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
1·0
0·8
Proportion not instutionalised
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,
0·6 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
0·4 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)
0·2 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
0 We included the classification of bladder incontinence in
the frailty scale to study whether incontinence on its own (a
Time to institutionalisation (months) common disorder among elderly people) was a marker for
1·0
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
0·8 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
Proportion surviving

classification 0 (12% were classified as 1, 16% as 2, 5% as

0·6 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
0·4 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]).
0·2 0 This operational definition of frailty gives readily
1
2
available data for physicians and extends classification
3 beyond activities of daily life and mobility. Although the
frailty scale predicts adverse outcomes, research is needed
0 on whether high-risk people are amenable to specific
0 20 40 60 80 preventive interventions. The scale also draws attention to
Time to death (months) the relation of cognitive and activities of daily life, which
Time to institutionalisation (A) and death (B) on frailty scale, may prompt better understanding of the complex factors
adjusted for age and sex underlying adverse outcomes in elderly people.

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RESEARCH LETTERS
1 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.
2 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.
3 Fillenbaum GG. Multidimensional functional assessment of older
adults: the duke older americans resources and services procedures.
Hillsdale, NJ: Lawrence Erlbaum Associates, 1988.
4 American Psychiatric Association. Diagnostic and statistical manual of
mental disorders, 3rd edn. Washington: American Psychiatric
Association, 1987.
5 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 rockwood@is.dal.ca); 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
Satu Alaluusua, Pirjo-Liisa Lukinmaa, Jorma Torppa, Jouko
Tuomisto, Terttu Vartiainen
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-tetrachlorodibenzo-
p-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 (I-
TEqs) 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
206
Degree of defective
mineralisation
3
2
1
0
0 20 40 60 80 100
Ranked values of ex posure to PCDD/ FS
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.
The study was supported by the Academy of Finland, by the European
Commission (grant number ENV4-CT96-0336), and by the Finnish
Dental Society.
1 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.
2 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.
3 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.
4 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 satu.alaluusua@helsinki.fi); Department of Oral
Pathology, Institute of Dentistry, University of Helsinki, Helsinki;
National Public Health Institute, Helsinki and Kuopio, Finland
Sex ratio after exposure to dioxin-
like 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