- Email: [email protected]
Endemic fluorosis
4 Endemic fluorosis PAUL
E. McGILL
'All substances are poison, there is none that is not a poison. The right dose differentiates a poison and remedy.' Paracelsus
Fluorine is widely distributed in variable concentrations in soil, rock and ground water. It is not an essential element for human health and no fluoride-deficiency syndrome has, as yet, been described. It has a recognized importance in the prevention of dental caries and in the treatment of osteoporosis. Exposure to high quantities of fluorine, either by ingestion or inhalation, results in the condition known as skeletal fluorosis. EPIDEMIOLOGY
Industrialfluorosis occurs when there is prolonged exposure to high atmospheric concentrations of fluoride in the aluminium, steel and glass industries. Endemicfluorosis results from the ingestion of excessive quantities of fluoride, usually in drinking water (Anon, 1981). In some areas, an additional source of pollution is atmospheric dust-containing suspended particles of fluoride (Rao et al, 1975) or contamination of foodstuffs from coal ash (Yan, 1990). There are well-known endemic areas in the tropics, in southern India around Madras and Hyderabad (Siddiqui, 1955) and in northern India in the Punjab (Jolly et al, 1968; Reddy et al, 1969). In Africa, fluorosis is endemic in the Rift Valley provinces of Tanzania, Kenya, Uganda and Ethiopia (Grech, 1966; Moller et al, 1970; Nair and Manji, 1982; Haimanot et al, 1987; Ndosi, 1989) and in the Sudan (Smith et al, 1953) and South Africa (Ockerse, 1945). PATHOGENESIS
Following absorption from the gastrointestinal tract, fluoride is taken up rapidly into bone and replaces hydroxyl ions in bone apatite. About half is sequestered in bone and the remainder excreted in urine and faeces. Fluoride bound to bone and teeth has a biological half-life of several years. Absorption is reduced in the presence of calcium, magnesium and aluminium. Bailli~re's Clinical Rheumatology-Vol. 9, No. 1, February 1995 ISBN 0-7020-1946-1
75 Copyright 9 1995, by Bailli6re Tindall All rights of reproduction in any form reserved
76
p.E. McGILL
The mechanism by which fluoride ions bring about such dramatic changes in skeletal tissue is not known. These changes include an overall increase in bone mass. Tendons, ligaments and muscles are infiltrated by mineral deposits and periosteal outgrowths. The vertebral column and ribs become fused following ossification of the intervertebral discs and spinal ligaments. The changes in bone density and characteristic ligamentous changes are vividly demonstrated on X-ray (Figure l(a)-(c)).
(b)
(a)
(c) Figure 1. (a), (b) Sclerotic vertebrae; (c) pelvis. Reproduced from Haimanot et al (1987, Tropical and Geographical Medicine 39: 209-217, with permission).
ENDEMIC FLUOROSIS
77
CLINICAL FEATURES Dental fluorosis
The incidence of dental fluorosis in endemic areas exhibits a linear relationship to the fluorine content of drinking water. The enamel of permanent teeth is affected by mottling and brownish discoloration and, in severe cases, pitting of the surface and chipping of the edges of teeth. Rarely, in highly endemic areas the deciduous teeth may be affected. Such teeth are usually caries-free but they are fragile and premature loss occurs due to periapical tooth absorption. In temperate climes dental fluorosis does not occur with water levels of less than 2 parts per million (ppm). Dental enamel mottling may be found in more than 80% of children resident since birth in endemic areas. Skeletal fluorosis
In temperate areas fluorosis affecting bone is not detectable until the concentration in drinking water is greater than 4 ppm. In the tropics more water may be consumed by those in physically strenuous jobs and fluorosis may develop at lower concentrations. There is an area of endemic fluorosis in the Persian Gulf (Qatar) where the water concentation of fluoride is less than 4 ppm. Excessive drinking of tea which contains very high concentrations of fluoride is considered to be an important contributory factor (Azar et al, 1961). There is generally a linear relationship between the development of skeletal fluorosis, the fluoride concentration of drinking water and the duration of exposure. Skeletal fluorosis is usually associated with the consumption of water with a fluoride content of more than 8 ppm for longer than 10 years. There are some areas in the Ethiopian and Kenyan Rift Valley where the fluoride content is 40 ppm. In endemic areas symptoms of back stiffness and limb pains are common and radiological evidence of skeletal fluorosis is present in 70% or more of symptomatic individuals. In established cases there is global restriction of spinal movements leading to a rigid kyphotic spine which outwardly resembles ankylosing spondylitis (Figure 2(a)). Involvement of joint capsule, ligaments and tendon insertions occurs in both the spine and at the periphery, mimicking the enthesopathy of ankylosing spondylitis (Figure 2(b)). Chest expansion is greatly limited due to involvement of the costosternal and costovertebral joints. Neurological manifestations of skeletal fluorosis
In endemic regions, it is estimated that about 10% of those with skeletal fluorosis exhibit neurological disease (Singh and Jolly, 1961; Haimanot et al, 1987). The neurological consequences are those of a radiculomyelopathy due to mechanical compression of the spinal cord and nerve roots by osteophytes. The brunt of the pathology falls on the cervical cord and usually consists of a myelopathy with progressive weakness of lower limbs
78
P . E . McGILL
(a)
(b) Figure 2. (a) Skeletal fluorosis with marked rigidity of the spine resembling ankylosing spondylifts. (b) Ligament and tendon calcification. Reproduced from Reddy (1979, Handbook of Clinical Neurology) with permission of Elsevier Science.
and difficulty walking with a combined motor and sensory defect and sphincter disturbances in the most severe cases (Figure 3(a) and (b)). In addition, there is frequently gross crippling deformities of the hips and knees, resulting in dual locomotor and neurological disability (Figure 3(c)). Root compression may lead to mixed neurological signs in the upper limbs with lower motor neurone lesions predominating. Very occasionally, cranial nerve palsies occur, usually the eighth nerve with a progressive high-frequency perceptive deafness due to compression of the nerve within the sclerosed auditory canal. DISABILITY
The impact of these locomotor changes on the workforce of certain rural communities is highlighted in a study from the EthiopianRift Valley where premature retirement (45-50 years) is common because of inability to perform physically strenuous work (Haimanot et al, 1987). PREVENTION AND TREATMENT
Prevention can only be undertaken by providing an alternative source of drinking water with a low fluoride concentration. In isolated villages
ENDEMIC FLUOROSIS
79
(a)
(c)
(b) Figure 3. (a) Dense sclerotic vertebrae with encroachment of canal. Reproduced from Singh and Jolly (1961, Quarterly Journal of Medicine 30: 357-372) with permission of Oxford University Press (b) Cervical radiculomyelopathy with paraplegia. (c) Crippling combined neurological and locomotor disease. Reproduced from Reddy (t979, Handbook of Clinical Neurology) with permission of Elsevier Science.
80
P . E . McGILL
dependent on a high fluoride ground water supply with no alternative sources, cheap methods of defluoridation need to be installed and the collection of rain water for drinking must be encouraged. In those with neurological disease surgical decompression of the cervical spine has been used with variable success (Reddy, 1979; Kak, 1988). SUMMARY The presence of excessive quantities of fluorine in drinking water is accompanied by a characteristic sequence of changes in teeth, bone and periarticular tissues. These changes lead to a variable degree of locomotor disability, ranging from simple mechanical back pain to severe, crippling, combined locomotor and neurological impairment. In endemic areas, a substantial proportion of the population may be affected, posing a severe public health problem. In some areas, the hazards to human health are not fully appreciated and are under-reported. The maximum impact is felt in those communities engaged in physically strenuous activities, either agricultural or industrial. The need of these often isolated communities in economically hard-pressed countries, for the provision of low-fluoride drinking water remains a hope rather than an expectation at the present time.
REFERENCES Anon (1981) Chronic fluorosis. British Medical Journal 282: 253-254. Azar HA, Nucho CK, Bayyuk SI and Bayyuk BW (1961) Skeletal Sclerosis Due to Chronic Fluoride Intoxication. Annals of Internal Medicine 55: 193201. Grech P (1966) Fluorosis in young persons. A further survey in Northern Tanganyika, Tanzania. British Journal of Radiology 39: 761-764. Haimanot RT, Fekadu A & Bushra B (1987) Endemic fluorosis in the Ethiopian Rift Valley. Tropical and Geographical Medicine 39: 20%217. Jolly SS, Singh BM, Mathur OC & Malhotra KC (1968) Epidemiological, clinical and biochemical study of endemic dental and skeletal fluorosis in the Punjab. British Medical Journal 4: 427-429. Kak VK (1988) Fluorosis of the cervical spine. Nimhans Journal Supplement 159-162. Moiler IJ, Pindborg JJ, Gedalia I and Roed-Petersen B (1970) The prevalence of dental fluorosis in the people of Uganda. Archives of Oral Biology 15: 213-225. -air KR & Manji F (1982) Endemic fluorosis in deciduous dentation: A study of 1276 children in a typically high fluoride area (Kiambu) in Kenya. Odontostomatologie Tropicale 4: 17%184. Ndosi NK (1989) Fluorosis with quadriplegia. A rare case. Post Graduate Doctor, Middle East 12: 84-88. Ockerse T (1945) Endemic fluorosis in South Africa, Pretoria (Thesis, University of Witwatersrand). Bulletin of Hygiene 20 (abstract): 20. Rao SR, Murty KJR, Murthy TVSD & Reddy SS (1975) Treatment of fluorosis in humans. Fluoride 8: 12-24. Reddy DB, Rao CM & Sarada D (1969) Endemic fluorosis. Journal of the Indian Medical Association 53: 275-281. Reddy DR (1979) Skeletal fluorosis. In Vinken PJ & Bruyn GW (eds) Handbook of Clinical Neurology (vol. 36), pp 456-504. Amsterdam: North Holland Publishing Company. -
ENDEMIC FLUOROSIS
81
Siddiqui AH (1955) Fluorosis in Nalgonda district, Hyderabad, Deccan. British Medical Journal 11: 1408-1413. Singh A & Jolly SS (1961) Endemic fluorosis with particular reference to fluorotic radiculomyelopathy. Quarterly Journal of Medicine (New Series) XXX: 357-372. Smith DA, Harris HA & Kirk R (1953) Fluorosis in the Butana, Sudan. Journal of Tropical Medicine and Hygiene 56: 57--58. Yan L (1990) Epidemiological survey of endemic fluorosis in Xiou Shan and Bao Jing areas. Chung-Hua-Liu-Hsing-Ping-Hsueh-Tsa-Chih 11(5): 302-306.
E. McGILL
'All substances are poison, there is none that is not a poison. The right dose differentiates a poison and remedy.' Paracelsus
Fluorine is widely distributed in variable concentrations in soil, rock and ground water. It is not an essential element for human health and no fluoride-deficiency syndrome has, as yet, been described. It has a recognized importance in the prevention of dental caries and in the treatment of osteoporosis. Exposure to high quantities of fluorine, either by ingestion or inhalation, results in the condition known as skeletal fluorosis. EPIDEMIOLOGY
Industrialfluorosis occurs when there is prolonged exposure to high atmospheric concentrations of fluoride in the aluminium, steel and glass industries. Endemicfluorosis results from the ingestion of excessive quantities of fluoride, usually in drinking water (Anon, 1981). In some areas, an additional source of pollution is atmospheric dust-containing suspended particles of fluoride (Rao et al, 1975) or contamination of foodstuffs from coal ash (Yan, 1990). There are well-known endemic areas in the tropics, in southern India around Madras and Hyderabad (Siddiqui, 1955) and in northern India in the Punjab (Jolly et al, 1968; Reddy et al, 1969). In Africa, fluorosis is endemic in the Rift Valley provinces of Tanzania, Kenya, Uganda and Ethiopia (Grech, 1966; Moller et al, 1970; Nair and Manji, 1982; Haimanot et al, 1987; Ndosi, 1989) and in the Sudan (Smith et al, 1953) and South Africa (Ockerse, 1945). PATHOGENESIS
Following absorption from the gastrointestinal tract, fluoride is taken up rapidly into bone and replaces hydroxyl ions in bone apatite. About half is sequestered in bone and the remainder excreted in urine and faeces. Fluoride bound to bone and teeth has a biological half-life of several years. Absorption is reduced in the presence of calcium, magnesium and aluminium. Bailli~re's Clinical Rheumatology-Vol. 9, No. 1, February 1995 ISBN 0-7020-1946-1
75 Copyright 9 1995, by Bailli6re Tindall All rights of reproduction in any form reserved
76
p.E. McGILL
The mechanism by which fluoride ions bring about such dramatic changes in skeletal tissue is not known. These changes include an overall increase in bone mass. Tendons, ligaments and muscles are infiltrated by mineral deposits and periosteal outgrowths. The vertebral column and ribs become fused following ossification of the intervertebral discs and spinal ligaments. The changes in bone density and characteristic ligamentous changes are vividly demonstrated on X-ray (Figure l(a)-(c)).
(b)
(a)
(c) Figure 1. (a), (b) Sclerotic vertebrae; (c) pelvis. Reproduced from Haimanot et al (1987, Tropical and Geographical Medicine 39: 209-217, with permission).
ENDEMIC FLUOROSIS
77
CLINICAL FEATURES Dental fluorosis
The incidence of dental fluorosis in endemic areas exhibits a linear relationship to the fluorine content of drinking water. The enamel of permanent teeth is affected by mottling and brownish discoloration and, in severe cases, pitting of the surface and chipping of the edges of teeth. Rarely, in highly endemic areas the deciduous teeth may be affected. Such teeth are usually caries-free but they are fragile and premature loss occurs due to periapical tooth absorption. In temperate climes dental fluorosis does not occur with water levels of less than 2 parts per million (ppm). Dental enamel mottling may be found in more than 80% of children resident since birth in endemic areas. Skeletal fluorosis
In temperate areas fluorosis affecting bone is not detectable until the concentration in drinking water is greater than 4 ppm. In the tropics more water may be consumed by those in physically strenuous jobs and fluorosis may develop at lower concentrations. There is an area of endemic fluorosis in the Persian Gulf (Qatar) where the water concentation of fluoride is less than 4 ppm. Excessive drinking of tea which contains very high concentrations of fluoride is considered to be an important contributory factor (Azar et al, 1961). There is generally a linear relationship between the development of skeletal fluorosis, the fluoride concentration of drinking water and the duration of exposure. Skeletal fluorosis is usually associated with the consumption of water with a fluoride content of more than 8 ppm for longer than 10 years. There are some areas in the Ethiopian and Kenyan Rift Valley where the fluoride content is 40 ppm. In endemic areas symptoms of back stiffness and limb pains are common and radiological evidence of skeletal fluorosis is present in 70% or more of symptomatic individuals. In established cases there is global restriction of spinal movements leading to a rigid kyphotic spine which outwardly resembles ankylosing spondylitis (Figure 2(a)). Involvement of joint capsule, ligaments and tendon insertions occurs in both the spine and at the periphery, mimicking the enthesopathy of ankylosing spondylitis (Figure 2(b)). Chest expansion is greatly limited due to involvement of the costosternal and costovertebral joints. Neurological manifestations of skeletal fluorosis
In endemic regions, it is estimated that about 10% of those with skeletal fluorosis exhibit neurological disease (Singh and Jolly, 1961; Haimanot et al, 1987). The neurological consequences are those of a radiculomyelopathy due to mechanical compression of the spinal cord and nerve roots by osteophytes. The brunt of the pathology falls on the cervical cord and usually consists of a myelopathy with progressive weakness of lower limbs
78
P . E . McGILL
(a)
(b) Figure 2. (a) Skeletal fluorosis with marked rigidity of the spine resembling ankylosing spondylifts. (b) Ligament and tendon calcification. Reproduced from Reddy (1979, Handbook of Clinical Neurology) with permission of Elsevier Science.
and difficulty walking with a combined motor and sensory defect and sphincter disturbances in the most severe cases (Figure 3(a) and (b)). In addition, there is frequently gross crippling deformities of the hips and knees, resulting in dual locomotor and neurological disability (Figure 3(c)). Root compression may lead to mixed neurological signs in the upper limbs with lower motor neurone lesions predominating. Very occasionally, cranial nerve palsies occur, usually the eighth nerve with a progressive high-frequency perceptive deafness due to compression of the nerve within the sclerosed auditory canal. DISABILITY
The impact of these locomotor changes on the workforce of certain rural communities is highlighted in a study from the EthiopianRift Valley where premature retirement (45-50 years) is common because of inability to perform physically strenuous work (Haimanot et al, 1987). PREVENTION AND TREATMENT
Prevention can only be undertaken by providing an alternative source of drinking water with a low fluoride concentration. In isolated villages
ENDEMIC FLUOROSIS
79
(a)
(c)
(b) Figure 3. (a) Dense sclerotic vertebrae with encroachment of canal. Reproduced from Singh and Jolly (1961, Quarterly Journal of Medicine 30: 357-372) with permission of Oxford University Press (b) Cervical radiculomyelopathy with paraplegia. (c) Crippling combined neurological and locomotor disease. Reproduced from Reddy (t979, Handbook of Clinical Neurology) with permission of Elsevier Science.
80
P . E . McGILL
dependent on a high fluoride ground water supply with no alternative sources, cheap methods of defluoridation need to be installed and the collection of rain water for drinking must be encouraged. In those with neurological disease surgical decompression of the cervical spine has been used with variable success (Reddy, 1979; Kak, 1988). SUMMARY The presence of excessive quantities of fluorine in drinking water is accompanied by a characteristic sequence of changes in teeth, bone and periarticular tissues. These changes lead to a variable degree of locomotor disability, ranging from simple mechanical back pain to severe, crippling, combined locomotor and neurological impairment. In endemic areas, a substantial proportion of the population may be affected, posing a severe public health problem. In some areas, the hazards to human health are not fully appreciated and are under-reported. The maximum impact is felt in those communities engaged in physically strenuous activities, either agricultural or industrial. The need of these often isolated communities in economically hard-pressed countries, for the provision of low-fluoride drinking water remains a hope rather than an expectation at the present time.
REFERENCES Anon (1981) Chronic fluorosis. British Medical Journal 282: 253-254. Azar HA, Nucho CK, Bayyuk SI and Bayyuk BW (1961) Skeletal Sclerosis Due to Chronic Fluoride Intoxication. Annals of Internal Medicine 55: 193201. Grech P (1966) Fluorosis in young persons. A further survey in Northern Tanganyika, Tanzania. British Journal of Radiology 39: 761-764. Haimanot RT, Fekadu A & Bushra B (1987) Endemic fluorosis in the Ethiopian Rift Valley. Tropical and Geographical Medicine 39: 20%217. Jolly SS, Singh BM, Mathur OC & Malhotra KC (1968) Epidemiological, clinical and biochemical study of endemic dental and skeletal fluorosis in the Punjab. British Medical Journal 4: 427-429. Kak VK (1988) Fluorosis of the cervical spine. Nimhans Journal Supplement 159-162. Moiler IJ, Pindborg JJ, Gedalia I and Roed-Petersen B (1970) The prevalence of dental fluorosis in the people of Uganda. Archives of Oral Biology 15: 213-225. -air KR & Manji F (1982) Endemic fluorosis in deciduous dentation: A study of 1276 children in a typically high fluoride area (Kiambu) in Kenya. Odontostomatologie Tropicale 4: 17%184. Ndosi NK (1989) Fluorosis with quadriplegia. A rare case. Post Graduate Doctor, Middle East 12: 84-88. Ockerse T (1945) Endemic fluorosis in South Africa, Pretoria (Thesis, University of Witwatersrand). Bulletin of Hygiene 20 (abstract): 20. Rao SR, Murty KJR, Murthy TVSD & Reddy SS (1975) Treatment of fluorosis in humans. Fluoride 8: 12-24. Reddy DB, Rao CM & Sarada D (1969) Endemic fluorosis. Journal of the Indian Medical Association 53: 275-281. Reddy DR (1979) Skeletal fluorosis. In Vinken PJ & Bruyn GW (eds) Handbook of Clinical Neurology (vol. 36), pp 456-504. Amsterdam: North Holland Publishing Company. -
ENDEMIC FLUOROSIS
81
Siddiqui AH (1955) Fluorosis in Nalgonda district, Hyderabad, Deccan. British Medical Journal 11: 1408-1413. Singh A & Jolly SS (1961) Endemic fluorosis with particular reference to fluorotic radiculomyelopathy. Quarterly Journal of Medicine (New Series) XXX: 357-372. Smith DA, Harris HA & Kirk R (1953) Fluorosis in the Butana, Sudan. Journal of Tropical Medicine and Hygiene 56: 57--58. Yan L (1990) Epidemiological survey of endemic fluorosis in Xiou Shan and Bao Jing areas. Chung-Hua-Liu-Hsing-Ping-Hsueh-Tsa-Chih 11(5): 302-306.