Volume 168 Issue 2

Apolipoprotein screening in Australian children: feasibility and the effect of age, sex, and ethnicity Judith F Lynch, Michelle D Marshall, Xing L Wang and David E L Wilcken MJA 1998; 168: 61-64 Abstract - Introduction - Methods - Results - Discussion - References - Authors' details - - ©MJA1998 Abstract Objectives: (i) To evaluate the feasibility of detecting adverse lipid profiles in schoolchildren by measuring capillary dried blood spot apolipoprotein levels, and (ii) to assess the effect of age, sex and ethnicity on apolipoprotein levels. Design: We measured capillary dried blood spot apolipoproteins B and A-I (apo B and apo A-I); assessed levels in relation to age, sex and ethnicity; and recalled children with elevated levels for a full lipid profile measurement. Participants and setting: 6992 children (3501 boys and 3491 girls), aged 5-13 years, from schools in eastern Sydney, 1991-1995. Main outcome measures: Capillary blood levels of apolipoproteins B and A-I, and serum total cholesterol level. Results: Of the 6951 children who provided an adequate fingerprick blood sample, we recalled 1465 children (21.1%) (640 boys [43.7%] and 825 girls [56.3%]) with elevated apo B levels and/or apo B : apo A-I ratios for further testing, either by us or by their family doctor (overall estimated compliance rate up to 70%). Among the 458 children who returned to us, there was a 90% positive predictive value for a total cholesterol level of over 4.5 mmol/L in those with both elevated apo B levels and high apo B : apo A-I ratios. Girls had higher apo B levels and apo B : apo A-I ratios than boys (P < 0.00001 for both), and in both sexes there was a trend downwards for apo B and upwards for apo B : apo A-I ratio over the age range tested, but levels were relatively stable between the ages of 6 and 10 years. Indian children (1.5% of the screened population) had the highest apo B levels, followed by white children (71.1%); Asian children (9.2%) had the lowest (P < 0.00001 compared with Indian and white children). Conclusions: The high positive predictive value of capillary blood apolipoprotein levels for an adverse lipid profile in children suggests that measuring apolipoprotein levels by this method is a useful initial approach to cardiovascular risk assessment. Introduction Despite a recent decline in cardiac deaths, coronary disease is still the largest single cause of premature death in Australia.1 It is known that atherogenesis, the underlying pathological process, may begin in childhood;2,3 that relevant risk factors may track from childhood to adulthood (particularly elevated levels of total and low-density lipoprotein [LDL] cholesterol and increased body weight); and that these factors tend to aggregate within families.4,5 With these considerations in mind, we explored the feasibility of screening for adverse lipid profiles in a target group of primary schoolchildren, with the aim of implementing family-based coronary prevention by secondarily identifying any parents at risk. We measured levels of apolipoprotein B (apo B), the carrier protein for the atherogenic LDL cholesterol, and apolipoprotein A-I (apo A-I), the principal carrier protein for the antiatherogenic high density lipoprotein (HDL) cholesterol, in capillary dried blood spots from 6992 primary schoolchildren aged 5-13 years. There is increasing evidence that high apo B and low apo A-I levels are as reflective of cardiovascular risk as are their respective lipoproteins.6 We describe here the positive predictive value of high apo B and/or apo B : apo A-I ratio for elevated total cholesterol levels and the effects of age, sex and eth nicity on lipid levels in Australian children. Methods School and population demographics We received permission from 70 schools in eastern Sydney (public primary schools, 45%; Catholic primary schools, 29%; and private fee-paying schools, 26%) to contact parents and offer them the option of their child participating in a "Heart Health Screening Program". Children were given consent forms to take home to their parents. On the forms, we asked for the country of origin of each family, and this information was confirmed by a family history questionnaire (sent to all parents within a week of the testing at school) asking each parent to identify their country of origin. Only 1% of the total declined to answer this question (the "unknown" group) (Table 1). Blood collection and apolipoprotein measurement Testing took place between 1991 and 1995. From each child we obtained a capillary blood sample by fingerprick, which was spotted directly onto filter paper (No. 903: Schleicher & Schuell Inc., Keene, NH, USA), allowed to air dry and stored at 2 70¡C until analysis. Concentrations of dried blood spot apo B, apo A-I and lipoprotein (a) (Lp(a)) were measured within two weeks by our previously described enzyme-linked immunosorbent assay methods,7-9 and from these results an apo B : apo A-I ratio was also calculated. These methods allowed us to carry out all three measurements on one small (minimum, 20 µL sample) capillary dried blood spot. We report here the results obtained for measurement of apo B and apo A-I only. Recall In the first school tested, we established the frequency distribution for apo B levels and apo B : apo A-I ratios and set the level for recall for each of these as at or above the 90th percentile. These cut-off points were adjusted from the apo lipoprotein results obtained from each of the next seven schools. However, a stable cut-off level was reached by the third school. We defined three categories of children for recall: those with an ele vated apo B level only (Criterion 1), those with a combination of elevated apo B level and apo B : apo A-I ratio (Criterion 2), and finally those with an elevated apo B : apo A-I ratio only (Criterion 3). We notified the parents of the children for recall by letter, explaining the results and suggesting that both parents, the child, and any other siblings might come to us for further lipid testing, or attend their family doctor. In those who returned to us, we measured total cholesterol level, as well as HDL cholesterol and triglyceride levels, in a venous blood sample by standard methods. LDL cholesterol level was calculated by the Friedewald formula,10 and we also measured serum apo B, apo A-I and Lp(a) by the methods outlined above.7-9 The parents of children with apo B levels and apo B : apo A-I ratios below the established cut-off points were also sent a letter explaining that their children's levels currently fell below the recall criteria. These families were sent a healthy lifestyle pamphlet specifically directed to maintaining a low level of cardiovascular risk; they were also asked if they would like to volunteer as a healthy control family and have complete lipid profiles measured as above. Statistical analysis As the distributions of age, apo B and apo A-I levels, and apo B : apo A-I ratios were normal, analyses by parametric methods were appropriate. We used one-way analysis of variance (ANOVA) for comparisons of measured quantitative variables when there were more than two groups; for example, when children were divided according to high apo B, high apo B : apo A-I ratio, or both, as categorical variables, and levels of total cholesterol and LDL cholesterol, and total cholesterol to HDL cholesterol ratio as the continuous outcome variables. When the comparison was between two groups -- for example, when lipid values were compared in girls and boys as categorical determinants -- Student's t test was used.11 We employed a chi-squared comparison for assessing associations between categorical variables, and used the SPSS statistical software package for all analyses.12 Ethical approval The study was approved by the ethics committee of the University of New South Wales. Results Initial testing The parental consent rate to initial testing was 63.9%. There were 6992 children aged 5-13 years available for testing, 3501 (50.1%) boys and 3491 (49.9%) girls. Only 41 children (0.6%) failed to provide an adequate finger-prick blood sample on the day, leaving a total population of 6951 children tested. Recall population The cut-off point for apo B level was set at 0.550 g/L or more and for the apo B : apo A-I ratio 1.200 or more. We recalled 1465 children (or 21.1% of the population tested). Of these recalls, 65.3% were for elevated apo B only (Criterion 1), 19.6% for elevated apo B and apo B : apo A-I ratio (Criterion 2), and 15.1% for elevated apo B : apo A-I ratio only (Criterion 3). In all, 458 of the children recalled returned with their families to our laboratory for lipid studies (31.2% compliance rate). To obtain an assessment of how many may have been seen by their family doctor (the other option we suggested), we contacted 205 of the remaining 1007 families. Among these, 118 had seen their family doctor for follow-up, and 89 had either moved or were not interested in further testing. This suggested an overall compliance rate of about 70%, if this sample was representative. Of the non-recalled "normal" population of 5486 (78.9%), only 151 families (2.7%) volunteered for lipid testing, an insufficient number for meaningful statistical analysis. Predictive value We used the results of the 458 children who returned for a full lipid profile to assess the positive predictive value of our screening method. The National Heart Foundation of Australia recommends a total cholesterol level of 4.5 mmol/L as the upper limit for children in this age range.13 With a level of over 4.5 mmol/L as the endpoint, Criterion 1 (elevated apo B only) had a positive predictive value of 84% (95% confidence interval [CI], 80%-88%), and with Criterion 2 (elevated apo B level and apo B : apo A-I ratio combined) the predictive value increased to 90% (95% CI, 85%-95%). However, Criterion 3 (elevated apo B : apo A-I ratio only) yielded only 66% (95% CI, 54%-77%), possibly reflecting children with low HDL cholesterol and normal total cholesterol levels. Raising the cut-off point did not substantially improve the positive predictive value of our screening method. When the cut-off point for apo B was increased from 0.550 g/L to 0.700 g/L, for example, the positive predictive value of Criterion 2, the most strongly predictive, only increased to 94% (95% CI, 91%-97%). ANOVA confirmed the association between high apo B levels from analysis of dried blood spot and an adverse lipid profile, and also that a combined high apo B level and apo B : apo A-I ratio was a stronger predictor. In this analysis, criteria established by high apo B, high apo B : apo A-I ratio and a combination of both were determinant categorical variables, and the total cholesterol and LDL cholesterol levels and total chol es terol to HDL cholesterol ratio were the continuous outcomes. Total (P < 0.0006) and LDL cholesterol (P < 0.0014) levels and the total cholesterol to HDL cholesterol ratio (P < 0.0006) were all significantly higher in Criterion 2 than in Criterion 1 or Criterion 3 (Table 2). Sex, age and ethnicity There was a highly significant difference in the apo B and apo B : apo A-I ratio levels between boys and girls (P < 0.00001 for each) (Figures 1 and 2), but no difference (P = 0.6) in apo A-I levels (data not shown). The girls had consistently higher apo B levels and apo B : apo A-I ratios over the age range studied (Figures 1 and 2). This resulted in a significant difference in the recall rate between girls and boys (chi-squared = 23.362; P < 0.00001). This sex difference was also reflected in the total cholesterol levels of children returning for further lipid tests (data not shown). As shown in Figures 1 and 2, there was a downward trend in apo B level and an upward one in apo B : apo A-I ratio in boys over the age range screened, while the opposite was observed in girls; but levels were relatively consistent in both between the ages of 6 and 10 years. Most of the 6951 children screened were white (71.1%); the remainder were of diverse ethnic origins (Table 1). The mixed-race group (8.3% of the total) included white/Asian (28.2%), white/Arabic (17.8%), white/South American (10.7%), and other combinations (56.7%). As age was a significant contributor to apo B concentrations, we compared the "age adjusted apo B levels" for both boys and girls to assess potential differences between major ethnic groups (Figure 3). Indian children had the highest apo B levels, followed by white children. Asian children had the lowest levels and these were significantly different from those of the Indian, white, mixed-race and South American children (P < 0.00001 for each). We did not include black, Australian Aboriginal or Pacific Islander ethnic groups in this analysis because of small numbers and highly skewed age distributions. In all ethnic groups, girls had higher levels than boys (Figure 3). Discussion We have established previously that apolipoprotein measurements provide a convenient and effective approach to the detection of dyslipidaemia,14 and that apo B levels in children are correlated with the occurrence of coronary events in their grandparents, which highlights the relevance of measurements in children to assessing risk of vascular disease in older family members.15 We have also established a clear-cut association between increased apo B levels and apo B : apo A-I ratios and body mass index in Australian children.16 Here, we extend these find ings by demonstrating the feasibility of screening of schoolchildren's capillary blood apolipoprotein levels as an approach to family-based primary coronary prevention. Although we do not have adequate data to determine the sensitivity or specificity of our screening method, the presence of both an elevated apo B level and raised apo B : apo A-I ratios had a positive predictive value of 90% for the detection of elevated total serum cholesterol level. Raising the apolipoprotein cut-off points only improved the predictive value to 94%. This method identified elevated apolipoprotein levels in 21.1% of our population, of whom 90% had elevated total cholesterol levels. Screening for apolipoprotein levels may be more relevant than screening for total cholesterol levels alone, as total cholesterol level does not show the interrelations between levels of the atherogenic LDL and the antiatherogenic HDL cholesterol.17 In a small number of children (0.48%) apo B levels were elevated without elevation of total cholesterol level.18 These families were also provided with dietary and lifestyle advice as this may also be associated with increased cardio vascular risk. Our findings clearly show highly significant differences between boys and girls at this age, with girls having higher apo B levels and apo B : apo A-I ratios than boys. We suspect this biological difference, which was evident before the onset of puberty in both boys and girls, to be hormonally based, although we have no data to support this. The vari ation in apolipoprotein levels within the age range studied could also be hormonally based. Whatever the mech anisms, these same age-related sex differences have been identified in several other studies in children.19,20 The consistency of these results clearly indicates a need to have different cut-off points in boys and girls for elevated apolipoprotein levels. Our results also define the age range (between 6 and 10 years) when levels are most stable and most appropriate for screening, findings which will be incorporated into future studies. There were uniform sex-related differences in apolipoprotein levels in each of the racial groups in our population, as well as very significant differences in levels between the various ethnic groups, as has also been found in previous studies.21,22 In our population, Indian and white children had the highest apo B and apo B : apo A-I ratios and Asian children had the lowest. It is well established that Chinese and Japanese populations have much lower cholesterol levels than whites and a correspondingly lower prevalence of coronary artery disease. Indian populations have a higher prevalence of cardiovascular disease.23 While these variations may relate to the genetic background of each ethnic group, diet and lifestyle undoubtedly make major contributions, and this is particularly evident in non-Western groups who have moved to live in a Western society. The higher prevalence of coronary disease in Indians living in the United Kingdom, for example, is well documented.24 Ethnic differences may become blurred with time if dietary habits become more uniform, and this has occurred among Asians emigrating to the United States and the United Kingdom; within a generation they acquired local lifestyles and a correspondingly higher prevalence of coronary artery disease than that in the communities they had left.25,26 In conclusion, our study demonstrates the feasibility of conducting a program of measuring apolipoprotein levels in capillary blood samples to assess lipid profiles in children to facilitate family-based coronary prevention. It documents wide acceptance by both schools and parents. Implicit in such a study is the potential for a multiplier effect in that, if a child has an elevated apolipoprotein level and therefore an adverse lipid profile, it is very likely that this will also be seen in at least one parent and other siblings.27 Our ongoing screening program requires the establishment of a concurrent intervention program to improve dietary and lifestyle habits of affected children and their parents. This is of more immediate relevance to affected parents as they are approaching the age of overt coronary disease. However, the program provides an ideal opportunity to establish healthy lifestyles in young children at a time of easy acceptance, and with the potential for preventing a disorder that may have its origins in childhood.28 References Heart and Stroke Facts. A report by the National Heart Foundation of Australia. Canberra: NHFA, 1996. Stary HC. Evolution and progression of atherosclerotic lesions in coronary arteries of children and young adults. Arteriosclerosis 1989; 9(1 Suppl): I19-I32. Tracy RE, Newman WP, Wattigney WA, Berenson GS. Risk factors and atherosclerosis in youth autopsy findings of the Bogalusa Heart Study. Am J Med Sci 1995; 310(Suppl 1): S37-S41. Berenson GS, Wattigney WA, Bao W, et al. Rationale to study the early natural history of heart disease: the Bogalusa Heart Study [review]. Am J Med Sci 1995; 310(Suppl 1): S22-S28. Sanchez-Bayle M, Gonzalez-Requjo A, Ruiz-Jarabo C, et al. Serum lipids and lipoproteins in Spanish children and adolescents: a 5 year follow-up. Acta Paediatr 1996; 85: 292-294. Bao W, Srinivassan SR, Berenson GS. Tracking of serum apolipoproteins A-I and B in children and young adults: the Bogalusa Heart Study. J Clin Epidemiol 1993; 46: 609-616. Wang XL, Dudman NP, Wilcken DE. Enzyme-linked immunosorbent assay of apolipoprotein B in blood spotted onto filter paper, suitable for neonatal screening. Clin Chem 1989; 35: 1000-1004. Wang XL, Dudman NP, Blades BL, Wilcken DE. Changes in the immunoreactivity of apo A-I during storage. Clin Chem 1989; 179: 285-293. Wang XL, Wilcken DE, Dudman NP. An indirect sandwich ELISA for Lp(a) in serum and dried blood spots. Clin Chim Acta 1992; 207: 73-86. Friedewald WT, Levy RI, Fredrickson DS. Estimation of the concentration of low-density lipoprotein cholesterol in plasma, without use of the preparative ultracentrifuge. Clin Chem 1972; 18: 499-502. Norusis MJ. General factorial analysis of variance. SPSS for Windows Advanced Statistics, release 6.0. Chicago: SPSS Inc, 1993: 31-56. McNeil D. Statistical methods II: one-way analysis of variance. In: McNeil D, editor. Epidemiological research methods. New York: John Wiley & Sons, 1996: 66-71. National Diet and Heart Disease Advisory Committee, National Heart Foundation of Australia. Guide to plasma lipids for doctors. Curr Therap 1992; 10(Suppl 1): S1-S8. Wang XL, Wilcken DE, Dudman NP. Apolipoprotein A- I and B and the B/A-I ratio in the first year of life. Pediatr Res 1991; 30: 544-549. Wilcken DEL, Wang XL, Greenwood J, Lynch JF. Lipoprotein (a) and apolipoproteins B and A-I in children and coronary vascular events in their grandparents. J Pediatr 1993; 123: 519-526. Wilcken DE, Lynch JF, Marshall MD, et al. Relevance of body weight to apolipoprotein levels in Australian children. Med J Aust 1996; 164: 22-25. Taylor CJ, Olpin S, Rattenbury J, et al. Familial hyper cholesterolaemia: pilot study to identify children at risk. J Clin Pathol 1993; 46: 730-733. Grundy S. Small LDL. Atherogenic dyslipidaemia and the metabolic syndrome. Circulation 1997; 95: 1-4. Resnicow K, Morley-Kotchen J, Wynder E. Plasma cholesterol levels of 6585 children in the United States: results of the know your body screening in five states. Pediatrics 1989; 84: 969-976. Christensen B, Glueck C, Kwiterovich P, et al. Plasma cholesterol and triglyceride distributions in 13,665 children and adolescents: the Prevalence Study of the Lipid Research Clinics Program. Pediatr Res 1980; 14: 194-202. Zhang W, Evans AE, Cambien F, et al. Distribution of lipid variables in subjects in Belfast, Northern Ireland and Taiyuan, PR China. Atherosclerosis 1993; 102: 175-180. Freedman DS, Lee SL, Byers T, et al. Serum cholesterol levels in a multiracial sample of 7,439 preschool children from Arizona. Prev Med 1992; 21: 162-176. Enas EA, Mehta J. Malignant coronary artery disease in young Asian Indians: thoughts on pathogenesis, prevention, and therapy. Coronary Artery Disease in Asian Indians (CADI) Study [review]. Clin Cardiol 1995; 18: 131-135. Bhatnagar D, Anand IS, Durrington PN, et al. Coronary risk factors in people from the Indian subcontinent living in west London and their siblings in India. Lancet 1995; 345: 405-409. Egusa G, Murakami F, Ito C, et al. Westernized food habits and concentration of serum lipids in the Japanese. Atherosclerosis 1993; 100: 249-255. Robinson D, Kawamura T, Hinohara S, Sakamoto Y. Levels of cardiovascular risk factors in Japanese people living in the UK. J Cardiovasc Risk 1995; 2: 449-458. Shaukat N, de Bono DP, Jones DR. Like father like son? Sons of patients of European or Indian origin with coronary artery disease reflect their parents' risk factor patterns. Br Heart J 1995; 74: 318-323. Resnicow K, Cross D, Lacosse J, Nichols P. Evaluation of a school-site cardiovascular risk factor screening intervention. Prev Med 1993; 22: 838-856. (Received 15 Apr, accepted 15 Oct, 1997) Authors' details Department of Cardiovascular Medicine, Prince Henry and Prince of Wales Hospitals, Sydney; and Community Health Services and Programs, South Eastern Sydney Area Health Service, Royal South Sydney Hospital, Sydney, NSW. Judith F Lynch, HTech, Heart Health Education Program Co-ordinator; Michelle D Marshall, BSc, Scientific Officer; Xing L Wang, PhD, Research Fellow; David E L Wilcken , MD, FRACP, Visiting Professor of Medicine. Reprints will not be available from the authors. Correspondence: Professor D E L Wilcken, Department of Cardiovascular Medicine, Room 163, Clinical Sciences Building, Prince Henry Hospital, Little Bay, Sydney, NSW 2036. Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/>

Judith F Lynch · Michelle D Marshall · Xing L Wang

The impact of catalytic converters on motor vehicle exhaust gas suicides Virginia H Routley and Joan Ozanne-Smith MJA 1998; 168: 65-67 Abstract - Introduction - Methods - Results - Discussion - Acknowledgments - References - Authors' details - - ©MJA1998 Abstract Objective: To examine the trends in motor vehicle exhaust gas suicides since 1970 and to investigate the impact of catalytic converters. Design: Australia-wide database analyses and a retrospective stratified series of 100 Victorian cases. Data sources: Australian Bureau of Statistics, 1970-1995; Australian Institute of Health and Welfare, National Injury Surveillance Unit, 1991/92-1995/96; Victorian Coroner's files, 1994-1996. Results: There were 509 motor vehicle exhaust gas suicides in Australia in 1995, representing 22% of total suicides. Since the 1986 requirements for reduced carbon monoxide emissions from new vehicles (and thus the use of catalytic converters), the absolute numbers and rates of such suicides have increased, and they have come to represent a larger percentage of total suicides. Of 75 Victorian victims' vehicles traced, 36% were manufactured during or after 1986, showing that exhaust gas suicides have occurred in vehicles with catalytic converters. Blood carboxyhaemoglobin levels did not differ between victims using vehicles with or without catalytic converters. Between 1976 and 1991 exhaust gas suicides increased at a faster rate than motor vehicle registrations. Australian hospital admissions for exhaust gas suicide attempts have increased substantially since 1991-1992. Conclusion: Catalytic converters and the associated lower CO emission limits of 9.3 g/km had not, by 1995, resulted in a reduction in numbers, rates or percentages of exhaust gas suicides in Australia. Introduction Suicide is a major problem in Australia, with approximately 2000 deaths from suicide annually in recent years. Since 1990 suicide has become a more common cause of death than motor vehicle crashes. In 1995, suicide by motor vehicle exhaust gas accounted for 509 deaths and was second only to hanging. It was most commonly used by males (85%), especially those aged 20-50 years. Rates of motor vehicle exhaust gas suicide per 100 000 population in Australia were 4.69 for males, 1.02 for females and 2.85 total (Australian Institute for Suicide Research and Prevention, 1996; unpublished data). Further, motor vehicle exhaust gas related self-harm represented a smaller proportion of patients hospitalised for attempted suicide than of successful suicides (2.0% v. 21.6%; Australian Institute of Health and Welfare, National Injury Surveillance Unit, 1996; unpublished data), indicating the high lethality of this means of suicide. Motor vehicle availability has been found to be related to exhaust gas suicides,1 and in Australia the rates of such suicides in different States vary to some extent with motor vehicle registration rates. For example, the Northern Territory has the lowest rates for each, while Western Australia has relatively high rates (Australian Institute of Health and Welfare, National Injury Surveillance Unit, 1996; unpublished data).2 Carbon monoxide (CO), the most toxic component of motor vehicle exhaust gas, is colourless, odourless and tasteless and is produced from the incomplete combustion of organic fuels. Mild CO poisoning produces headache and drowsiness; more severe poisoning leads to collapse, coma and death.3 Other effects can include myocardial infarction, deterioration of personality and impaired memory.4,5 Environmental regulations have required carbon monoxide emission levels from vehicle exhausts to be reduced over past decades. The required maximum levels have been 24.3 g/km from July 1976 (Australian Design Rule [ADR] 27A), 9.3 g/km from 1986 for new passenger vehicles (ADR 37-00) and 2.1 g/km for new models (ADR 37-01) from 1997 and for all new passenger vehicles from 1998. To cope with the unleaded petrol legally required since 1986 to reduce environmental air pollution from exhaust emissions, vehicles usually require catalytic converters (ADR 37-00; Australian Standard 2877). These convert carbon monoxide and other pollutants into the by- products, carbon dioxide and water. The purposes of this study were to examine overall trends in exhaust gas suicides, and to investigate the impact of the 1986 reduction in allowable carbon monoxide emissions (or the effects of catalytic converters) on that suicide rate. Methods To examine the trends in exhaust gas suicide between 1970 and 1995, we analysed Australia-wide data for mortality from motor vehicle exhaust gas suicides and for total suicides by age, sex and State of residence obtained from the Australian Bureau of Statistics (ABS). We examined Australian hospital admissions data from the Australian Institute of Health and Welfare, National Injury Surveillance Unit for admissions related to motor vehicle exhaust gas suicide attempts. Rates for suicide by motor vehicle exhaust gas were obtained from the Australian Institute for Suicide Research and Prevention. Data on vehicle numbers, rates per head of population and year of manufacture were obtained from ABS publications. Australian exhaust gas suicides and motor vehicle registration rates were compared for the ABS Motor Vehicle Census years since 1970. To examine the effects of catalytic converters, we undertook a retrospective stratified case series study of 100 exhaust gas suicides in Victoria between 1 January 1994 and 31 December 1996, noting the year of manufacture of the motor vehicles involved and victims' blood levels of carboxyhaemoglobin (COHb) -- a reflection of carbon monoxide levels. We compared COHb levels in victims whose suicides involved vehicles manufactured before 1986 with those whose vehicles were manufactured from 1986 (when CO emission levels were reduced). Cases of exhaust gas suicide in 1994 were obtained from a Victorian State Coroner's Office publication,6 while those in 1995 and 1996 were obtained from the Victorian Coroner's Facilitation System database. Results Since 1975 there have been approximately 7000 motor vehicle exhaust gas suicides in Australia. Suicides show an increasing trend, with dips in 1979 and 1993 (R2 = 0.58), while motor vehicle registrations follow an exponential trend (R2 = 0.88), showing a steady rise (Figure 1). Between 1979 and 1991 such suicides increased at a faster rate than motor vehicle registrations. Motor vehicle exhaust gas suicides have steadily increased as a percentage of total suicides since at least 1970 (7% in 1970, 13% in 1980 and 22% in 1995). Hospital admissions for Australian motor vehicle exhaust gas suicide attempts have increased steadily in recent years (1994/95 data are not available), with the data showing an exponential trend (R2 = 0.99). Deaths also increased, but show no clear trend (Figure 2). The 100 cases of exhaust gas suicide obtained from the records of the Victorian Coroner comprised 33 of a total of 96 in 1994, 33 of 140 in 1995, and 34 of 136 in 1996. The year of vehicle manufacture had been recorded for only 75 of these cases (25 in each of 1994, 1995 and 1996). Of these 75, 20% in 1994, 56% in 1995 and 32% in 1996 involved vehicles manufactured in 1986 or later. In total, 27 of the 75 vehicles (36%) were 1986 models or later. This proportion is not significantly different (P = 0.62) from the 39% of vehicles manufactured in 1986 or later in the total Victorian fleet of 2 799 310 vehicles in May 1995 (ABS 1995 Motor Vehicle Census).2 For the 74 cases in which both the victim's COHb level and the age of the vehicle was known, 26 involved vehicles manufactured in 1986 or later and 48 involved earlier models. The median COHb level of victims in these two groups was identical (77.1%). Discussion Motor vehicle exhaust gas suicide is a major public health problem in Australia, accounting for 22% of suicides in 1995. Despite the introduction of catalytic converters and the 1986 reduction in CO exhaust limits, motor vehicle exhaust gas suicides have increased in number, rate and as a proportion of total suicides since 1986. Hospitalisations, however, have doubled, suggesting an increase in failed attempts, and the rate curve for successful suicides also appears to be flattening in the 1990s. In 1995, 43% of registered Australian motor vehicles were manufactured in 1986 or later.2 If exhaust gas suicide had been made impossible by catalytic converters and the 1986 reduced CO emission standard of 9.3 g/km, then rates for such suicides should have reduced from 2.08 to about 1.19 per 100 000 population between 1985 and 1995 (assuming a similar distribution of vehicles to that of the Australian fleet and an unchanged number of attempts). In fact, rates per 100 000 population have been about 2.5 for the past five years and peaked at 2.85 in 1995. It is clear from our investigation of the sample from the Victorian Coroner's files that vehicles manufactured since 1986 have been used in exhaust gas suicides. Our finding that there was no difference in median COHb levels between victims who used vehicles with and without catalytic converters is consistent with the results of a New South Wales study.7 Given that CO emissions from vehicles with catalytic converters are lower, it can be deduced that time (and possibly other factors) need further investigation. The few overseas studies which have examined the relationship between suicides and motor vehicle exhaust gas have found that imposing emission controls reduces the incidence of such suicides.8-10 Vehicle emission limits for CO in the US have been lower than those in Australia, being at our 1986 limit (9.3 g/km) as early as 1975 and at just under our 1997 limit (2.1 g/km) in 1981.11 Thus, US trends should shed some light on the Australian situation, especially as the test conditions are similar. However, it should be noted that the average age of vehicles in the US is seven years, compared with 11 years in Australia, which suggests that there would be a longer lag time for exhaust emission changes to affect suicide rates in Australia. Motor vehicle exhaust gas is a less popular method of suicide in the United States than in Australia (1991 rates per 100 000 population being 0.73, compared with 2.78 for Australia).12 Data available for the US to 1991 show a decline in the exhaust gas suicide rate from the years 1963 to 1979, an increase from 1981 to 1987, followed by a decline to below the pre-1982 rates. Exhaust gas suicides in the US have decreased from 8.9% of suicides in 1970 to 7.4% in 1980 and 5.6% in 1991.8,12 Despite some conflicting evidence in Australia and the US as to the reductions in CO exhaust emission levels ne cessary for influencing exhaust gas suicide rates, these emission reductions do not appear to have produced the success suggested by early reports in the international literature.8-10 There are a variety of possible explanations for this. Firstly, exhaust gas suicides usually involve a hose or pipe being used to feed exhaust gas from an idling vehicle into the sealed interior of a vehicle. Clearly, CO emission levels set for environmental reasons may not be particularly relevant in this situation, and if suicides are to be prevented it would be more appropriate to set CO emission limits in relation to each vehicle's cabin volume. Further, testing vehicles for compliance with environmental standards involves three phases, none of which involve engine idling (during which CO emission could be higher) only. Secondly, CO emissions from vehicles with catalytic converters may exceed the legislated limit. Specific examples are: the engine idles from a cold start, with a delay of 1.5-3 minutes before the catalytic converter has warmed up and is operating efficiently (as blood COHb concentration rises most rapidly when first exposed to CO the initial absorption rate would be particularly high3 ); the condition of the catalytic converter has deteriorated or the engine may require tuning (under ADR 37-00 a catalytic converter is required to operate effectively for 80 000 km or five years, whichever occurs first); and for reasons that are unclear, the pollution performance of 4-9-year-old cars has been found to deteriorate faster than that of older cars.13 A 1989 US report noted that, even with reduced CO emission limits and catalytic converters, it is still possible to use car exhaust for suicide.10 If exposure is prolonged, residual CO content would eventually cause death, or suffocation might occur. Also, destruction of the engine management system, by the use of leaded petrol and neglect, or physical disconnection of the engine management system, could increase the CO content, and thus the lethality of this method for suicide.8 Further research needs to be undertaken in this technically complex area. A study of the vehicles used for unsuccessful exhaust gas suicide attempts and of other factors contributing to their failure would assist in understanding the relationship between vehicles and exhaust gas suicides. New regulations in Australia have not yet reduced suicides from motor vehicle exhaust gas. There is a need to monitor the situation, especially in the light of the 1997 reduction in CO to 2.1 g/km, and to review the regulations, vehicle design and testing methods. Acknowledgments The study was funded by the Victorian Health Promotion Foundation through its funding of the Victorian Injury Surveillance System, a project of Monash University Accident Research Centre. We thank the Victorian State Coroner's Office for providing access to relevant records, Associate Professor David Ranson (Victorian Institute of Forensic Medicine), David Lester (Richard Stockton College of New Jersey), Jerry Moller and Stan Bordeaux (Australian Institute of Health and Welfare, National Injury Surveillance Unit) for providing data, Christine Chesterman and Voula Stathakis (Monash University Accident Research Centre) for assisting with data collection and analysis, respectively, and Dr Ella Sugo (formerly of the NSW Institute of Forensic Medicine), Brian Hobsbawn (Environment Australia) and Jerry Moller for providing valuable comment. References Lester D. Car ownership and suicide by car exhaust in nations of the world. Percept Motor Skills 1994; 79: 898. Australian Bureau of Statistics. May 1995, Motor Vehicle Census. Canberra: ABS, 1996. (Catalogue No. 9309.0.) Ernsting J, King P. Aviation medicine. 2nd ed. London: Butterworths, 1988. Willis Hurst J, Schlant R, Rackley C, et al. The heart. 7th ed. New York: McGraw-Hill, 1990. Smith JS, Brandon S. Morbidity from acute carbon monoxide poisoning at three-year follow-up. BMJ 1973; 1: 318-321. Unnatural deaths, 1993/94. Melbourne: Victorian State Coroner's Office, December 1995. Sugo E, Duflou J, Sercombe J, Brown J. Suicidal inhalation of carbon monoxide -- a reappraisal of variables affecting lethal levels. Paper presented at the Annual Scientific Meeting of the Royal College of Pathologists of Australasia;1996 Sep 16-19; Sydney. Sydney: The College, 1996. Lester D. Changing rates of suicide by car exhaust in men and women in the United States after car exhaust was detoxified. Crisis 1989; 10: 164-168. Clarke R, Lester D. Toxicity of car exhausts and opportunity for suicide: comparison between Britain and the USA. J Epidemiol Community Health 1987; 41: 114-120. Lester D, Abe K. Car availability, exhaust toxicity and suicide. Ann Clin Psychiatry 1989; 1: 247-250. Code of Federal Regulations. Title 40: Protection of environment. Part 86 -- control of air pollution from new and in-use motor vehicles and new and in-use motor vehicle engines: certification and test procedures. Washington, DC: Office of the Federal Register National Archives and Records Administration, 1997. Centers for Disease Control and Prevention, National Center for Health Statistics. Vital statistics of the US. Vol. II. Mortality. Part A. Washington: Public Health Service, May 1996. Federal Office of Road Safety. Motor vehicle pollution in Australia. Report on the national in-service vehicle emission study. Canberra: AGPS, 1996. (Received 18 Mar, accepted 27 Sep, 1997) Authors' details Monash University Accident Research Centre, Melbourne, VIC. Virginia H Routley, BEc, GradDipSocStats, Research Fellow; Joan Ozanne-Smith, MB BS, MPH, Professorial Fellow. No reprints will be available. Correspondence: Ms V H Routley, Monash University Accident Research Centre, Wellington Road, Clayton, VIC 3168. Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/>

Virginia H Routley · Joan Ozanne-Smith

Medical truth and legal proof Changing expectations of the expert witness Gordon Samuels MJA 1998; 168: 84-87 Introduction - Matters of opinion - The role of the expert - Expert qualifications - From adversaries to truth... - Science v Law - Expert error - Judging the experts - References - Authors' details - - ©MJA1998 Introduction When Dr Julian Lee wrote inviting me to give the 1997 AMA (NSW) Oration, he suggested that I might care to address the relationship "between our two professions and its current implications". Plainly, one of the two professions to which he referred was that of medicine. The other could scarcely have been the profession of Governor, which, so far as I am aware, lacks the formal structure, the need to have survived rigorous inquiry into some intellectual qualification and the right of self-regulation which normally denote a profession. So I concluded that he was referring to the profession which I pursued in a former incarnation when I was, as most of you will know, a barrister and, later, a judge. As a lawyer in both of those roles I enjoyed close professional relationships with the medical profession. As a barrister I was retained by a medical insurer and did my best to act as shield and buckler for those doctors -- in those days a small number -- who had the misfortune to find themselves in the courts as defendants. I often relied on the expert evidence of medical practitioners, and on different occasions did my best to destroy the testimony of others. As a judge I sat on varied cases involving doctors in one capacity or another, and throughout the time I much enjoyed the intellectual comradeship presented by the Medico Legal Society of New South Wales and the Australian Academy of Forensic Sciences. It seemed to me, however, that what Dr Lee had in mind was the professional relationship which exists between the medical and the legal professions, and which links them as the leading participants in the litigious process in the courts. It is to that aspect which I propose to direct my remarks tonight. Despite changes in the procedure for recovering damages for injury sustained on the roads and in the workplace, such actions remain regular fixtures in the common law lists. It follows that doctors are still the expert witnesses who are most in demand, and their evidence is the scientific testimony most commonly presented to the courts. I propose to say a word or two about expert witnesses and their evidence, with particular reference to medical witnesses, and to describe shortly the way in which our current forensic procedure prescribes how that evidence is to be given and its cogency tested. Then I will say something about the problem which exercises -- I might say, in some cases, agitates -- both doctors and lawyers of ensuring that expert testimony is of a standard which the court may accept and act upon. There has been a recent decision of the Supreme Court of the United States,1 which, although not directly of authority in Australia, may well produce a substantial effect upon the way in which Australian courts in the future assess and admit scientific evidence, including, of course, evidence concerning medical science. Matters of opinion Expert witnesses have not always enjoyed a good reputation. They have tended to present the same image in legal literature as the lawyer does in Shakespeare: venal, grasping and fit to be hanged. The following acrid passage is a fair sample: "These witnesses are usually required to speak, not to facts, but to opinions; and when this is the case, it is often quite surprising to see with what facility, and to what extent, their views can be made to correspond with the wishes or the interests of the parties who call them." That observation comes from the celebrated text book Taylor on evidence, but there are judicial comments to the same effect, referring, for example, to the "kind of unconscious bias which is a well known characteristic of expert evidence".2 However, judicial comment has also included pleasing accolades, such as those bestowed in a case in New South Wales upon medical witnesses who were demonstrating with singular tenacity the philosophical dichotomy between physician and surgeon.3 The physicians who gave evidence preferred proof by scientific means; the surgeons by experience and observation. Some of the criticism made of the expert witness may be justified. But, in all fairness, it should be shared with the lawyers, who have cast expert witnesses in a particular role which they often find uncomfortable and restricting. It was the lawyers who originally altered the expert's function from that of assessor to that of witness. The allegation of undue adherence to the client's cause is made by those who have created, and who perpetuate, the forensic techniques to which the expert has been forced to adapt. It is not the expert's own choice to be a partisan, but a consequence of the pressures and temptations exerted by the adversarial system in which he or she has to play a part. The role of the expert The function of expert witnesses is to inform the tribunal, judge or jury, of matters about which its lack of specialist skill or experience would leave it ignorant. It is intended to substitute knowledge for speculation. The duty of the expert has been defined in this way: "...to furnish the judge or jury with the necessary scientific criteria for testing the accuracy of their conclusions so as to enable the judge or jury to form their own independent judgement by the application of these criteria to the facts proved in evidence."4 The expert's task is twofold. First, to furnish basic scientific or technical data. Second, to present inferences and conclusions from the facts which the judge or jury, for lack of specialised knowledge, cannot draw themselves. The expert is introduced to carry the proof to the conclusion for which the party presenting that evidence contends. But the limits of the role are drawn where the expert's special knowledge ceases to be significant. Expert qualifications Before the expert can perform the assigned function, he or she must be qualified to furnish the evidence to be tendered. This question of qualification rarely presents itself in the average case where the evidence of doctors, engineers and accountants, let us say, is primarily concerned. It is not the qualification to give the evidence which has generated recent controversy, but rather the quality of the evidence which a qualified expert offers. The High Court of Australia has dealt in detail with the skill necessary to qualify a witness as an expert, and with the circumstances in which the testimony of a skilled person is admissible. The putative expert must have undertaken a professional course of study which has given him or her more opportunity of judging the matters in question than other people; or must have completed the professional study of what has been described as "an organised branch of knowledge" relevant to the subject matter of the inquiry.5 A leading text writer on the law of evidence has suggested that the only true criterion is whether "on this subject can [the tribunal] from this person receive appreciable help".6 The standard to be applied is somewhat indefinite; and from this it follows that any medical practitioner may be (and nearly always is) admitted to give evidence upon any branch of medicine. And one can always be found who will. It is unfortunately true that the law does not require the best possible witness as it requires the best possible evidence; and the safeguard is said to be the good sense of the tribunal of fact which must itself determine which of the witnesses it will accept. Up to the present, Australian law has not contained any criterion for evaluating the quality of expert evidence as a threshold element to be satisfied as a test for admission. In the average case where there is a conflict of medical evidence, the dispute is most often about a commonplace medical condition in which specialised support for any of the assertions that might be made may readily be found. In the unusual case, the most novel proposition will have its adherents, who may compensate in vehemence for what they may lack in scientific authority. There is a prime example of this situation, and of the difficulties of applying any stringent limitation upon the testimonial capacity of persons prima facie qualified. The issue in a case was whether the deceased's acute lymphatic leukaemia had resulted from trauma. The evidence of a doctor was admitted (and accepted by the jury) which answered the question affirmatively, on the footing of a scientific phenomenon known to the witness as "autonomic dyspraxia", but not at all within the professional experience of any of the eminent practitioners who gave evidence on the other side.7 From adversaries to truth... The nature of expert evidence and the way in which it is given will be largely determined by the procedure of the court; and its effect is greatly influenced by the capacity of the court to understand and apply it. The basic forensic procedure which applies, with variations, in all Australian courts is the adversarial system or procedure. Its essence is that the parties, and not the court, determine the issues which they will fight, and themselves select and call the evidence in support of them. The cases are generally conducted by advocates for the parties, and, as a general rule, the judge's intervention is, and is intended to be, comparatively minor. It is thus the responsibility of the parties to prepare their cases and marshal their witnesses. The court provides the formal means, backed by sanctions, by which the witnesses may, if necessary, be summoned to the trial and documents procured for inspection and tender. It is an essential consequence of the adversarial system that the parties are not obliged to call all the relevant evidence which they may have in their possession. They are entitled to call only that which favours their own case, and, with certain important exceptions, may properly not disclose that which does not. Traditionally, the adversarial trial has been regarded as a gladiatorial combat, and sporting metaphors abound. They are not always accurate, but, as Lord Devlin has observed,8 our system is a trial of strength rather than an inquiry on the European model produced by the traditions of the Roman law, in which the judge, rather than the parties, conducts and controls the proceedings as an inquisitor rather than a referee. Since our mode of trial does not involve painstaking and wide-ranging investigation conducted by an impartial inquisitor, it is not designed to ferret out the truth in any absolute sense. The judge, for example, is limited by the material which the parties choose to offer; and, in a criminal case, save in the most exceptional circumstances, is not permitted to call a witness of his or her own motion.9,10 Although the position in Australia is uncertain, there is authority for the view that in a civil action the prohibition upon the judge's calling a witness is absolute.11-14 The adversarial trial is, above all, intended to produce a winner. In our system the question is not "What is the truth of the matter?". It is not "Who killed X?". It is not even "Did the accused kill X?". It is "Has the prosecution proved beyond reasonable doubt that the accused killed X?", because the issue is whether the party carrying the burden of proof has discharged it. I think that in most cases the adversarial conflict does elicit the truth, but it cannot be regarded as designed to do so. Science v Law The procedure adopted in our courts tends to exacerbate fundamental differences in approach between doctors and lawyers. Medicine is a science and law is not. Developments in medicine are made by experiment and observation; in law they are made by the decisions of legislatures and judges. A medical fact is one which can be empirically supported or clinically determined; a legal fact is one which is more probable than other countervailing facts. A trial lawyer seeks to win by tipping the scales of proof in his or her favour by the preponderance of cogent evidence. Hence, the search is for positive answers and firm conclusions; for the means of establishing the proposition that will prove the issue in dispute and end the case. Beyond that the lawyer has no commitment. Thus, lawyers often find difficulty in dealing with the expert, whether forensic scientist or medical practitioner, who does have a continuing commitment to the search for a final answer which, nevertheless, the scientific methodology tends to deny. Karl Popper has said: "When we think we have found an approximation to the truth in the form of a scientific theory which has stood up to criticism and to tests better than its competitors, we shall, as realists, accept it as a basis for practical action, simply because we have nothing better (or nearer to the truth). But we need not accept it as true; we need not believe in it (which would mean believing in its truth)."15 Furthermore, the details of forensic procedure place restrictions sanctioned by the rules of evidence upon the scientist's, and the doctor's, accustomed method of exegesis and description. The need to deploy closely reasoned opinion by means of question and answer, and the danger of fatal disconnection if the interrogating counsel is inept or the judge's interventions unduly copious, are not designed to promote lucidity. Further, expert witnesses are irritated by the way in which cross-examining counsel is able to detach and attack certain portions of their evidence or force them into logical qualifications. An expert witness, of course, whatever the field, needs to bear in mind the necessity of separating ego from opinion. Expert error Against this background some alarm has been generated in recent years by a number of cases in the United Kingdom and Australia in which a miscarriage of justice (that is to say, a wrong result) has occurred as a result of the admission of highly dubious scientific evidence. In a paper which I delivered to the Australian Academy of Forensic Sciences in 199116 I cited the "Chamberlain Case" in Australia, in which a Royal Commission finally established that some of the vital evidence for the prosecution was simply wrong;17 the case of "The Birmingham Six" in England where, again, the scientific evidence and the methodology used to produce it were fatally flawed;18,19 and finally the case of "McLeod-Lindsay", in which scientific developments subsequent to the trial refuted the evidence upon which the case for the prosecution largely depended.20 The question raised by instances of this kind is how does "bad" scientific evidence -- what is known as "junk science" in the United States -- get into the court room? How does it find its way into evidence and thus into the deliberations of the tribunal? Some commentators would answer that instantly by ascribing it to judicial incompetence, and the evasion by judges of their responsibility to evaluate expert testimony.21 Another view is that "scientific test evidence is frequently misused in criminal trials because of its unreliability".22 I think that the problem is complex, but I do not have the space here to analyse it. However, it is possible that the judges are about to modify their methods of dealing with expert evidence. Judging the experts A recent decision of the United States Supreme Court (Daubert v Merrell Dow Pharmaceuticals) has changed the test for admission of expert evidence in United States Federal Courts.1 Before that judgment was published, the test for the admission of expert evidence was much the same as that in Australia. In the case Frye v United States the test enunciated was that expert testimony was admissible if it was "deduced from a well recognised scientific principle or discovery, the thing from which the deduction is made [being] sufficiently established to have gained general acceptance in the particular field to which it belonged".23 Some commentators have expressed the view that there is a relatively close resemblance between the Frye test and the principles of admissibility employed in Australia.24,25 But there are contrary views as well.26,27 The decision in Daubert addressed the issue whether a small group of "impressively credentialled" scientists and doctors could present evidence which seemed to be scientific, but was of too recent origin to have been generally accepted.24 The majority judgment established two criteria for the admissibility of expert evidence: relevance and reliability. It was thus for the judge to ensure that all scientific testimony in evidence "is not only relevant, but reliable" (Daubert at 2795).1 The judges suggested four indicators for assessing whether the testimony met the test of reliability. These were whether the assertion can be and has been tested (i.e., whether it was capable, in Popper's terms, of falsification); whether the theory or technique has been subjected to peer review and publication; the known or potential rate of error; and whether there has been "general acceptance" within a relevant scientific community.24 The effect of Daubert is to impose upon the judge the task of assessing the reliability of a scientific opinion. If the Daubert test is accepted in Australia, the change may be described as transforming "the criteria for admissibility of scientific knowledge claimed, from one based on an expert community's 'general acceptance' of a particular theory to a focus upon the internal practices of the various sciences in combination with certain professional checks and balances such as peer review and error rate in conjunction with consideration of 'general acceptance'".24 It has been said that the shift in legal practice in the United States has transformed the role of the judge "from relatively passive assessor to an active inquisitor searching for the underlying essence of scientific knowledge claims".24 Regarding this, my question is whether this responsibility can be discharged by a judge working within the constraints of the adversarial system. I would think that there may be cases in which the judge, in order to evaluate the scientific evidence, would need to seek the assistance of interim instruction, as I might call it, to provide some basis of knowledge from which to understand the further processes which had produced the opinion offered. Assume, for example, that a judge must examine the reliability of an opinion about the cause of some cardiac condition. It is likely that the judge would need some instruction in basic medical theory and practice in order to understand the process of experiment, observation, and reasoning which has led to the theory from which the final opinion has been deduced. If a judge is confined to the evidence which the parties place before him or her, this process of instruction will be extremely difficult to manage. On the other hand, if every trial in which expert evidence is to be adduced involves subjecting the judge to a crash course of physiological, pathological or anatomical instruction, the trial will be infinitely prolonged and judges very rapidly exhausted. Questions of expert evidence and the difference between the scientific and the legal approach are, I think, both fascinating and critical in the administration of justice. The problem of how a judge is to choose between two scientific witnesses, each of whom appears to be thoroughly well qualified but who cannot agree upon a single particular, is one of perennial difficulty. The attempt to solve it by the device of relying upon the witness's demeanour, although championed by the High Court,28,29 is, in my respectful view, greatly open to question. But the growing incidence of novel medical and other scientific theories -- in particular, the challenge offered by syndrome evidence, leading to what has been called "forensic abuse syndrome"30 -- requires novel modes of judicial response. References Daubert v Merrell Dow Pharmaceuticals 113 Sct 2786 (1993). Miller Steamship Co Pty Ltd v Overseas Tankships (UK) Ltd. (1963) NSWR 737 at 753 per Walsh J. Burgess v Brownlow (1964) NSWR 1275 at 1277 per Manning J. Davie v Edinburgh Magistrates (1953) SC 34 at 40 per Lord President Cooper. Clark v Ryan (1961) 103 CLR 486 at 491-2 per Dixon CJ, at 501 per Menzies J and at 508 per Windeyer J. Wigmore on Evidence, Vol VII, s 1923. 3rd ed. Boston: Little, Brown & Company, 1940. Commissioner for Government Transport v Adamcik (1961) 106 CLR 292. Devlin P. The Judge. Oxford: Oxford University Press, 1981: 54. Whitehouse v The Queen (1983) 152 CLR 657. The Queen v Apostilides (1984) 154 CLR 563 at 571. Re Enoch & Zaretsky, Bock & Co's Arbitration (1910) 1 KB 327. Bassett v Host (1982) 1 NSWLR 206 at 207, 213. Obacelo Pty Ltd v Toveraft Pty Ltd (1986) 66 ALR 371. Cross on Evidence (Aust ed.) Vol 1 at 17080 et seq . Sydney: Butterworths, 1991. Popper K. Unended quest. Glasgow: Fontana-Collins, 1976: 151. Samuels G. Is this the best we can do? Aust J Forensic Sci 1993; 25: 3. Report of the Commission of Inquiry into Chamberlain Convictions, May 1987 (the Morling Report), especially at 324. Canberra: AGPS, 1987. Makler I. The Court of Appeal meets its Waterloo. Legal Service Bull 1991; 16(3): 107. Woffinden B. Miscarriages of justice. Sevenoaks: Coronet, 1989: 392. Report of the Royal Commission of Inquiry into the conviction of Alexander Lindsay, July 1991 (the Loveday Report), at 185. Bell D. Aust J Forensic Sci 1994; 26: 74 and 83. Bourke J. Misapplied science -- unreliability in scientific test evidence. Aust Bar Rev 1993; 10: 124. Frye v United States 293 F 1013 (1923) at 1014. Edmond G, Mercer D. Keeping "junk" history, philosophy and sociology of science out of the courtroom. U N S W Law J 1997; 20: 48-59. Arson M, Hunter J. Litigation: evidence and procedure. 5th ed. Sydney: Butterworths, 1995: 965. Freckelton J. The trial of the expert. Oxford: Oxford University Press, 1987: 60. Odgers S, Richardson J. Keeping bad science out of the courtroom: changes in American and Australian expert evidence law. U N S W Law J 1995; 18: 108, at 123. Abalos v Australian Postal Commission (1990) 171 CLR 167. Devries & Anor v Australian National Railways Commission & Anor (1993) 177 CLR 472, especially at 479. Freckelton I. Contemporary comment: when plight makes right -- the forensic abuse syndrome. Crim Law J 1994; 18: 29. Originally delivered as the 1997 AMA (NSW) Oration in the Great Hall of the University of Sydney, Tuesday, 17 June 1997. Authors' details Office of the Governor, Macquarie Street, Sydney, NSW. Gordon Samuels, AC, Governor of New South Wales. Correspondence: The Honourable Gordon Samuels, Governor of New South Wales, Macquarie Street, Sydney, NSW 2000. - Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/>

Gordon Samuels