Statement by L.G.S. Rao, Ph.D. Bellshill Maternity Hospital Bellshill, Scotland, U.K. Regarding H.R. 4957 S. 1929
Date: 09 Mar 1982
Length: 37 pages
Jump To Images
Length: 37 pages
Jump To Images
- Rao, Lgs
- SPCH, SPEECH/PRESENTATION
- BIBL, BIBLIOGRAPHY
- CHAR, CHART/GRAPH
- LEGAL DEPT FILE ROOM
- Named Organization
- Bellshill Maternity Hospital
- Boston City Hospital
- Rao, Lgs
- Named Person
- Surgeon General
- Date Loaded
- 07 Jan 1999
- Master ID
- 03607523-8364 Comprehensive Smoking Prevention Education Act of 810000 Hearing Before the Committee on Labor and Human Resources United States Senate Ninety-Seventh Congress Second Session on S. 1929
- 03607531-7540 97th Congress 1st Session S. 1929 to Amend the Public Health Service Act and the Federal Cigarette Labeling and Advertising Act to Increase the Availability to the American Public of Information on the Health Consequences of Smoking and Thereby Improve Informed Choice, and for Other Purposes.
- 03607587-7594 National Institute on Drug Abuse Technical Review on Cigarette Smoking As An Addiction
- 03607618-7620 Coaliion on Smoking or Health Seeks to Influence Legislators
- 03607621-7623 Coalition on Smoking or Health .. A Public Policy Project with the National Interagency Council on Smoking and Health
- 03607624-7626 Former Ftc Counsel to Staff Coalition on Smoking or Health
- 03607627-7629 Statement of the American Lung Association to the House Subcommittee on Health and the Environment on H.R. 5653, the Comprehensive Smoking Prevention Education Act
- 03607630-7636 the Importance of the Federal Government in the Prevention of Smoking Related Diseases Testimony in Support of H.R. 5653, A Revised Version of H.R. 4957 the Comprehensive Smoking Prevention Education Act by the American Lung Association
- 03607681-7692 Lung Cancer, Coronary Heart Disease and Smoking
- 03607717-7724 Statement on S. 1929 'comprehensive Smoking Prevention Education Act of 810000' of Dan G. Mcnamara, M.D., F.A.C.C. President to Honorable Orrin G. Hatch Chairman Committee on Labor and Human Resources
- 03607725-7726 File No. 792-3204
- 03607727-7730 Statement of the American Medical Association to the Labor and Human Resources Committee U.S. Senate Re: S. 1929 Comprehensive Smoking Prevention Education Act
- 03607731-7734 Statement on S. 1929 the Comprehensive Smoking Prevention Education Act of 810000 by John R. Walton, Rrt President
- 03607735-7740 Statement of the American College of Physicians on S. 1929, the 'comprehensive Smoking Prevention Education Act of 810000'
- 03607741-7749 Testimony of the American College of Chest Physicians Submitted by Thomas L Petty, M.D., F.C.C.P. President Regarding S. 1929 'the Comprehensive Smoking Prevention Education Act of 820000'
- 03607750-7751 Testimony of Action on Smoking and Health (Ash), by Its Executive Director and Chief Counsel, John F, Banzhaf III, Before the Senate Committee on Labor and Human Resources, Chaired by the Honorable Orrin G. Hatch, on the Comprehfnsive Smoking Prevention Education Act (S. 1929) Submitted 820402
- 03607752-7763 Federal Trade Commission Staff Report on the Cigarette Advertising Investigation
- 03607764-7770 Statement of the Bakery, Confectionery & Tobacco Workers International Union to the Senate Committee on Labor and Human Resources Re: S. 1929 'the Comprehensive Smoking Prevention Education Act of 820000
- 03607771-7790 Comments on H.R. 4957 - - Proposed 'comprehensive Smoking Prevention Education Act of 810000'
- 03607791-7793 Cigarette Smoking of Pregnant Women
- 03607794-7809 Peter L. Berger
- 03607810-7813 Gilgamesh on the Washington Shuttle
- 03607814-7848 Statement Rodger L. Bick, M.D.
- 03607849-7854 Statement of Theodore H. Blau Ph.D. Presented Before Subcommittee on Health and the Environment House of Representatives
- 03607855-7858 Statement of Walter M. Booker, Ph.D.
- 03607859-7864 Statment Smoking and Fetal Growth
- 03607865-7873 Curriculum Vitae Oliver Gilbert Brooke
- 03607874-7884 Statement of Barbara B. Brown, Ph.D.
- 03607885-7892 Statement of Dr. Victor Buhler
- 03607893-7896 Statement of Jack Matthews Farris, M.D.
- 03607897-7909 Statement of Sherwin J. Feinhandler, Ph.D.
- 03607910-7936 Statement of Edwin R. Fisher, M.D.
- 03607937-7945 Statement of H. Russell Fisher, M.D.
- 03607946-7979 Statement of Jean D. Gibbons
- 03607980-7983 Statement of Katherine Mcdermott Herrold, M.D.
- 03607984-7997 Statement of Arthur Furst, Ph.D.
- 03607998-8015 Statement of Richard J, Hickey, Ph.D.
- 03608016-8021 Statement of Duncan Hutcheon, M.D., D.Phil. Departments of Pharmacology and Medicine 820312
- 03608022-8053 Statement of Leon O. Jacobson
- 03608054-8065 State Ment of Lawrence L, Kupper, Ph.D.
- 03608066-8085 Statement of Hiram Thomas Langston M.D. Clinical Professor of Surgery (Emeritus) Northwestern University Medical School
- 03608086-8091 the Alleged Cost of Cigarette Smoke
- 03608092-8121 Statement of Eleanor J. Macdonald Professor Emeritus of Epidemiology Department of Cancer Prevention University of Texas System Cancer Center M.D. Anderson Hospital and Tumor Institute, Houston, Texas
- 03608122-8129 Statement of John E. O'toole, Chairman, Foote, Cone & Belding Communications, Inc.
- 03608170-8173 Statement of Henry Rothschild, M.D., Ph.D.
- 03608177-8190 Statement of Bernice C. Sachs, M.D., Seattle, Washington
- 03608191-8195 Concerning the 'comprehensive Smoking Prevention Act of 820000'
- 03608205-8236 Statement of Sheldon C. Sommers, M.D.
- 03608237-8246 Statement Professor T.D. Sterling
- 03608247-8275 Statement of Professor Yoram J. Wind for Submission to the Subcommittee on Health and the Environment
- 03608276-8277 for Use at 10 A.M. Tuesday, 820316
- 03608278-8287 Statement of Robert Casad Hockett
- 03608288-8317 Relationships Between Family Smoking Habits, Individual Differences in Personality, and the Smoking Behavior of College Students
- 03608318-8337 Personality and Smoking Behavior
- 03608338-8364 on the Relation Between Family Smoking Habits and the Smoking Behavior of College Students
Page 1: alv99d00
Statement by L. G. S. Rao, Ph.D. Bellshill Maternity Hospital Bellshill, Scotland, U.K. Regarding H.R. 4957 S. 1929 My name is Dr. L.G.S. Raor I am Senior Biochemist at Bellshill Maternity Hospital in Glasgow, Scotland. I obtained mv Ph.D. in Biochemistry from the University of Newcastle in 1966. I am the author of numerous scientific publications and have made presentations at scientific meetings in Europe andI the United States. My experience in clinical biochemistry over the past 20 years has been varied and has resulted in the development of interests in several methodological and clinical problems including perinatal medicine. Over the past several years, I have become deeply interested in the investigation of the - causes of the high incidence of low birth weight and perinatal4 mortality which is found among the poorer patients of Bellshil Maternity Fbspital. I have attempted to define in biochemica terms the risk factors associated with the "poor social condi- tions"'which are supposed to be the caus= of the poor reproduc- tive performance of these mothers. I have found, as have otheN researchers in this fiel of the poorer social gr growth ret3rdation is the has been claimed, their s of considerable practical ciencies can be correcte tion. A program of such striking reduction -.in th. nerinatal mortality and m- o' the scientific researct- Introduction - There is a widely h~ -cause of low birthweight (the "causal" hypothesis) cause the statistical ass PNM lacks the specificity significance and because causal hypothesis.
Page 2: alv99d00
in Glasgow, Scotland. I obtained :)m the University of Newcastle in nerou s scientific publications and scientific meetings in Europe and al biochemistry over the past 20 as resulted in the development of :)dological and clinical problems . Over the past several years, I ted in the investigation of the of low birth weight and perinatal ng the poorer patients of Bellshill attemote d t o define in biochemical ziated with the "poor social condi- be the caus.e of the poor reproduc- )thers. I have found, as have other 607 researchers in this field, that the biological characteristic of the poorer social groups that is of relevance to fetal growth retardation is their poor nutritional status and not, as has been claimed, their smoking habits. This finiing could be of considerable practical iaportance because nutritional defi- ciencies can be corrxted by dietary advice or supplementa- tion. A program of such dietary intervention could lead to a striking reduction in the incidence of low birth weight and perinatal mortality and morbidity. Set forth below is a review of the scientific research supporting the above conclusion: Introduction There is a widely t~eld view that maternal smoking is a -cause of low birthweight (LBW) and perinatal mortality* (PNM) (the "causil" hypothesis). That view is challenged herein be- cause th e statistical associatio n between smoking and LBW and PNM lacks the specificity and the consistency to be of causal significance and because of evidence inconsistent with the causal hypothesis. *The term perinatal mortality includes both stillbirths and infant death within the first few weeks after birth. - 2-
Page 3: alv99d00
608 Most of the stu9ies which favour the causal hypothesis have not corrected for factors which are already k mwn to have a marked effect on LBW and PNM. The most conspicuous fact that emerges from a scrutiny of all the studies on smoking in preg- nancy is that the so-called "effect" of smoking is seen only in the poorer underprivileged mothers and not in th e mothers who have a good family income. Low family income could lea9 to nutritional deficiencies which can caus e fetal growth retar3a- tion. Therefore, the so-called "effect" of smoking seen in only th e poorer mothers may no t b e du e to smoking itself, but due to deficiencies in maternal nutrition during pregnancy. Evidence for this has come from a recent study on the protein intake in pregnancy in Bellshill Maternity Hospital which ~ showed that among mothers with normal protein intake, there was no difference in the proportion of LBW infants between smokers and non-smokers. Other evidence a gainst the c ausal hypothesis from a review of the available literature is also presented. - Smoking in pregnancy has become such an emotioral issue that it is difficult to be unbiased in the design of the studies on this subject or in the interpretation of the results. As there is a great deal of evidence against the -3- "causal" hypothesis, o the higher incidence perinatal mortality fo, nancy. There is consic growth-retardation is m pregnancy, possibly du denoted as the "nutrit hypothesis is th e view certain type of persor. reproductive performan: -his hypothesis will b thesis. The latter tw common and are compler favour of th e "causal" in the 1979 U.S. Surge discussed in detail, t alternative hypotheses merits discussed. For a valid discuss o-° factors that are a: perinatal mortality nee
Page 4: alv99d00
the causal hypothesis have already known to have a sost consoicuous fact that :udies on smoking in preg- of smoking is seen only in ad not in the mothers who sily income could lead to ,use fetal growth retarda- =fect" of smoking seen in ue to smoking itself, but itrition during pregnancy. -cent study on the protein Maternity Hospital which protein intake, there was BW infants between smokers 1 hypothesis from a review -esented. : such an emotion3l issue sd in the design of the he interpretation of the . o f ev idenc e aga ins t the 609 "causal" hypothesis, o ther hypotheses are required to explain the higher incidence of low birt'hweight infants and higher perinatal mortality found in sone studies o n smoking and preg- nancy. There is considerable evidence for the view that fetal growth-retardation is mediated through a reduced weight gain in pregnancy, possibly due to undernutrition. This view will be dem ted as the "nutritional" hypothesis. Another alternative hypothesis is the view that smoking is a characteristic of a certain type of person or a group of people who have a poor reproductive performance because of constitutional re3sons. This hypothesis will be denoted as the "constitutional" hypo- thesis. The latter two hypotheses have several features in common and are compleroentarx to each other. The evidence in favour of the "causal" hypothesis is presented in great detail in the 1979 U.S. Surgeon-General's report .(1) and will not be discussed in detail, but the evidence in favour of the two alternative hypotheses will be presente3 and their relative merits discussed. For a valid discussion of smoking and pregnancy, the effect of factors that are already known to affect birthweight and perinatal mortality needs a brief consideration. -4 -
Page 5: alv99d00
610 Factors that are known to affect fetal arowth: 8iological Factors The biological factor which shows the best correlation with the weight of the infant is the functional capacity of the placeita, which is determined mainly by the size of the pla- centa and the quantity and quality of th_ blood supply to the fetus. The size of the pla centa is largely determined by the height and weight of the mother. The factors that influence the quantity of blood flow are not well understood except in pathological states such as pre-eclamosia and extensive infarc- tions in the placenta. There is some evidence that uterine blood flow is under hormonal control (26). The quility of the blood supply is mainly determined by the nutritional status of the mother. It is well-known that in poorer countries with nutritional d eficiencies, the weight of the mother and the infant are both lower than that of those in the more prosperous countries (2) . Thus, maternal stature and the nutritional status during the pregnancy appear to be important factors on theoretical grounds and are, in fact, found to be so in pra c tice. The other biological factors which are known to affect birthweight are:- 1. The length of gestation, the shorter the gestational period, the smaller the baby, 2. Sex of the infant, males being slightly heavier than females (about 200g) after about 36 weeks of gesta- tion, and -5- 3. The pregnancy n lighter than lat Socio-e conon ic f actors In addition to these that there are important to influ ence birthweight status could have an in tries, probably b y affec even in some prosperous infant is related to the husband. 1hus, social c have a higher birthweig -perinatal mortality and 1 in social classes 4 ar. These socio-economic fact in their effect on perir Thus, the perinatal mort 1,000 births and was 32.0 - ~: The striking effect c appears to be mainly duc rity, low birthweight bab fact, social class has st
Page 6: alv99d00
ws the best correlation with functional capacity of the ly by the size of the pla- of tha blcod supply to the s largely d etermined by the The factors that influence t well u nderstood except in amnsia and extensive infarc- some evidence that uterine 1 (26). The quality of the ~y the nutritional status of t in poorer countries with 3ht of the mother and the thos e i n th e mor e prosperou s tature and the nutritional to be important factors on .ct, found to be so in prac- s which are known to affect 611 3. The pregnancy number, the first chi13 being slightly lighter than later children (about 200g). Socio-econanic factors In addition to these biological factors, it is well known that there are imnortant socio-°conomic factors which are known to influ ence birthweight. It is not surprising that economic status could have an influence on birthweight in poor coun- tries, probably by affecting the nutrition of the mother, but even in some prosperous western countries the weight of the infant is related to the social a nd educatioaal status of the husband. Thus, social classes I and 2 (professional workers) have a higher birthweight longer gestational periods, lower -perinatal mortalit y and lower congenital deformities than those in social classes 4 and 5 (manual and unskilled workers). 'hiese socio-economic factors appear to be particularly striking in their effect o n perinatal mortality in the Unitei Kingdom. 'Ihus, the perinatal mortality in social class 1 was 9.5 per 1,000 birtl-s and was 32.0 per 1,000 in social class 5(3). The striking effect of social class on perinatal mortality appears to b e mainly due to the higher incidence of prematu- rity, low birthweight babies, and congenital abnormalities. In fact, s ocial c lass h as such a striking effect on the health of -6- Y -
Page 7: alv99d00
612 the pooulation in certain countries (4) that there is a higher incidence of shorter mothers (449! ) in social classes 4 an9 5 comoarefl to social classes I an3 2 (?0.5$). The nunber of mothers delivered before 36 weeks gestation was twice as high for c lasses 4 and 5( 8.48 ) a s that o f I an3 2 (4.2$ ). ( See Table 1). This higher incidence of prematurity alone can ac- count for the higher perinatal problems of the social classes 4 and 5. The socio-economic differences persist even when mater- nal stature has been accouzted for (5) . It has been shown that the incidence of prematurity is associated with th e social class of the mother's father, for any given social class of the mother's husband (6). This indicated that the socio-economic status (prcbably nutritional status) of the mother when she was a child had a striking effect on her growth in chill3hoo3 and -her reproductive performance in later life. Thus, in Britain, social class appears to affect the maternal size and nutrition, and could b e a very important f actor which affects birthweight and perinatal mortality. In the United States also, similar socio-econonic factors appear to affect perinatal mortality. Thus, black populations in general and the less educate3 among the whites have a higher perinatal mortality than the better educated whites (29). In a large study on perinatal mortality conducted in Canada, the hospital status of the mother, whether private or ward patient, which is probably determine d by the educational status of the father, has been shown to be an -7- imoortant risk factor, the perinatal mortalitv than tha Thus, there are sever 'actors which affect birth :hese must be taken into ac tion between smoking and per Sone Methodoloaical consider Most studies on the sut not taken the above factor, clusions, therefore, are op Seneral's report has pointe of adjustment for differenc in the distribution of su economic status and race smoking to perinatal mortali ?he usua 1 definition of '"eighe3 less than 2500 grams zient definition, it cou1d 9estational age, the parity taken into consideratio n t o `-etal growth retardation. I
Page 8: alv99d00
;4) that there is a higher n social classes 4 and 5 (?0.58). The number of station was twice as high of 1 an3 2 (4.2$). (See prematurity alone can ac- :ms of the social classes 4 r life. Thus, in Britain, ternal siz e an d nutrition, - which affects birthweight .ited States also, similar 'fect perinatal mortality. .: .. ~. t -- ~ . . . id the less educated among m ortality than the better ad y o n perinata 1 mortality itus of the mother, whether ,robably determined by the has been shown to be an 613 imoortant risk factor, the private patients having a much lower perinatal mortality than that of the ward patients (21) . Thus, there are several import3-it biological ani social factors which affect birthweight and perinatal mortality and these must be taken into account when cor.sidering the associa- tion between smoking and perinatal mortality. Some Methodological considerations Most studies on the subject of smoking and pregnancy have not taken the above factors into consideration and their con- clusions, therefore, are ope n to question. The 1979 Surg eon- , General's report has pointed out that "problems arise from lack of adjustment for differences between smokers and non-smokers in the distribution of such factors as age, parity, socio- economic status and race when th e relationship of maternal smoking to perinatal mortality is under study." (1) The usua 1definition of a low-birthweight baby i s one that weighed less than 2500 grams at birth. Although it is a conve- nient definition, it co.ild be subject to serious errors. The gestational age, the parity, and the sex of the infant must be taken into consideration to obtain some degre e of validity of fetal groath retardation. It is obvious that for a small woman -8-
Page 9: alv99d00
614 weighing 100 pounds, a 2500 gram baby born at 34 weeks is not a small baby but it is for a tall woaan weighing 160 poilds and delivering at 40 weeks of her pregnancy. In fact, the 2500 gram limit appears to be absurd in some situations as it has been shown that the perinatal morta?ity for the under 2500 gram babies increases with the increase in maternal height (7). Although it would become too cumbersome to take the mother's height and weight into consideration in defining low birth- weight, at least the gestational age, parity and sex of the in fan t shoul d b e take n int o account . An important c oncept in d efining fetal growth retardation was described by GYuenwal3 (8) and adopted in a study by Miller and co-workers (9) . According to this concept, fetal growth . -retardation is divided into two types. One is the 1ong, thin baby," which is the result of wasting that occurs during a period of days prior to birth, resulting in a low ponderal index. The second type has a general decrease in growth pro- bably extending over a period of weeks before birth, with the result that the deficits in body length and weight at birth are proportional resulting in a normal ponderal index. 'Ihe second type is described as short for dates (SHFD). The infants of the first type with the low ponderal index, have large appe- tites and will catch up within a few months with the weight of 'infants with a normal birthweight. On the other hand, the SHFD -9- infants a nd their sibling disease, suggestive off a be seen later in this pape fetal growth retardation i question of smoking ?ind pr The "Oausal" T.lypothesis - Several studies have birthweight babies and a h be statistically a ssociate rancy. FYbwever. there a ssoci ation i s not _-;eppr association has bee n inter -in spite of considerable e worthwhile to assess _crit this hypothesis. If maternal smoking is tion and an increase in smoking should be found }n the population. 5b~.$ve.r, effect is seen only in p upper socio-economic,group
Page 10: alv99d00
~y born at 34 weeks i s not a man weighinq 150 Do1n3s and gnancy. In fact, the 2500 some situations as it has !ity for the under 2500 gram e in maternal height (7) : arsome to take the mother's .on in defining low birth- ige, parity and sex of the zg fetal growth retardation idopted in a study by Miller this concept, fetal growth es. One is the "long, thin sting that occurs during a ssulting in a lo+ ponderal ~ral decrease in growth pro- eeks before birth, with the ngth and weight at birth are oonderal index. ltie second tes (SHFD). The infants of :al index,-have large appe- !w months with the weight of On the other hand , the SHFD 615 infants a nd their siblings have a notable incidence of organic disease, suggestive of a genetic or familial pattern. It can be seen later in this paper that this tvpe of classification of fetal growth retardation is useful in the understanding of the question of smoking and pregnancy. 'lh e "Causal " !iypothesi s Several studies have reported a higher incidence of low birthweight babies and a higher rate of perinatal mortality to be statistically associated with maternaL smoking during preg- n3ncy. Fbwever, there are some studies in which. this association is not reported. Nevertheless, this statistical association has been interpreted as having causal significance, I -in soite of considerable evieience against this view. : It may be worthwhile t o asses s_critically the evidence for and against this hypothesis. If maternal s moking is,the cause of fetal growth retarda- tion and an increase in perinatal mortaLity, this effect of smoking should be found in all countries and in a1l sections of the population. [iowever, this is not found to be true. 'ihis effect is seen only in poorer social groups, but not in the upper socio-economic groups (See Table 2). Many studies have -10-