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A brief clinical instrument to classify frailty in elderly people
RESEARCH LETTERS
Research letters
A brief clinical instrument to classify frailty in elderly people Kenneth Rockwood, Karen Stadnyk, Chris MacKnight, Ian McDowell, Réjean Hébert, David B Hogan
Increasingly, the term frailty is used to describe combinations of ageing, disease, and other factors (eg, fitness, nutritional status) that make some people vulnerable. There is no broadly accepted definition or standard system for classification of elderly people who are at risk for adverse health outcomes. 1 We assessed the criterion validity of a short candidate measure of frailty in prediction of death and institutionalisation. In 1991–92, we selected from Canadian provincial
Proportion not instutionalised
1·0
0·8
0·6
0·4
0·2
0 Time to institutionalisation (months) 1·0
Proportion surviving
0·8
0·6
0·4
0 1 2 3
0·2
0 0
20
40
60
80
Time to death (months) Time to institutionalisation (A) and death (B) on frailty scale, adjusted for age and sex
THE LANCET • Vol 353 • January 16, 1999
comprehensive sampling frames a random sample of 9008 community residents stratified by age (65–74 years, 75–84 years, Ä85 years), with 2/1 and 2·5/1 oversampling of the two older cohorts, respectively, and clustered by area. 2 As described elsewhere,2 baseline data included self-reported functional status (Older Americans Resources and Services Activities of Daily Living Scale 3) and clinical assessment of cognition for dementia (DSM-III-R criteria 4) and cognitive impairment with no dementia (CIND, based on exclusion of dementia 2). In 1996–97, we contacted surviving members of this cohort, and proxy informants of decedents to find out vital status and residential history since first contact. The frailty scale is based on the classification scheme of the geriatric status scale (GSS), 5 which was used to target patients in hospital eligible for a specialised geriatric intervention. Patients were classified at four levels, appropriate for people living in the community, representing fitness to frailty: (0) Those who walk without help, perform basic activities of daily living (eating, dressing, bathing, bed transfers), 3 are continent of bowel and bladder, and are not cognitively impaired; (1) bladder incontinence only; (2) one (two if incontinent) or more of needing assistance with mobility or activities of daily living, has CIND, or has bowel or bladder incontinence; and (3) two (three if incontinent) or more of totally dependent for transfers or one or more activities of daily life, incontinent of bowel and bladder, and diagnosis of dementia. 4 We included the classification of bladder incontinence in the frailty scale to study whether incontinence on its own (a common disorder among elderly people) was a marker for adverse outcomes. All data were analysed with SAS (version 6.12). We used Cox’s proportional hazards modelling to generate relative risks (adjusted for age and sex) for death and institutionalisation (compared with classification 0) and 95% CIs for each category of the frailty scale. At baseline, 67% of the cohort met the criteria for the classification 0 (12% were classified as 1, 16% as 2, 5% as 3). By 1996–97, 24% of the cohort had died and 12% were institutionalised. The frailty scale showed a dose-response relation between grades of frailty and subsequent institutionalisation (for 1, relative risk 1·7 [95% CI 1·3–2·1; for 2 3·6 [3·1–4·3]; for 3 9·4 [7·7–11·5]) and death (for 1 1·2 [1·0–1·4]; for 2 2·0 [1·8–2·2]; for 3 3·1 [2·7–3·6]). This operational definition of frailty gives readily available data for physicians and extends classification beyond activities of daily life and mobility. Although the frailty scale predicts adverse outcomes, research is needed on whether high-risk people are amenable to specific preventive interventions. The scale also draws attention to the relation of cognitive and activities of daily life, which may prompt better understanding of the complex factors underlying adverse outcomes in elderly people.
205
1 2
3
4
5
Rockwood K, Fox RA, Stolee P, Robertson D, Beattie BL. Frailty in elderly people: an evolving concept. Cam Med Assoc J 1994; 150: 489–95. Graham JE, Rockwood K, Beattie BL, McDowell I, Eastwood R, Gauthier S. Standardization of the diagnosis of dementia in the Canadian Study of Health and Aging. Neuroepidemiol 1996; 15: 246–56. Fillenbaum GG. Multidimensional functional assessment of older adults: the duke older americans resources and services procedures. Hillsdale, NJ: Lawrence Erlbaum Associates, 1988. American Psychiatric Association. Diagnostic and statistical manual of mental disorders, 3rd edn. Washington: American Psychiatric Association, 1987. Hogan DB, Fox RA. A prospective controlled trial of a geriatric consultation team in an acute-care hospital. Age Aging 1990; 19: 107–13.
Division of Geriatric Medicine, Dalhousie University and Centre for Health Care of the Elderly, Queen Elizabeth II Health Science Centre, Halifax, Nova Scotia, Canada B3H 2E1 (Prof K Rockwood; email [email protected]); Gerontology and Geriatrics Research Centre, Department of Epidemiology and Community Medicine, University of Ottawa; Sherbrooke Geriatric University Institute, Sherbrooke; and Division of Geriatric Medicine, University of Calgary
Developing teeth as biomarker of dioxin exposure
Degree of defective mineralisation
RESEARCH LETTERS
3 2 1 0 0
20 40 60 80 Ranked values of ex posure to PCDD/ FS
100
Mineralisation defects by exposure to PCDD/Fs Mineralisation degrees: 0=normal; 1=mild defect in only one tooth; 2=moderate defect or mild defect in more than one tooth; 3=severe defect.
congeners (p=0·07). In the regression analysis, the multiple correlation square did not increase when PCB-TEqs were added into the model after I-TEqs. The high frequency of hypomineralised dental defects among normal children may be a sign of exposure to PCDD/Fs. Since the dental hard tissues do not undergo remodelling, defects that occurred in infancy can be diagnosed even after many years. Also, because defects are seen after exposure to very low concentrations, they may be the best available indicator of dioxin exposure.
Satu Alaluusua, Pirjo-Liisa Lukinmaa, Jorma Torppa, Jouko Tuomisto, Terttu Vartiainen
The study was supported by the Academy of Finland, by the European Commission (grant number ENV4-CT96-0336), and by the Finnish Dental Society.
Polychlorinated aromatic hydrocarbons are environmental contaminants that occur as heterogeneous mixtures, enrich in the food chain, and bioaccumulate in tissue lipid. Breast feeding infants are at risk from those contaminants. Evidence implies that dioxins interfere with tooth development. An association between dioxin exposure in children and developmental dental defects has been shown after heavy accidental exposure and at prevailing concentrations.1 We have previously shown that experimental exposure of rats to the most toxic dioxin congener, 2,3,7,8-tetrachlorodibenzop-dioxin (TCDD), leads to developmental defects of dental hard tissues2 and that mouse embryonic teeth are affected in culture dependent on epidermal growth-factor-receptor expression.3 To find out whether teeth could be used as a biomarker of exposure to polychlorinated aromatic hydrocarbons in a normal breastfed child population we examined dentitions of 102 children aged 6–7 years in Finland for the presence of hypomineralised enamel defects. The permanent first molars, which are mineralised during the first 2 years of life, were the target teeth. The lesions, when present, were classified as established.1 We measured concentrations of the 17 most toxic polychlorinated dioxin/furan (PCDD/F) and 33 biphenyl congeners in milk samples, collected from the mother when the child was aged 4 weeks, by high-resolution gas chromatography mass spectrometry.4 The concentrations of PCDD/Fs were expressed in TCDD toxic equivalents (ITEqs) and those of biphenyl congeners in PCB-TEqs. We calculated total exposure of the infants from the duration of breastfeeding (mean 10·5 months) and the concentrations in milk (after having taken into account a yearly 25% first-order decline during lactation). Placental exposure was estimated to correspond to the exposure via milk for two months. Hypomineralised enamel defects were seen in the target teeth of 17 children (17%). Severity varied from chalky lesions to localised loss of enamel associated with affected dentin. The sum of I-TEqs and PCB-TEqs ranged from 7·7 pg/g to 258 pg/g milk fat (mean 48·8 [SD 29·1] pg/g). Mineralisation defects occurred more often and were more severe in children who had been exposed to higher amounts of polychlorinated aromatic hydrocarbons than in those exposed to lower amounts (p=0·02). Defects were clearly associated with the total exposure to toxic dioxins and furans (figure, p=0·004) but weakly with exposure to biphenyl
1
206
2
3
4
Alaluusua S, Lukinmaa P-L, Vartiainen T, Partanen M, Torppa J, Tuomisto J. Polychlorinated dibenzo-p-dioxins and dibenzofurans via mother’s milk may cause developmental defects in the child’s teeth. Environ Toxicol Pharmacol 1996; 1: 193–97. Alaluusua S, Lukinmaa P-L, Pohjanvirta R, Unkila M, Tuomisto J. Exposure to 2,3,7,8-tetrachlorodibenzo-para-dioxin leads to defective dentin formation and pulpal perforation in rat incisor tooth. Toxicology 1993; 8: 1–13. Partanen A-M, Alaluusua S, Miettinen PJ, et al. Epidermal growth factor receptor as a mediator of developmental toxicity of dioxin in mouse embryonic teeth. Lab Invest 1998; 78: 1473–81. Vartiainen T, Saarikoski S, Jaakkola JJ, Tuomisto J. PCDD, PCDF, and PCB concentrations in human milk from two areas in Finland. Chemosphere 1997; 34: 2571–83.
Department of Pedodontics and Orthodontics, Institute of Dentistry, POB 41, FIN-00014 University of Helsinki, Helsinki, Finland (S Alaluusua; e-mail [email protected]); Department of Oral Pathology, Institute of Dentistry, University of Helsinki, Helsinki; National Public Health Institute, Helsinki and Kuopio, Finland
Sex ratio after exposure to dioxinlike chemicals in Taiwan Walter J Rogan, Beth C Gladen, Yue-Liang Leon Guo, Chen-Chin Hsu
Between 1977 and 1984, 48 girls but only 26 boys were born to parents exposed to 2,3,7,8 tetrachlorodibenzo-p-dioxin (TCDD, or dioxin) in Seveso, Italy.1 The 1976 industrial accident at Seveso produced the highest documented community exposures to TCDD, and the period 1976–83 represents about one half-life of TCDD in adult human beings.2 Although TCDD is perhaps the most toxic and carcinogenic synthetic chemical known, has hormonal agonist/antagonist properties, and alters hormone metabolism,3 how it might have led to such a large departure from the expected sex ratio at birth of about 49 girls to 51 boys is unknown. Polychlorinated biphenyls (PCBs) and polychlorinated dibenzofurans (PCDFs) are also persistent and are toxicologically similar to (although less potent than) TCDD. They can occupy the Ah receptor, which is thought to mediate the toxic effects of TCDD.3 In two instances in Asia, thousands of people consumed cooking oil contaminated with PCBs and PCDFs, ingesting gram quantities of PCBs and milligram quantities of PCDFs. The two major PCDFs
THE LANCET • Vol 353 • January 16, 1999
Research letters
A brief clinical instrument to classify frailty in elderly people Kenneth Rockwood, Karen Stadnyk, Chris MacKnight, Ian McDowell, Réjean Hébert, David B Hogan
Increasingly, the term frailty is used to describe combinations of ageing, disease, and other factors (eg, fitness, nutritional status) that make some people vulnerable. There is no broadly accepted definition or standard system for classification of elderly people who are at risk for adverse health outcomes. 1 We assessed the criterion validity of a short candidate measure of frailty in prediction of death and institutionalisation. In 1991–92, we selected from Canadian provincial
Proportion not instutionalised
1·0
0·8
0·6
0·4
0·2
0 Time to institutionalisation (months) 1·0
Proportion surviving
0·8
0·6
0·4
0 1 2 3
0·2
0 0
20
40
60
80
Time to death (months) Time to institutionalisation (A) and death (B) on frailty scale, adjusted for age and sex
THE LANCET • Vol 353 • January 16, 1999
comprehensive sampling frames a random sample of 9008 community residents stratified by age (65–74 years, 75–84 years, Ä85 years), with 2/1 and 2·5/1 oversampling of the two older cohorts, respectively, and clustered by area. 2 As described elsewhere,2 baseline data included self-reported functional status (Older Americans Resources and Services Activities of Daily Living Scale 3) and clinical assessment of cognition for dementia (DSM-III-R criteria 4) and cognitive impairment with no dementia (CIND, based on exclusion of dementia 2). In 1996–97, we contacted surviving members of this cohort, and proxy informants of decedents to find out vital status and residential history since first contact. The frailty scale is based on the classification scheme of the geriatric status scale (GSS), 5 which was used to target patients in hospital eligible for a specialised geriatric intervention. Patients were classified at four levels, appropriate for people living in the community, representing fitness to frailty: (0) Those who walk without help, perform basic activities of daily living (eating, dressing, bathing, bed transfers), 3 are continent of bowel and bladder, and are not cognitively impaired; (1) bladder incontinence only; (2) one (two if incontinent) or more of needing assistance with mobility or activities of daily living, has CIND, or has bowel or bladder incontinence; and (3) two (three if incontinent) or more of totally dependent for transfers or one or more activities of daily life, incontinent of bowel and bladder, and diagnosis of dementia. 4 We included the classification of bladder incontinence in the frailty scale to study whether incontinence on its own (a common disorder among elderly people) was a marker for adverse outcomes. All data were analysed with SAS (version 6.12). We used Cox’s proportional hazards modelling to generate relative risks (adjusted for age and sex) for death and institutionalisation (compared with classification 0) and 95% CIs for each category of the frailty scale. At baseline, 67% of the cohort met the criteria for the classification 0 (12% were classified as 1, 16% as 2, 5% as 3). By 1996–97, 24% of the cohort had died and 12% were institutionalised. The frailty scale showed a dose-response relation between grades of frailty and subsequent institutionalisation (for 1, relative risk 1·7 [95% CI 1·3–2·1; for 2 3·6 [3·1–4·3]; for 3 9·4 [7·7–11·5]) and death (for 1 1·2 [1·0–1·4]; for 2 2·0 [1·8–2·2]; for 3 3·1 [2·7–3·6]). This operational definition of frailty gives readily available data for physicians and extends classification beyond activities of daily life and mobility. Although the frailty scale predicts adverse outcomes, research is needed on whether high-risk people are amenable to specific preventive interventions. The scale also draws attention to the relation of cognitive and activities of daily life, which may prompt better understanding of the complex factors underlying adverse outcomes in elderly people.
205
1 2
3
4
5
Rockwood K, Fox RA, Stolee P, Robertson D, Beattie BL. Frailty in elderly people: an evolving concept. Cam Med Assoc J 1994; 150: 489–95. Graham JE, Rockwood K, Beattie BL, McDowell I, Eastwood R, Gauthier S. Standardization of the diagnosis of dementia in the Canadian Study of Health and Aging. Neuroepidemiol 1996; 15: 246–56. Fillenbaum GG. Multidimensional functional assessment of older adults: the duke older americans resources and services procedures. Hillsdale, NJ: Lawrence Erlbaum Associates, 1988. American Psychiatric Association. Diagnostic and statistical manual of mental disorders, 3rd edn. Washington: American Psychiatric Association, 1987. Hogan DB, Fox RA. A prospective controlled trial of a geriatric consultation team in an acute-care hospital. Age Aging 1990; 19: 107–13.
Division of Geriatric Medicine, Dalhousie University and Centre for Health Care of the Elderly, Queen Elizabeth II Health Science Centre, Halifax, Nova Scotia, Canada B3H 2E1 (Prof K Rockwood; email [email protected]); Gerontology and Geriatrics Research Centre, Department of Epidemiology and Community Medicine, University of Ottawa; Sherbrooke Geriatric University Institute, Sherbrooke; and Division of Geriatric Medicine, University of Calgary
Developing teeth as biomarker of dioxin exposure
Degree of defective mineralisation
RESEARCH LETTERS
3 2 1 0 0
20 40 60 80 Ranked values of ex posure to PCDD/ FS
100
Mineralisation defects by exposure to PCDD/Fs Mineralisation degrees: 0=normal; 1=mild defect in only one tooth; 2=moderate defect or mild defect in more than one tooth; 3=severe defect.
congeners (p=0·07). In the regression analysis, the multiple correlation square did not increase when PCB-TEqs were added into the model after I-TEqs. The high frequency of hypomineralised dental defects among normal children may be a sign of exposure to PCDD/Fs. Since the dental hard tissues do not undergo remodelling, defects that occurred in infancy can be diagnosed even after many years. Also, because defects are seen after exposure to very low concentrations, they may be the best available indicator of dioxin exposure.
Satu Alaluusua, Pirjo-Liisa Lukinmaa, Jorma Torppa, Jouko Tuomisto, Terttu Vartiainen
The study was supported by the Academy of Finland, by the European Commission (grant number ENV4-CT96-0336), and by the Finnish Dental Society.
Polychlorinated aromatic hydrocarbons are environmental contaminants that occur as heterogeneous mixtures, enrich in the food chain, and bioaccumulate in tissue lipid. Breast feeding infants are at risk from those contaminants. Evidence implies that dioxins interfere with tooth development. An association between dioxin exposure in children and developmental dental defects has been shown after heavy accidental exposure and at prevailing concentrations.1 We have previously shown that experimental exposure of rats to the most toxic dioxin congener, 2,3,7,8-tetrachlorodibenzop-dioxin (TCDD), leads to developmental defects of dental hard tissues2 and that mouse embryonic teeth are affected in culture dependent on epidermal growth-factor-receptor expression.3 To find out whether teeth could be used as a biomarker of exposure to polychlorinated aromatic hydrocarbons in a normal breastfed child population we examined dentitions of 102 children aged 6–7 years in Finland for the presence of hypomineralised enamel defects. The permanent first molars, which are mineralised during the first 2 years of life, were the target teeth. The lesions, when present, were classified as established.1 We measured concentrations of the 17 most toxic polychlorinated dioxin/furan (PCDD/F) and 33 biphenyl congeners in milk samples, collected from the mother when the child was aged 4 weeks, by high-resolution gas chromatography mass spectrometry.4 The concentrations of PCDD/Fs were expressed in TCDD toxic equivalents (ITEqs) and those of biphenyl congeners in PCB-TEqs. We calculated total exposure of the infants from the duration of breastfeeding (mean 10·5 months) and the concentrations in milk (after having taken into account a yearly 25% first-order decline during lactation). Placental exposure was estimated to correspond to the exposure via milk for two months. Hypomineralised enamel defects were seen in the target teeth of 17 children (17%). Severity varied from chalky lesions to localised loss of enamel associated with affected dentin. The sum of I-TEqs and PCB-TEqs ranged from 7·7 pg/g to 258 pg/g milk fat (mean 48·8 [SD 29·1] pg/g). Mineralisation defects occurred more often and were more severe in children who had been exposed to higher amounts of polychlorinated aromatic hydrocarbons than in those exposed to lower amounts (p=0·02). Defects were clearly associated with the total exposure to toxic dioxins and furans (figure, p=0·004) but weakly with exposure to biphenyl
1
206
2
3
4
Alaluusua S, Lukinmaa P-L, Vartiainen T, Partanen M, Torppa J, Tuomisto J. Polychlorinated dibenzo-p-dioxins and dibenzofurans via mother’s milk may cause developmental defects in the child’s teeth. Environ Toxicol Pharmacol 1996; 1: 193–97. Alaluusua S, Lukinmaa P-L, Pohjanvirta R, Unkila M, Tuomisto J. Exposure to 2,3,7,8-tetrachlorodibenzo-para-dioxin leads to defective dentin formation and pulpal perforation in rat incisor tooth. Toxicology 1993; 8: 1–13. Partanen A-M, Alaluusua S, Miettinen PJ, et al. Epidermal growth factor receptor as a mediator of developmental toxicity of dioxin in mouse embryonic teeth. Lab Invest 1998; 78: 1473–81. Vartiainen T, Saarikoski S, Jaakkola JJ, Tuomisto J. PCDD, PCDF, and PCB concentrations in human milk from two areas in Finland. Chemosphere 1997; 34: 2571–83.
Department of Pedodontics and Orthodontics, Institute of Dentistry, POB 41, FIN-00014 University of Helsinki, Helsinki, Finland (S Alaluusua; e-mail [email protected]); Department of Oral Pathology, Institute of Dentistry, University of Helsinki, Helsinki; National Public Health Institute, Helsinki and Kuopio, Finland
Sex ratio after exposure to dioxinlike chemicals in Taiwan Walter J Rogan, Beth C Gladen, Yue-Liang Leon Guo, Chen-Chin Hsu
Between 1977 and 1984, 48 girls but only 26 boys were born to parents exposed to 2,3,7,8 tetrachlorodibenzo-p-dioxin (TCDD, or dioxin) in Seveso, Italy.1 The 1976 industrial accident at Seveso produced the highest documented community exposures to TCDD, and the period 1976–83 represents about one half-life of TCDD in adult human beings.2 Although TCDD is perhaps the most toxic and carcinogenic synthetic chemical known, has hormonal agonist/antagonist properties, and alters hormone metabolism,3 how it might have led to such a large departure from the expected sex ratio at birth of about 49 girls to 51 boys is unknown. Polychlorinated biphenyls (PCBs) and polychlorinated dibenzofurans (PCDFs) are also persistent and are toxicologically similar to (although less potent than) TCDD. They can occupy the Ah receptor, which is thought to mediate the toxic effects of TCDD.3 In two instances in Asia, thousands of people consumed cooking oil contaminated with PCBs and PCDFs, ingesting gram quantities of PCBs and milligram quantities of PCDFs. The two major PCDFs
THE LANCET • Vol 353 • January 16, 1999