). “Phossy jaw” and “bis-phossy jaw” of the 19th and the 21st centuries: The disunity of John Walker and the friction match. Craniomaxillofacial Trauma & Reconstruction, 8(3), 262-270.

Rasmusson, L., & Abtahi, J. (2014). Bisphosphonate associated osteonecrosis of the jaw: An update on pathophysiology, risk factors, and treatment. International Journal of Dentistry, 1-9.

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