Drinking and driving among US high-school students

position, mortality from SIDS has fallen strikingly.5 This example illustrates the potential value of risk-factor epidemiology. The methods of epidemiological studies should be questioned, the possibility of confounding and bias should always be taken into account, and the validity of apparent associations in observational studies should be assessed by accepted criteria. If doubt remains, the issue can be further investigated with randomised trials or in animal models. Risk-factor epidemiology is an essential source of hypotheses, be tested in more controlled environments. much is occasionally made of weak associations, Although and causality can sometimes be wrongly inferred, it is absurd to condemn all risk-factor epidemiology as unconvincing and

which

can

too

unscientific. Peter Rothwell Department of Clinical Neurosciences, Neurosciences Trials Unit, University of Edinburgh, Western General Hospital, Edinburgh EH4 2XU, UK

1 Fleming PJ, Gilbert R, Azaz Y, et al. Interaction between bedding and sleeping position in the sudden infant death syndrome: a population based case-control study. BMJ 1990; 301: 85-89. 2 Wailoo MP, Petersen SA. Bedding and sleeping position in the sudden infant death syndrome. BMJ 1990; 301: 492-93. 3 Southall D, Stebbens V, Samuels M. Bedding and sleeping position in the sudden infant death syndrome. BMJ 1990; 301: 492. 4 Dwyer T, Ponsonby AB, Newman NM, Gibbons LE. Prospective cohort study of prone sleeping position and sudden infant death syndrome. Lancet 1991; 337: 1244-47. 5 Wigfield RE, Fleming PJ, Berry PJ, Rudd PT, Golding G. Can the fall in Avon’s sudden infant death rate be explained by changes in sleeping position? BMJ 1992; 304: 282-83.

SiR-Risk-factor epidemiology established itself as a science at least four decades ago. It has identified the smoking and lung cancer link, the increased risk of oesophageal cancer with alcohol consumption, the relation of paan-tobacco chewing to oral cancer, and the reproductive risk factors for breast cancer, to give just four examples important to public health. If Skrabanek is unaware of these facts, perhaps he should learn something about epidemiology: Lilienfeld and Lilienfeld’s excellent introduction is easy reading for a beginner.l

Stephen W Duffy MRC Biostatistics Unit, Institute of Public Health, University Forvie Site, UK

Cambridge CB2 2SR, 1

Lilienfeld AM, Lilienfeld DE. Foundations of epidemiology. New York: Oxford University Press, 1980.

Drinking and driving among US high-school students SiR-In the USA, deaths from motor-vehicle-related accidents account for more than 37% of all deaths among persons aged 15-24 years.’In 1990, over half of all crash-related deaths were alcohol related.2 Therefore, reducing adolescent drink driving has become a public health priority.3 In the 1991 Youth Risk Behaviour Survey (a representative sample of US high-school students) 12 272 students were asked whether in the past month they had driven a car or other vehicle when they "had been drinking alcohol" and whether they were a passenger with someone driving "who had been drinking alcohol". Multivariate models were created to assess factors associated with these behaviours. Of all students, 17% reported drinking and driving at least once in the past month and 40% reported being a passenger with someone who was drinking and driving. Drinking and driving increased with age and was highest among whites and Latinos (table). Drinking

*Driving vehicle when drinking alcohol at least once in past month. tRode in a vehicle driven by had been drinking alcohol at least once in past month. tORs for one subgroup were adjusted for other subgroups—eg, ORs for age were adjusted for race/ethnicity, sex, and school performance. §Significantly different from referent group (p<0 05). IAsian, Pacific someone who

islander, native Amencan, Alaskan native, or other. Ref referent, Prev= prevalence.

Table : Prevalence and odds ratio (OR) for drinking and driving and riding with someone who drinks and drives by age, race/ ethnicity, sex, and school performance

driving was higher among males than among females and decreasing school performance. Being a with who was drinking and driving was someone passenger more often than reported drinking and driving, though in differences this subgroup respect were less striking (table). About 1 in every 3 adolescents aged 14 and younger reported being a passenger in a car driven by someone who was drinking. Previous estimates of self-reported drinking and driving or riding with someone who was drinking and driving among US and

increased with

adolescents are unavailable. However, studies show substantial declines in both alcohol-related accidents and the percentage of drivers with a blood alcohol concentration of 0-01% or more who were involved in fatal crashes.4 Because of the high rates of drinking and driving behaviours across population subgroups, effective strategies are needed to address these behaviours. Recent studies have suggested that punitive laws toward drunk driving have had little effect in reducing motor-vehicle-related deaths.5 However, taxes on beer and wine and enforcement of minimum age drinking laws can decisively reduce drunk

driving.6,7 Despite legal minimum drinking ages of 18-21 and driver licensing ages of 16-17 in many states in the USA, millions of adolescents drink and drive. Although adolescence is a period of change, growth, and, inevitably, experimentation, physicians need to recognise and address patterns of destructive behaviour at the earliest possible opportunity. Medical care providers are in a position to screen youths for drinking and driving behaviour, and to offer counselling that promotes responsible behaviour. No society can afford the devastating consequences of drunk driving. Luis G Escobedo Centers for Disease Control and Prevention, Atlanta, GA 30341, USA

1

2

National Center for Health Statistics, Centers for Disease Control. Health, United States, 1990. Hyattsville, Maryland: National Center for Health Statistics, Centers for Disease Control, 1991. US Dept of Health and Human Services publication no 91-1232. National Highway Traffic Safety Administration. Fatal accident reporting system 1990; a review of information on fatal traffic accidents in the United States. Washington, DC: US Dept of Transportation, 1991. Dept of Transportation publication (DOT) HS 807 794.

421

Public Health Service. Healthy people 2000; national health promotion and disease prevention objectives. Washington, DC: US Dept of Health and Human Services, 1991. Dept of Health and Human Services publication (PHS) 91-50212. Centers for Disease Control. Alcohol-related traffic fatalities among youth and young adults: United States, 1982-1989. MMWR 1991; 40: 178-87. Evans WN, Nevill D, Graham JD. General deterrence of drunk driving: evauation of recent American policies. Risk Anal 1991; 11:

3

4

5

279-89.

Decker MD, Graitcer PL, Schaffner W. Reduction in motor vehicle fatalities associated with an increase in the minimum drinking age. JAMA 1988; 260: 3604-10. Ferrell S. Policy alternatives for alcohol-impaired driving. Health Educ

6

7

1989; 16: 413-27.

Approval of pharmaceutical products SiR-According to Garattini et al (Nov 13, p 1191) 10 out the top 50 pharmaceutical products sold in Italy and France during 1992 are drugs "for which there is no evidence of efficacy". The criteria for such a statement are not given (according to Greek mythology, Venus was preferred to Athena as the finest, but Athena’s opinion was quite different!). There are well-known mechanisms for the approval of pharmaceutical products in Italy and France. So to accept Garattini’s

statement we must

admit that: the committee

applications for the marketing of the above mentioned drugs approved products without efficacy; such approvals were based on reports from Italian and French pharmacologists and clinicians, evidently stating the products had "no efficacy"; and that many Italian and French doctors prescribed such products knowing their inefficacy. These doctors would be deceiving their patients and-due to the mechanism of payment-also their country. Or may be they made their own judgment on "clinical efficacy" (and we should admit Athena may, at least in some cases, to be preferred to Venus, contrary to Garattini’s statement). examining

the

While there is wide debate on the value of randomised clinical trials as the only valid way to choose medicines in English-speaking countries,i it is disturbing that this criterion is coming to be accepted in countries like Italy and France, with a long medical history and culture. Giovanni Ceccarelli Via C

1

Cipolla 42, 00179 Roma, Italy

Hellman S, Hellman D S. On mice but not men: problems of the randomized clinical trial. N Engl J Med 1991; 324: 1585-89.

Hodgkin’s disease: a malignancy of follicular dendritic cells? SiR-For many years the origin of the malignant cells in Hodgkin’s disease, the Reed-Sternberg (RS) cell, has been an enigma. Almost every cell type in the normal lymph node has been proposed as the possible progenitor for Hodgkin’s disease

including, as the strongest candidates, T and B lymphocytes. A number of RS cells have been found to express CD21 which is an antigen present also in follicular dendritic cells.’ Earlier studies have also shown similarities in the metallophilic staining properties of dendritic cells and RS cells.2 Therefore, we have studied the presence of a follicular dendritic cell marker, the acid cysteine proteinase inhibitor (ACPI), in Hodgkin’s disease. The follicular dendritic cells in lymph nodes consistently contain ACPP which is a protein of 12 000 D that inhibits the action of cysteine proteinases. Lymphocytes and mature macrophages in lymph nodes do not contain ACPI in similar stains.3 Sections of 20 cases of Hodgkin’s disease were stained immunohistochemically with a rabbit antibody to ACPI with 422

Figure: Immunohistochemical disease for ACPI

staining of MC type of Hodgkin’s

Classical binucleated Reed-Sternberg cell is stained (arrow) as well several mononuclear Hodgkin cells (h). Haematoxylin background staining, x 1000.

as

complex method. 3 of the cases were of the lymphocytic predominant type (LP), 10 mixed cellularity (MC), 3 nodular sclerosis (NS), and 4 lymphocytic depletion (LD). The same cases were also stained for CD20 (L26, B-lymphocyte marker, Dako), CD3 (T-lymphocyte marker, Dako), CD30 (BerH-2, Dako), and CD15 (LeuMl, RS cell marker).

the avidin-biotin

Our results showed that the RS cells were stained for ACPI in 88% of the cases studied with the exception of the LP type. In the LP type the RS cells were not stained. The RS cells of 1 NS and 1 LD case did not stain for ACPI. In the positive cases not all RS cells were stained, but the amount of positive cells varied from about 20-60% of all RS cells. In addition to the classical binucleated RS cells, the mononuclear malignant Hodgkin cells also showed the same pattern of staining for ACPI (figure). Especially in the MC type, the cytoplasm of the RS cells was often intensely stained filling the whole cytoplasm, but in the RS cells with less intense staining there was often a perinuclear granular staining pattern. Furthermore, in the periphery of the lesions a more follicular pattern of dendritic types of ACPI positive cells was found. This could not be seen in routine stains. With the exception of the LP type where the RS cells were CD20 positive, the results showed that some RS cells were stained with markers for T and B cells, but the staining was faint and consisted of only a few cells. CD30 and CD 15 were usually positive in RS cells. Frozen tissue was available from 6 cases. Gene rearrangement studies for the immunoglobulin heavy chain, kappa, and lambda chains as well as for the T-cell receptor P-chain were all negative. The suggestion that RS cells are derived from T or B lymphocytes has been based on immunohistochemical studies showing the presence of markers for T and B cells on RS cells, and on studies that demonstrate immunoglobulin and T-cell receptor gene rearrangements in Hodgkin’s disease and in accepted cell lines of RS cells. The pattern of expression of both markers for T and B cells in RS cells is, however, inconsistent and shows considerable variation, which, therefore, is not certain proof of cell lineage. In contrast, markers of follicular dendritic cells have been detected in RS cell lines and the protein composition of RS cell lines resembles that of follicular dendritic cells and has few similarities with lymphoid or myeloid cell lines. The results of gene rearrangement studies are conflicting,4.5 but it seems possible that rearrangement of the immunoglobulin or T-cell receptor genes may occur in