Addictive Behaviors 30 (2005) 77 88

Childhood IQ, smoking, and cognitive change from age 11 to 64 years$

Lawrence J. Whalleya,*, Helen C. Foxa, Ian J. Dearyb, John M. Starrc
a

Department of Mental Health, University of Aberdeen, Aberdeen, Scotland, UK b Department of Psychology, University of Edinburgh, Scotland, UK c Department of Geriatric Medicine, University of Edinburgh, Scotland, UK

Abstract We investigated whether smoking is a risk factor for relative cognitive decline from age 11 to 64 years. The potentially confounding effects of childhood IQ, occupational status, level of education, presence of heart disease, hypertension, and lung function were examined. Subjects were nondemented and living independently. They were all born in 1936, had been participants in the same Scottish national IQ survey in 1947, and were reexamined at age about 64 years in 2000 2002. Current smokers and nonsmokers had significantly different mental test scores at age 64. This difference remained after adjustment for childhood IQ. Multiple linear regression identified childhood IQ, level of education, occupational code, lung function, and smoking history as significant independent predictors of mental function at age 64. In this sample, smoking makes a small ( < 1% variance) independent negative contribution to cognitive aging. D 2004 Elsevier Ltd. All rights reserved.
Keywords: Cognitive aging; Smoking; Lung function; Childhood intelligence

Follow-up studies of the Scottish Mental Survey 1932 are a series of ongoing collaborations among the Department of Mental Health, University of Aberdeen; Departments of Psychology, Universities of Edinburgh and Aberdeen; Scottish Council for Research in Education; and the Department of Geriatric Medicine, University of Edinburgh. * Corresponding author. Department of Mental Health, Royal Cornhill Hospital, Foresterhill, Aberdeen AB25 2ZH, Scotland, UK. Tel.:+44-1224553880; fax: +44-1224557401. E-mail address: l.j.whalley@abdn.ac.uk (L.J. Whalley). 0306-4603/$ see front matter D 2004 Elsevier Ltd. All rights reserved. doi:10.1016/j.addbeh.2004.04.014

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1. Introduction Some people continue to smoke and do so in the face of personal and public pressures to stop (Goodman & Glantz, 1998; Seigel, 1998). Among the immediate rewards claimed by smokers, there is the belief that smoking can stimulate pleasurable feelings (Pomerleau & Pomerleau, 1994) and enhance vigilance or selective attention (Koelega, 1993) or memory (Rusted, Graupner, Tennant, & Warburton, 1998). 1.1. Chronic smoking and cognition Hill (1989) showed that smokers performed less well on the Digit Symbol (DS) test of psychomotor speed than did nonsmokers or former smokers. He suggested that impaired lung function could contribute to cognitive impairment and that preventing smokers from smoking during cognitive test sessions could hinder test performance. By contrast, a lower risk of agerelated dementia has also been claimed for smokers than nonsmokers (Almeida, Hulse, Lawrence, & Flicker, 2002) although the largest studies to date do not support any health advantage for chronic smokers (Doll, Peto, Boreham, & Sutherland, 2000; Ott et al. 1998). At present, therefore, smoking cannot be consistently linked to either positive or negative longterm cognitive effects. Examination of smoking and cognition later in life benefits from knowledge of childhood IQ for the following reasons. First, it is helpful to have an assessment of cognitive function at an early age, before people have begun smoking. Second, it allows an assessment of cognition before adult occupational status is attained. This is important because occupational settings might maintain smoking behaviour, which might reduce cognition. Third, a measure of mental ability is needed from youth to assess cognitive change across the life. As far as we are aware, only one study to date examined cognition and smoking history in old age after adjusting for childhood IQ (Deary et al., 2003). They compared never-smokers, former smokers, and current smokers at age about 80 in a volunteer sample of 470 people who were born in 1921 and had taken part in the Scottish Mental Survey of 1932. The same mental test (the Moray House Test) was administered at age 11 and 80. After adjusting for childhood IQ, sex, and education, current smokers had significantly lower cognitive test scores than never- and former smokers at age 80, and smoking accounted for 1.4% of the variance in cognition at age 80. 1.2. Smoking and cognition: mechanisms Follow-up studies of the Scottish Mental Survey of 1932 (Deary, Whiteman, Starr, Whalley & Fox, 2004) did not examine possible mechanisms by which smoking might have affected cognition in old age. Either smoking and impaired lung function could act independently on cognition, or the effects of smoking could be mediated all or in part by lung function or through a general aging process (Anstey & Smith, 1999). To date, no study of chronic smoking and cognition has adjusted for childhood IQ and examined the mediating effect of lung function.

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1.3. The present study We examined surviving participants of the Scottish Mental Survey of 1947 (Scottish Council for Research in Education [SCRE], 1947). The Scottish Mental Surveys of 1932 and 1947 are reviewed by Deary et al. (2004). Here, we examine the contribution of smoking to cognitive change between the ages of 11 and 64 years. In addition, we examine whether any deleterious effect of smoking on cognitive change is mediated by its effects on lung function and whether any effect survives adjustment for major medical and social confounders. 2. Methods 2.1. Participants and procedures In 1999, with the agreement of the Grampian Ethics of Research Committee, local people who had taken part in the Scottish Mental Survey of 1947 were matched with a local health register. Exact matches were made by birth date and birth name. Subjects were aged about 64 years when invited to take part. Approaches continued until 465 subjects were recruited. Research procedures were completed during one visit (approximately 3 h) to the Clinical Research Centre. Written, informed consent was obtained by a trained research nurse at interview. Occupations were categorised using the Office of National Statistics, Standard Occupational Classification (2000) of the United Kingdom. Usual consumption of alcohol was recorded using a standardised questionnaire as units of alcohol in a typical week. Alcohol intake was not normally distributed and was categorised before entry into the statistical models as (1) nondrinker, (2) drinks up to 7 units per week, (3) drinks between 8 and 14 units per week, (4) drinks 1428 units per week, (5) drinks 2856 units per week, and (6) drinks more than 56 units per week. Smoking history was classified as never smoked, former smoker, or current smoker. Pack years were calculated as usual number of cigarettes per day times years as a smoker, divided by 20. A medical history of past and current treated episodes of illness was obtained. Specific details were sought about drug treatments in the previous year. History of hypertension, heart disease, and chronic lung disease was recorded. The research nurse also completed a clinical examination that included lung measurements made with a vitalograph spirometer with the subject standing. The highest of three expirations was recorded after an initial practice blow. Blood pressure was recorded both sitting and standing, each on three occasions at intervals of about 5 min. Hypertension was identified by a mean systolic pressure above 140 mm Hg and/or a mean diastolic pressure above 90 mm Hg. Subjects with treated hypertension were included in the hypertensive group. Time taken (in seconds) to walk 6 m was included as a measure of functional mobility. 2.2. Mental tests 2.2.1. The moray house test (MHT, tested when age about 11) On the 4th of June 1947, almost all children born in 1936 and attending schools in Scotland took a version of the Moray House Test which is an omnibus, group-

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administered mental test containing 71 numbered questions (75 items in total). SCRE gave access to their archived mental ability records (Scottish Mental Survey 1947, SMS47) for the present study. The following cognitive tests were administered in the same session as the clinical interview and examination described above, when subjects were about age 64. 2.2.2. Ravens Standard Progressive Matrices Ravens Standard Progressive Matrices (RPM; Raven, 1960) were used to measure nonverbal reasoning. Subjects were allowed 20 min to complete the test. 2.2.3. Rey Auditory Verbal Learning Test The Rey Auditory Verbal Learning Test (AVLT, Lezak, 1995; Rey, 1964, pp. 438446) measures memory and learning. 2.2.4. Uses of Common Objects Test Lezak (1995, uses of objects, p. 667) described the Uses of Common Objects Test (UOT) as a test of executive function or purposive action. 2.2.5. Digit symbol The DS subtest of the Wechsler Adult Intelligence ScaleRevised (WAIS-R; Wechsler, 1981) was used as an indicator of speed of information processing (Salthouse, 1996). 2.2.6. Block design The Block Design (BD) subtest of the WAIS-R (Wechsler, 1981) was used to examine constructional ability. 2.2.7. Mini-Mental State Examination A standardised brief cognitive screening instrument, the Mini-Mental State Examination (MMSE; Folstein, Folstein, & McHugh, 1975; Tombaugh & McIntyre, 1992), was used as part of a two-stage design with subjects falling below a set cutoff (24 points), undergoing a more detailed clinical examination by one of us (LJW). 2.3. Hypotheses and statistical analyses The general hypothesis to be tested was that smoking contributed to mental test scores as measured by DS, AVLT, BD, UOT, RPM and to a composite score derived from all of these when combined. Of specific interest to the present study was the hypothesis that the contribution of smoking would remain after adjustment of mental scores for childhood intelligence. Testing the general hypothesis to detect the contribution of smoking led to the specific hypothesis that in never-smokers, lung function measures would contribute to mental test scores after adjustment for childhood intelligence. Scores from the Moray House Test in 1947 were adjusted by age (in days) at testing in 1947 and transformed into conventional type IQ test results (mean = 100, S.D. = 15). Analysis was

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performed using the Statistical Package for the Social Sciences (Version 11). Scores from RPM, AVLT, BD, DS, and UOT were entered into a principal components analysis which extracted a single component accounting for 52% of the total score variance. Standardised scores on this component were converted to a conventional IQ-type scale (mean = 100, S.D. = 15). Lung function measurements were forced expiratory volume (FEV), vital capacity, and peak expiratory flow rate (PEFR) expressed as percentages of the value predicted from a linear regression of lung function on height for each sex (Hole et al., 1996). Comparisons between subjects grouped as never-smokers, past smokers, and current smokers were made using parametric and nonparametric statistics as appropriate. After the removal of one outlier, the analysis proceeded to a multivariate analysis of covariance, performed between the main, between-subjects factors of smoking history and sex on the dependent cognitive variables (RPM, AVLT, BD, DS, and UOT) with IQ11 as the covariate. Univariate analyses of covariance were then performed with post hoc Scheffes test to locate the source of any differences between subjects grouped by smoking history with IQ11 as covariate. Next, to examine the contribution of IQ at age 11 (IQ11) with other independent variables to the prediction of cognitive performance at age 64, a stepwise multiple regression analysis was performed on composite cognitive score (IQ64) as the dependent variable, with the independent variables childhood IQ, sex (as a dummy variable), occupational status, level of education, usual alcohol consumption (category of units/week), history of lung disease and/or current use of medications for chronic lung symptoms, hypertension, and smoking history. Pack years, mean systolic BP, and diastolic BP were introduced into the analysis but did not contribute to the model and were excluded. Two outliers were identified and removed from the regression analysis. We then added lung functions (expressed as a percentage of predicted values) to the model to determine if the effects of smoking could be accounted for by impaired lung function. This last analysis was repeated after excluding current and former smokers.

3. Results 3.1. Participants Of the 635 subjects invited to participate, 465 (73%) agreed. People who scored more than 24 points on the MMSE were excluded (and 3 subjects who also showed features suggestive of early dementia on further examination), 55 subjects had missing or unusable lung function tests, and 49 subjects had one or more missing cognitive test score. Those with missing lung data did not differ by childhood IQ or current occupational code from participants, but those with missing cognitive data had lower childhood IQ scores (mean = 92.0, S.D. = 16.0) than participants (mean = 100.7, S.D. = 15.0, P < .001) and lower status occupations (mean = 5.9, S.D. = 2.1; mean participants = 4.7, S.D. = 2.1. P < .01). At recruitment, the mean age of the study sample was 64.6 years (S.D. = 0.7 years), and there were approximately equal numbers of men (210) and women (203). We first analysed data for subjects with complete cognitive test scores (n = 413) before proceeding to analyse only those subjects with both complete cognitive data and lung function data (n = 358).

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Table 1 shows that alcohol consumption differed significantly between subjects grouped by smoking status and sex. Alcohol consumption was more frequent in men than women (v2 = 60.1, df = 4, P < .001) and less frequent in nonsmokers (v2 = 15.72, df = 8, P < .05). Level of education and category of occupation did not distinguish between current, former, and never-smokers (Tables 1 and 2). 3.2. Mental tests The combined dependent variables differed between the main factors (smoking history: Wilks lambda=.942, F = 2.42, P < .02; partial g2 = 0.029; sex: Wilks lambda=.733, F = 29.25, P < .001, partial g2 = 0.267; Table 2). There was no significant sex-by-smoking
Table 1 Alcohol consumption, level of education, and occupational categories in subjects grouped by smoking history and sex (n = 413) Sex (n) Never-smokers Men (79) Women (105) Former smokers Men (89) Women (50) Current smokers Men (42) Women (48) Significance

Alcohol (units/week) None 18 (23%) 55 (52.4%) 18 (20%) 16 (32%) 10 (24%) 22 (46%) Sex: v2 = 60.1, df = 4, P < .001; 17 28 (35%) 36 (34%) 23 (26%) 22 (44%) 13 (31%) 17 (35%) Smoking: v2 = 15.7, df = 8, P < .05 8 14 19 (24%) 12 (11%) 23 (26%) 11 (22%) 9 (21%) 8 (17%) 15 28 9 (11%) 2 (2%) 21 (24%) 1 (2%) 8 (19%) 1 (2%) 29 56 5 (6%) 0 4 (5%) 0 2 (5%) 0 More than 56 0 0 0 0 0 0 Level of education No qualifications 15 (19%) 24 (23%) Lower (age 16 years) Higher (age 17 years) Trade diploma Professional qualification Graduate (or equivalent) 31 (39%) 33 (31%) 4 (5%) 11 (11%)

19 (22%) 5 (10%)

10 (24%) 18 (38%) Smoking: v2 = 17.9, ns; Sex: v2 = 4.8, ns 38 (43%) 23 (46%) 19 (45%) 16 (33%) 6 (7%) 5 (10%) 0 (0%) 5 (12%) 7 (17%) 1 (2%) 0 (0%) 6 (13%) 7 (15%) 1 (2%)

14 (18%) 17 (16%) 11 (14%) 18 (17%) 4 (5%) 2 (2%)

10 (11%) 13 (26%) 10 (11%) 4 (8%) 2 (2%) 0 (0%)

Occupational category Profess/admin 21 (27%) 26 (25%) Skilled manual 46 (58%) 57 (54%) Unskilled manual 12 (15%) 22 (21%)

24 (27%) 10 (20%) 12 (29%) 11 (23%) Smoking: v2 = 1.1, ns; Sex: v2 = 1.7, ns 45 (51%) 33 (66%) 18 (43%) 28 (58%) 19 (22%) 7 (14%) 12 (29%) 9 (19%)

Profess/admincombined professional and administrative categories.

L.J. Whalley et al. / Addictive Behaviors 30 (2005) 7788 Table 2 Cognitive performance scores by smoking status and sex (n = 358) Cognitive variable AVLT Never-smokers M (79) 53.9 (12.2) BD 27.4 (8.4) DS 43.4 (11.0) UOT 15.2 (5.9) RPM 36.3 (7.8) F (105) 63.7 (11.0) 24.0 (7.5) 47.7 (11.3) 13.4 (4.9) 36.4 (8.7) Former smokers M (89) 54.1 (11.8) 26.0 (8.5) 41.9 (10.1) 14.0 (6.0) 37.0 (8.3) F (50) 66.0 (14.1) 22.6 (6.8) 47.4 (9.7) 12.9 (4.1) 35.4 (7.4) Current smokers M (42) 51.3 (12.0) 24.8 (8.1) 36.4 (11.7) 13.1 (5.2) 33.9 (7.9) F (48) 61.5 (10.4) 21.8 (8.5) 41.78 (9.7) 12.0 (4.2) 34.0 (8.1) Total (413) 58.4 (12.8) 24.7 (8.1) 41.4 (11.0) 13.6 (5.3) 34.0 (8.2)

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Analysis of covariance with IQ11 as covariate [partial g2] df (sex) Smoking: F = 1.56, ns [.008] Sex: F = 74.80, P < .001 [.156] Smoking: F = 1.62, ns [.008] Sex: F = 26.23, P < .001 [.061] Smoking: F = 9.06, P < .001 [.043] Sex: F = 18.43, P < .001 [.043] Smoking: F = 1.73, ns [.008] Sex: F = 10.69, P < .001 [.026] Smoking: F = 2.44, ns [.005] Sex: F = 2.44, ns [.006]

AVLTAuditory Verbal Learning Test; BDBlock Design; DSDigit Symbol; UOTUses for Objects Test; RPMRavens Progressive Matrices.

interaction ( F=.307, ns). The covariate IQ11 was associated with the dependent variables ( F = 53.0, P < .001, partial g2 = 0.397). There were significant differences by smoking history for DS ( F = 9.06, P < .001, partial g2=.043). There were differences by sex for AVLT ( F = 74.80, P < .001, partial g2=.156); BD ( F = 26.23, df = 1, P < .001, partial g2=.061); and UOT ( F = 10.69, df = 1, P < .01, partial g2=.026). 3.3. Physical health measures Disease status did not distinguish between subjects grouped by smoking status. Twenty-one subjects reported current treatment of chronic lung symptoms. A positive history of heart disease was given by 23/156 never-smokers, 26/125 former smokers, and 11/77 current smokers (v2 = 1.47, df = 2, ns). Subjects with hypertension (treated or untreated) did not differ between smoking groups (never-smokers = 86/156; former smokers = 77/125; current smokers = 45/77, (v2 = 1.45, df = 2, ns). Lung functions, expressed as percentages of values expected by height and sex, were entered into statistical analyses. Table 3 shows that all lung function indices were lower ( P < .001) in current smokers than in nonsmokers (never-smokers and former smokers), and both FEV and vital capacity were lower in women than in men ( P < .001). There were no differences between subjects grouped by smoking history in mean

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Table 3 Lung function in subjects grouped by smoking history and sex Lung function PEFR (l/min) %PEFR FEV (l) %FEV Vital capacity (l) %Vital capacity Never-smokers M (64) 399 (115) 93.8 (18.8) 2.82 (0.55) 93.8 (16.4) 3.28 (0.68) 84.9 (16.0) F (92) 276 (71) 92.9 (17.4) 2.06 (0.41) 101.4 (19.4) 2.36 (0.53) 96.5 (20.5) Former smokers M (83) 372 (127) 89.3 (20.7) 2.50 (0.64) 82.7 (20.3) 3.01 (0.78) 77.6 (18.8) F (42) 257 (93) 87.7 (24.1) 1.82 (0.48) 89.0 (23.4) 2.12 (0.60) 86.4 (22.8) Current smokers M (33) 327 (93) 82.1 (20.7) 2.37 (0.54) 78.8 (17.5) 2.98 (0.69) 77.4 (7.9) F (44) 250 (74) 84.9 (19.7) 1.73 (0.39) 82.8 (19.0) 2.01 (0.46) 80.4 (18.9) Total (358) 319 (117) 89.7 (20.1) 2.26 (0.63) 85.9 (19.3) 2.66 (0.79) 85.1 (20.5) Smoking: F = 6.38, P < .01; Sex: ns Significance

Smoking: F = 22.29, P < .001; Sex: F = 9.69, P < .01 Smoking: F = 11.88, P < .001; Sex: F = 12.4, P < .001

% Values refer to percentage of values predicted by sex and height in nonsmokers free of respiratory disease.

time taken to walk 6 m (nonsmokers: n = 182, mean F S.D. = 4.98 F 1.9; former smokers: n = 137, mean F S.D. = 5.06 F 0.95; current smokers: n = 87, mean F S.D. = 5.28 F 1.19, F = 1.12, df = 2, ns). 3.4. Multiple regression analyses Stepwise multiple linear regression analyses were performed between the dependent variable IQ64 and the independent variables IQ11, smoking history, and occupational
Table 4 Summary of three stepwise multiple regression analyses of childhood IQ (IQ11), educational qualifications, occupational category (1highest, 3lowest), health variables, smoking history, and lung functions on a composite score of cognitive ability at age 64 (IQ64) Model Variable Change df in R2 .409 .009 .012 .048 .407 .034 .008 .046 .008 .415 .029 .020 F b .475 .116 .115 .196 .468 .168 .114 .172 .092 .545 .191 .142 Significance < .001 < .01 < .01 < .001 < .001 < .001 < .05 < .001 < .02 < .001 < .01 < .025

Model 1: all subjects excluding lung function test IQ11 Occupation results (n = 411; R2=.477; adjusted R2=.472) Smoking Education Model 2: including lung function test results IQ11 (n = 357; R2=.502; adjusted R2=.495) PEFR Occupation Education Smoking Model 3: excluding current and former IQ11 smokers (n = 156; R2=.464; adjusted R2=.454) Education PEFR

409 280.20 408 24.26 407 10.08 406 8.56 355 208.30 354 25.31 353 20.30 352 5.82 351 5.92 154 109.35 153 6.69 152 5.34

PEFRpeak expiratory flow rate (l/s); Smokingsmoking history (never-, former, and current smoker).

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status, level of education, hypertension, and sex. Two subjects were excluded because IQ64 values were > 3 standard deviations outside the sample mean. Table 4 summarises the three regression analyses that were performed for the total sample (n = 411, Model 1), in subjects with lung data (n = 357, Model 2), and in nonsmokers with lung data (n = 156, Model 3). In all models (Table 4), IQ11 accounted for the greatest proportion of variance in IQ64 (range = 40.541.5%). In Model 1 (all subjects, n = 411), IQ11 contributed 40.9% with additional modest contributions made by level of education (4.8%), smoking history (1.2%), and occupational category (0.9%). After inclusion of lung data in Model 2 (n = 357), the contributions made were 40.7% for IQ11, 4.6% for level of education, 3.4% for percentage PEFR, 0.8% for occupational category, and 0.8% for smoking history. In Model 3 (nonsmokers only, n = 156), these were 41.5% for IQ11, 2.9% for level of education, and 2.0% for percentage PEFR. Pack years did not contribute to any of the regression models.

4. Discussion We report an observational study of a population-based sample derived from a single birth cohort now at about usual retirement age. Childhood IQ, level of education, and category of occupation did not distinguish between current, former, and never-smokers. After adjustment for childhood IQ, a positive smoking history was associated with lower performance on tests of psychomotor speed (DS) and on a composite score derived from all five cognitive tests (RPM, AVLT, BD, DS, and UOT). Multiple regression analyses showed that smoking history made a minor, independent contribution to cognitive function aged 64 (IQ64) when this was fully adjusted for childhood IQ (IQ11), lung function, sex, occupation, and education. In never-smokers, cognitive function aged 64 was associated with IQ11, education, and lung function. Pack years of smoking did not contribute to any of the regression models. The first aim of the study was to identify lasting cognitive benefits or decrements of longterm smoking. There were no differences in IQ at age 11 by smoking status, but by age 64; current smokers were performing less well on cognitive tests than nonsmokers and former smokers. Psychomotor speed (measured by the DS test) was lower in smokers. The association between smoking and impaired lung function was seen in both current and former smokers. This suggests that the effects of smoking on lung function are relatively enduring, whereas these effects on cognition are more evident in current smokers than non- or former smokers. The latter result was also observed by Deary et al. (2003); they found that, after adjusting for IQ at age 11, current smokers, but not former smokers, had lower IQ scores at age 80 when compared with life-long nonsmokers. This observation raises the possibility that cognitive impairment attributable to smoking occurs only after protracted exposure or in later life when age-associated mental impairment is first observable. This latter interpretation is consistent with that of Richards, Jarvis, Thompson, and Wadsworth (2003) who found an association between lower cognitive performance and smoking history in smokers aged 53 years after adjustment for performance aged 43 years but not between cognitive performance and smoking aged 43 years.

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Our second aim was to compare cognitive ability of smokers and nonsmokers after taking account of childhood IQ. With full adjustment in the regression models for potential contributors to late life IQ, smoking made a small independent negative contribution and was placed lower than childhood IQ, PEFR, and education. In contrast to the findings of Richards et al. (2003), we did not detect an association between smoking and verbal memory. However, we did find that smokers performed less well on a test of information-processing speed. We conclude that long-term smoking does not produce long-term cognitive benefits; to the contrary, smoking makes a small but significant contribution to cognitive decline from age 11 to 64, in agreement with our findings at age 80, where smoking affected verbal reasoning (Deary et al., 2003). The third goal was to examine the association between cognitive function and smoking after taking account of childhood IQ, variation in lung function, and the presence of lung and cardiovascular disease. We interpret the regression models (Models 1, 2, and 3) as indicators that, after controlling for childhood IQ, important positive contributions to lifelong cognitive change are made by higher occupational status and education. There is a small additional significant negative contribution of smoking to change in cognitive performance in late life. The extent of this independent contribution was estimated at 1.2% when lung function was not included (Model 1) and was lower (0.8%) when lung function was included (Model 2). In never-smokers (Model 3), the contribution of lung function was lower (2.0%) than found in the larger sample in which smokers were included (lung function contributed 3.4%). Earlier studies have examined associations between smoking and risk of dementia and agerelated cognitive decline. Although some suggest a possible dementia-protective effect of smoking, later studies (reviewed by Almeida et al., 2002) indicated that smoking does not reduce the age-specific onset rate of dementia. Cervilla, Prince, and Mann (2000) agreed and reported contrary evidence that smoking was associated with an increased risk of age-related cognitive decline. Doll et al. (2000) commented that, if anything, persistent smoking may increase rather than decrease the onset rate of dementia, but the net effect cannot be large in either direction. The results of the present study are consistent with that view. Comparable data are also available from previous studies on the association between smoking and cognitive function. Most have reported that current smokers perform less well than expected on cognitive tests when compared with never-smokers and former smokers (Elwood et al., 1999; Hill, 1989), but most do not examine multiple cognitive domains and are crosssectional in nature. Kalmijn, van Boxtel, Verschuren, Jolles, and Launer, (2002) completed a follow-up study of 1894 middle-aged subjects (mean age = 56.4 years, range = 4570 years). After adjustment for confounders (including education), these authors found that current smokers had reduced psychomotor speed compared to never-smokers. Their observation is directly comparable to our finding that, without adjustment for childhood IQ, performance on the DS test (a test of psychomotor speed) was better in nonsmokers than in current smokers. However, after adjustment for childhood IQ, this advantage of nonsmokers was lost but retained for women (Table 2). Associations between smoking, lung function, and long-term change in cognitive function require explanation. The harmful effects of smoking on lung function are well established,

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both epidemiologically and experimentally (Doll et al., 2000). An association between smoking, impaired lung function, and reduced long-term cognition may be attributable to impaired cardiorespiratory support of brain function or harmful direct effects of smoking on both lung and brain tissue. The data obtained here suggest that about 5.7% of the variance in cognitive function at age 64 is attributable to the effects of education and occupation after adjustment for IQ at age 11. Thereafter, small but significant negative contributions amounting to no more than about 4% are made by a combination of smoking and impaired lung function acting both together and alone. Although negative effects on cognition are relatively small in terms of a single individual, these effects are important at the population level. As a lifestyle choice, they are open to modification and thereby to enhancement of retention of cognitive function.

Acknowledgements The present new analyses were supported by a grant from the Biotechnology and Biological Sciences Research Council and grants from the Medical Research Council and Scottish Executive Health Departments Chief Scientist Office. We thank Valerie Wilson and Graham Thorpe (Scottish Council for Research in Education) for providing access to age-11 Moray House Test scores from the Scottish Mental Surveys of 1947. We thank Steven Leaper, Helen Lemmon, and Marietta Struth for assistance with data collection and John R. Crawford for advice and training on the psychometric tests. Jon Ayres made helpful criticisms of the manuscript.

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