NYSA TI Single-Page 4
1959. J Nat Cancer Instit 1964; 32: 115
Abstract
Ham~-ond EC. Smoking in relation to ~ortality and =orbidity. Findings in first 34 ~onths of follow-up in a prospective study started in 1959. J Nat Cancer Instit 1964; 32: 115.
Fields
- Named Organization
- Addiction Research Foundation of Toronto
- Agricultural Research Service
- Agriculture Department (USDA)
- Alcohol, Drug Abuse and Mental Health Administration
- American Association of Advertising Agencies
- American Cancer Society
- American Health Foundation (Health Research)
Plaintiff- American Heart Association (Voluntary health organization that focuses on cardiac health)
Voluntary health organization that focuses on cardiac health and stroke. AHA occasionally teams with tobacco retailers to engage in promotions/fund-raisers (see http://www.smokefree.net/doc-alert/messages/247136.html and http://www.rawbw.com/~jpk/stand/Pictures.html).- American Public Health Association (Public health organization)
Professional organization for people working in public health- ASH (Action on Smoking and Health)
Action on Smoking and Health- ASHRAE (Am Society of Heating, Refrig and AC)
American Society of Heating, Refrigeration and Air Conditioning- Association of National Advertisers (Ad group)
Group of advertising entities nationwide.- Avon (Makeup)
- British Medical Journal (BMJ) (scientific periodical)
scientific periodical- Californians for Nonsmokers' Rights (Americans for Nonsmokers rights precursor)
Precursor organization to Americans for Nonsmokers Rights- Canadian Council on Smoking and Health
- Chilton Research Services
- CPD (Curriculum and Professional Development Dept., TX Ed Agency)
Curriculum and Professional Development Department of the Texas Education Agency- Dell
- Department of Commerce (DOC)
- *Department of Health and Human Services
- *Department of Health, Education, and Welfare (HEW) (use United States Departmen (use @hew_dept)
- *Department of Transportation (use United States Department of Transportation)
- Doctors Ought to Care (Activist physician group on tobacco)
Founded by Alan Blum M.D- Education Department (ED)
- Environmental Protection Agency (EPA)
- Federal Aviation Administration (Ruled on smoking on U.S. flights)
- Federal Communications Commission (FCC)
- Federal Highway Administration
- Federal Trade Commission (Enforcement agency for laws against deceptive advertising)
Enforces laws against false and deceptive advertising, including ads for tobacco products. Ensures proper display of health warnings in ads and on tobacco products;collects and reports to Congress information concerning cigarette and smokeless tobacco advertising, sales expenditures, and the tar, nicotine, and carbon monoxide content of cigarettes.- Federal Trade Commission (FTC)
- Gastroenterology (scientific periodical)
- Harvard Medical School
- *Health and Human Services (HHS) (use United States Department of Health and Hum (US)
- Institute of Psychiatry (London)
- ITC (India Tobacco Company)
India Tobacco Company- Journal of Preventive Medicine (scientific periodical)
- Kaiser-Permanente
- Lakartidningen (Swedish medical journal)
- Lancet
- Ministry of Health (Located in Singapore)
- MRD
- National Academy Press
- National Center for Health Statistics (Keeps statistics on health-related matters)
Plaintiff- National Institute of Education
- National Institute on Drug Abuse (An addiction research center in Baltimore, MD)
An addiction research center located in Baltimore, MD- National Institutes of Health (NIH)
- National Research Council
- Naylor Dana Institute for Disease Prevention (unit of AHF)
- New England Journal of Medicine
- New Scientist (scientific periodical)
- New York State Department of Health
- Newsweek (Weekly News Magazine (U.S.A.))
- Office on Smoking and Health
Responsible for creating reports on the health effects of smoking. Created by the Public Health Service.- Preventive Medicine (periodical)
- Reader's Digest
- Red Cross
- Research Council
- Roper Organization (Consumer Research/Public Relations Org.)
Interested in finding out what drives consumer behavior; surveys consumers on their prime areas of concern; assists corporations with reputation-building and public image based on its findings.- Royal College of Physicians (Monitors the quality of Canadian/U.K. medical education)
- Smokers Clinic
- Tobacco Institute (Industry Trade Association)
The purpose of the Institute was to defeat legislation unfavorable to the industry, put a positive spin on the tobacco industry, bolster the industry's credibility with legislators and the public, and help maintain the controversy over "the primary issue" (the health issue).- U.S. Department of Agriculture
- University of California Los Angeles (UCLA)
- University of California San Francisco
- University of Edinburgh (Located in Scotland)
- University of Houston
- University of London
- University of Manchester
- University of Minnesota
- University of New Mexico
- University of Nottingham
- University of Toronto
- University of Vienna
- University of Western Australia
- University of Western Ontario
- Veterans Administration
- World Conference on Smoking and Health
- World Health Organization (Concerned with global public health)
International organization concered with public health worldwide- Yale University
- Agricultural Research Service
- Named Person
- Armstrong, Bruce K.
- Bailey, Jeffry
- Bishop, Jr., Mike A. (RJR Corp. Public Relations)
Manager Smoking- *Bock, F.G. (Fred)
Associate Cancer- Bray, Jeremy
- Brown, Ron
- Dekker, Marcel
- Elizabeth, Queen, II
- Evans, Richard (smoking in teenagers)
- Fisher, Deborah A.
- Glantz, Stanton A.
- Gritz, Ellen R., Ph.D.
Plaintiff- Hall, Russell
- Harris, John (District Supervisor in Florida Police)
- Heart, Stanford
- Hill, J. Stanley
- Howe, Holly L.
- Jacob, Micheal
- Johnson, Anderson
- Jones, R.T. (BATCO GR&DC)
R. T. Jones was with BATCO-GR&DC. (Source: NM Tobacco Companies Personnel List)- Leathar, D.S.
- Lee, J.D. (ATLA Tobacco Litigation Gp Chair, Knoxville, TC attorney)
J.D. Lee is an attorney in Knoxville, TN and chairman of the ATLA Tobacco Litigation Group in 1994. The telephone number is (615) 544-0101.- Loeb, Barbara Keely
- Mah, Russell
- Mantel, Nathan (Biostatistician, American U., Industry Expert)
PM witness- Parker, Gillian
- Pederson, Linda
- Pellegrino, Ed
- Pindborg, J.J., M.D. (Studied the effects of smoking on Leukoplakia)
- Randell, Jane
- Rawson, Nigel
- Reid, Donald
- Samet, Jonathan M.
- Schwartz, Tony
Plaintiff- Shephard, Roy J.
- Stephens, Thomas
- *Todd, G.F. (use Geoffrey Todd)
- Tso, T.C., Ph.D. (PM Tobacco Working Group)
Defense - Bailey, Jeffry
- Master ID
- TI08350674-1466
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TABLE 1.
EARLY C~ILDDOOD I~ESPIRATORY I~CTIO~ ~ PASSIVE
O
C~
CO
C~1
CO
CO
STUDY POPULATI(M
10,672 blrlths in
Israel, 1907-1968
(3) births
2,205 in
England, 1963-196§
(~)
12,068 blzths in
Y[nlandp )66
(5)
1,265 blr is in
New Zealar , 1977
(~).
3~ chEldr~n
hospital i~ ed with
ItS virus t~ronch|tls
in infanc~,
England (~).
130 childlen with
RS virus Infection
in infancy, England
(8).
• RR e reative risk.
STUDY DESIGN EFFEC~ OF PASSlV~ S~OKING
COld~NTS
Antenatal m~ternal smoking
history, monitoring of
hospital adsisslons in
first year of Ills.
Prospective cohort with
annual questionnaire.
Prospective cohort with
follow-up of hospttallza-
tions, physician v/slts,
and mortality.
Prospecti~ cohort with
diaries, physician and
hospital record review.
Significant increase in
hospitalization for
pneumonia and bronchitis,
8R* - 1.38.
81gniflcant increase in
bronchitis or pneumonia in
first 7ear of life, I~R- 1.73
if one parent smoked,
RR = 2.60 if both smoked.
Significant increase of
hospitalization for resplra-
tory diseases during first
5 years, RR - 1.7~.
Significant increase in
bronchitis or p~eumonia during
the first 7ear of l~fe,
~= 2.0~p if m~ther smoked.
Case-control with 35
matched controls performed
g years after index
illness.
Borderline slsniflcant effect
of materna! sm0klns during
first year of life~
Case-control with III
controls performed I0
years after index illness.
Significant effect of maternal
smokinS st time of illness,
Calculated from published data if not provided by the authors.
Dose-response relationship
present. Maternal amokin~
only.
Sex of mokin~ parent not
examined.
Effect largest durin8
first year. Naternal
smoklns only and measured
during pregnancy.
No effect of paternal
smokinS. Effect of mater-
nal smoking equivocal in
second year, absent in
~hird. Dose-response
present in first,
Significant increase in
daily numbers of cigs-
reties smoked during the
first year of life by
parents of cases.
Effect of paternal smoking
also present.
respiratory illness 1>~fore age t~o and with respiratory illness in the last
year (9,10). In data from the 1979 National Health Interview Survey, parent
smoking was associated with significantly more days of restricted activity
from acute respiratory illness (2).
TABLE 2. RESPIRATORY SYMPTOMS ZN CHILDHOOD AND PASSIVE SMOKING
STUDY POPULATION
EFFECT OF PASSIVE SMOKING
COMMENTS
2,426 children, ages
4-14 yr, in England
(n).
~ prevalence of cough with
number of smoking parents.
Effect re~ved ~heu
parents' symptom
status controlled.
626 children under
age 15
United States (12).
Non-significant ÷ in preva-
lence of cough and phle~n
if smoking household.
Effect reduced by con-
trolling symptom status
of adults.
816 children, age 7
yr and above,
United States (13).
No effect on symptom
prevalence.
Small numbers in
specific subgroups.
5,835 children,
first year of
secondary school,
England (14).
÷ prevalence of cough and
breathlessness.
Child's smoking
controlled.
1,937 children, age
6-Ii yr, Japan (15).
÷ prevalence of lower air-
way symptoms.
Composite symptom
index. Effect varied
with residence location
650 children, age
5-9 yr,
United States (16).
676 elementary
school children,
United States (17).
4,071 children, age
5-14 yr,
United States (I0)
+ prevalence of persistent
wheeze.
~ prevalence of wheeze,
sputum, and cough.
No effect on prevalence of
symptoms or asthma.
Effect not significant
for chronic cough and
phlegm.
Effect not significant
for asthma.
Multivariate analysis
with maternal smoking
as the exposure
variable.
For respiratory symptoms, the evidence for effects of passive smoking is
less convincing (Table 2). The differing results may reflect tmcharacter-
iz~d v~riation--b~rween--wradie~--i~h~--~v~--6mb~d£~g exposure Yt~T.f~--In
each, the level of passive s~king has ~eu assessed with simple questions
about smoking by parents or household ~mbers. Variation in residence
construction and ventilation ~y result in differing concentrations of
tobacco smoke components at equivalent levels of passive smmking, as assess-
TI03350584
202
SAMET ARD ~PEIZE£
ed by questionnaire. Additionally, differing symptom questionnaires have
been used in these studies.
The evidence concerning effects of passive smoking on children's lung func-
tion is also conflicting. Most investigations have been cross-sectlonal and
preliminary data from longitudinal evaluations have only become available
recently. In general, studies with positive results have examined the
effects of passive smoking on flows at low lung volumes; those with negative
results have utilized lung function parameters less sensitive to smut1 air-
ways function or have involved relatively small populatlon samples.
Cross-sectional analyses involving a sample of five to nine year-old chil-
dren in East Boston, Massachusetts, provided an important early demonstra-
tion of passive smoking effects (16,18). In subjects with data available
for both parents, a dose-response relationship was demonstrated between the
level of FEF25_75 (forced expiratory flow from 25% to 75% of the forced
vital capacity) and the number of smoking parents. By multiple regression
analysis, the effects of passive smoking were prinmrily attributable to
maternal and not paternal smoking. Other cross-sectional investigations
have confirmed these results. Yarns11 and St. Leger (19) described
reductions of lung function consistent with a passive smoking effect, but
did not statistically assess the association. In a very large U.S. investi-
gation, statistically significant, but very small reductions of FEVo.75
(forced expiratory volume in 0.75 seconds) were associated with maternal
smoking (20). Vedal et al. (21) found significant reductions of several
spirometric measures in children with smoking parents. The effect primarily
reflected maternal smoking and was larger in girls.
Methodological limitations may explain the negative findings of other
studies. The population studied in England by Leeder e~ al. (22) was
relatively small and the PEFR (peak expiratory flow rate) is an insensitive
index of subtle changes in lung function. The methods of analysis may have
resulted in overadjustment for passive smoking in this study and that
conducted by Schilling et al. (13). Speizer et al. (9) did not find effects
of parental smoking in a large investigation of children from six U.S.
co~nlties. With expansion of the study group and the use of a more robust
adjustment for lung size, however, small effects were present in a preliml-
nary longitudinal analysis (24). Several investigations in Arizona were
limited by relatively small samples (17,23).
In summary, during the past ten years, the health effects of passive smoking
on children have been investigated with increasing intensity. The available
data are most convincing for an increased incidence of lower respiratory
tract infection during pregnancy. The evidence meets conventional epidem-
iological criteria for a causal relationship. Although associated with only
modest elevations of relative risk, passive smoking could be an important
source of morbidity in infancy. Assuming a 30% prevalence of
maternal smoking and a relative risk of 2.0, then 23% of lower
re~pira~orS'--rra~cr-~i-~f~c-vi~ffs--dfi-rTng EnTa~y ar~-~att~fa~q~ to th~s
exposure.
For s)nnpto=s and lung function level, the data on passive s~king effects
are conflicting. Because of the low prevalence of symptoms and the large
variance of function measurements, large study samples are needed. Some
TI08350885
pAS$1VE S]40KIRC AMD THE LUNGS
203
published investigations have not met this requirement and others have used
insensitive measures of function. Crude assessment of exposure also limit
their findings. The investigations least affected by the limitations of
sample size and insensitive lung function measurements suggest that passive
smoking does impair lung function in children. The effects are small and
their biological importance is uncertain. Longitudinal investigations may
clarify this issue.
PASSIVE SMOKIRG ARD ADULTS
Although less well characterized, the health effects of passive smoking on
adults are equally controversial. As with children, exposure is widespread
and involuntary when sustained in public areas or the workplace. For
respiratory symptoms, the available data do not demonstrate a consistent
pattern of passive smoking effects. Symptoms have generally not been
increased in non-smokers exposed to cigarette smoking by other household
members and sources of exposure outside of the home have not been evaluat-
ed. With regard to pulmonary function, exposure to passive smoking has been
associated with reduction of the FEF25_75 in two cross-sectional investiga-
tions, though others have been negative. White and Froeb (25) compared
spirometric test results in middle-aged non-smokers, with at least 20 years
of passive smoking exposure in the workplace, to values of controls. Flow
rates in the exposed group were significantly reduced. Criticism of this
investigation has focused on the test procedures, the determination and
classification of exposures, and the handling of former smokers. Bias may
have been introduced by uncontrolled correlates of social class. ~owever,
the findings of a populatlon-based French investigation of over 7800 adults
were similar and not subject to these limitations (26), Above age 60, the
FEF25-75 was reduced in non-smoking men and women with a smoking spouse.
The small reductions of FEF25_75 found in these studies would not be asso-
ciated with clinically important impairment and their long-term implications
must be established.
CONCLUSIONS
While clarification of the effects of passive smoking is an important
scientific objective, sufficient data for the development of preventive
strategies are already available. Prevention of active smoking will remain
the best approach for reducing the effects of smoking, regardless of the
results of additional research.
National Research_Counc_i_l_.~!~doo_r__poilR~aruLs~__WaahingtQn,_D.C:: Nation-
hal Academy Press, 1981.
Bonham GS, Wilson RW. Children's health in families with cigarette
s~okers. Am J. Public Health 1981; 71: 290-293.
TI08350886
204
SAMET ARD SPEIZER
o
8.
9.
10.
ii.
12.
13.
14.
15.
16.
Harlap S, Davies AM. Infant admissions to hospital and =internal s~ok-
ing. Lancet 1974; 1: 529-532.
Leeder SR, Corkhill R, Irwig ]hi, Holland ~q#, Coley JRT. ~nfluence of
family factors on the incidence of lower respiratory illness during the
first year of life. Br J Prey Soc Hed 1976; 30: 203-212.
Rantakallio P. Relationship of maternal smoking to morbidity and
mortality of the child up to the age of flve. Acta Paediatr Stand
1978; 67: 621-631.
Fergusson DM, Horwood LJ, Shannon l~r, Taylor B. Parental smoking and
lower respiratory illness in the first three years of life. J
Epidemiol Community Health 1981; 35: 180-184.
Sims DG, Downham MAPS, Gardner PS, Webb JKG, Weightman D. Study of
8-year-old children with a history of respiratory syncytial virus
bronchiolitis in infancy. Br Med J 1978; I: 11-14.
Pullan CR, Hey EN. Wheezing, asthma, and pulmonary dysfunction 10
years after infection with respiratory syncytial virus in infancy. Br
Med J 1982; 284: 1665-1669.
Speizer FE, Ferris B Jr, Bishop YHM, Spengler J. Respiratory disease
rates and pulmonary function in children associated with NO2 exposure.
Am Rev Respir Dis 1980; 121: 3-I0.
Schenker KB, Samet JM, Speizer FE. Risk factors for childhood respira-
tory disease: the effect of host factors and home environmental expo-
sures. Am Rev Respir Dis 1983; 128: 1038-1043.
Colley JRT. Respiratory symptoms in children and parental smoking and
phlegm production. Br Med J 1974; 2:201-204.
Lebowitz HD, Burrows B. Respiratory symptoms related to smoking habits
of family adults. Chest 1976; 69: 48-50.
Schilling RSF, Letal AD, Hui SL, Beck GJ, Schoenberg JB, Bouhuys A.
Lung function, respiratory disease, and smoking in families. Am J
Epidemiol 1977; 106: 274-283.
Bland M, Bewley BR, Pollard V, Banks
parents' smoking on respiratory symptoms.
If0-115.
Effect of children's and
Arch Dis Child 1978; 53:
Kasuga H, Hasebe A, Osaka F, Matsuki H. Respiratory symptoms in =choo]
children and the role of passive smoking. Tokai J Exp C1in Med 1979;
4: 101-114.
Weiss ST, Tager IB, Speizer FE, Rosner B. Persistent wheeze. Its
relation to respiratory illness, cigarette smoking, and level of pul-
monary function in a population sample of children. Am Rev Respir Dis
1980; 122: 697-707.
TI08350887
PASSIVE ~)~ING ~[D ~HE LU~S
17. Dodge R. The effects of indoor pollution on Arizona children. Arch
Environ Health 1982; 37: 151-155.
18.
Tager IB, Weiss ST, Rosner B, Speizer FE: Effect of parental cigarette
smoking on the pulmonary function of children. Am J Epidemiol 1979;
110: 15-26.
19. Yarnell JWG, St. Leger AS. Respiratory illness, maternal smoking habit
and lung function in children. Br J Dis Chest 1979; 73: 230-236.
20.
Hasselblad V, Humble CG, Graham MG, Anderson HS. Indoor environmental
determinants of lung function in children. Am Rev Respir Dis 1981;
123: 479-485.
21. Vedal S, Schenker MB, Samet JM, Speizer FE. Risk factors for childhood
respiratory disease: analysis of pulmonary function. Am Rev Respir
Dis 1984; 130: 187-192.
22. Leeder SR, Corkhill RT, Wysocki MJ, Holland WW. Influence of personal
and £amily factors on ventilatory function in children. Br J Prey Soc
Med 1976; 30; 219-224.
23. Lebowitz MD, Armet DB, Knudson R.
pulmonary function in children.
8:371-373.
The effect of passive smoking on
Environment International 1982;
24. Dockery DW, Ware JH, Speizer FE, Ferris BG Jr. Preliminary longitudi-
nal analyses of pulmonary function in school children in the slx-cities
study (Abstract). Am Rev Respir Dis 1982; 125:145 (Part 2).
25. White JR, Froeb HF. Small-airways dysfunction in non-smokers chronic-
ally exposed to tobacco smoke. N Eng J Med 1980; 302: 720-723.
26.
Kauffmsnn F, Tessier JF, Oriol P. Adult passive smoking in the home
environment: a risk factor for chronic airflow limitation. Am J
Epidemiol 1983; 117: 269-280.
T108350888
207
EFEECT OF SMOKING ON GASTROINTESTINAL ~RM01qE SECRETION
Yutaka Seino
Kinsuke Tsuda
Kozaburo Mori
Shozo Li
Jiro Takemura
Shigeru Matsukura
Hiroo Imura
Second Division, Department of Medicine
and Division of Metabolism and Clinical Nutrition*
Faculty of Medicine, Kyoto University
Kyoto 606, Japan
INTRODUCTION
Recent studies have reported the frequent occurrence of peptic ulcer and
chronic pancreatitis in smokers. Previously, it has been demonstrated also
that smoking reduces exocrine gastric (i) and pancreatic secretions (2) and
gastrointestinal contractile activity (3).
Several gut and pancreatic hormones have a close relationship with gastric
and pancreatic secretions and gastrointestinal motor activity: gastrin is
secreted from the gastric antrum; most pancreatic pol~peptide (PP) is found
to be distributed in the pancreas; and motilin and gastric inhibitory poly-
peptide (GIP) are located in the upper part of the small intestine. The
biological activities of these hormones are well known: gastrin stimulates
gastric acid secretion; motilin produces gastrointestinal motor activity
(4); and PP is related to pancreatic and biliary secretions (5). On the
other hand, GIP suppresses gastric secretions. In addition, the main GIP
action is thought to be the enhancement of insulin secretion.
The effect of smoking on endocrine gastrointestinal hormone secretions has
remained unclear, however. The present study was undertaken, therefore, to
elucidate the effect of smoking on the release of gut hormones such as gas-
trin, motilin, PP, and GIP.
SUBJECTS AND ~THODS
For each hormone, two experiments were performed. In experiment I, in order
to compare the effects of smoking 2 mg. nicotine cigarettes with non-
Address - .'_, ,___._
.~_Seco~d_D~ri-s~u~--Dep~rt~__nt
correspondence.~o'~_in~ ~ ~
of Medicine, Faculty of Medicine, Kyoto University, Shogoin Kawahara-cho,
Sakyo-ku, Kyoto 606, Japan.
T10~350889
smoking, six males aged 20-42 yrs were given a 280 Real. meal to stimulate
hormone release after an overnight fast. In experiment 2, six males aged
20-40 yrs smoked 1.2 mg D-nicotine (an isome_r of L-nicotlne) cigarettes to
compare the effects with those of 1.2 mg L-nicotine cigarette smoking on
200 Kcal. meal-induced motilin and PP release. Blood was withdrawn at
intervals of 5-15 mln. for two hours before and after the meal. The volun-
teers smoked one cigarette every 15 minutes for a total of 16 cigarettes in
four hours. Gastrin, GIP~ motilin, and PP were measured by specific radio-
immunoassay.
RESULTS
No significant difference in gastrin or GIP release was observed with or
without smoking, as shown in Figures I and 2. Motilin has an intermittent
secretory behavior which causes hunger gastrointestinal contractile activi-
ty. Smoking reduced the intermittent fluctuation of motilin release in the
fasting state, although the interval of fluctuation was different in each
subject, and also blunted the significant rise after meal ingestion, as
indicated in Figure 3.
FIGURE I. EFFECT OF SMOKING ON GASTRIN SECRETION
BEFORE AND AFTER MEAL INGESTION
~/ml
I~0
5O
'T~n':| { Mrn)
Tl08350890
FIC[TRE 2. EFFECT OF SMOKI~G ON GIP SECRETION
BEFORE AND AFTER MEAL INGESTION
FIGURE 3. EFFECT OF SMOKING ON MOTILIN SECRETION
BEFORE AND AFTER MEAL INGESTION
TI08350891
210
~IBO L~ AL.
Figure 4 shows the effect of smoking on PP release. In the non-smoking
controls, PP showed a biphasic secretory pattern after meal ingestion.
Smoking suppressed the significant rise in PP secretion after the ~eal,
especially the second phase of meal-induced PP secretion found with non-
smoking. When we calculated the total amount of meal-induced second phase
PP secretion, Z pP was significantly reduced by smoking (P < 0.05).
FIGURE 4. EFFECT OF SMOKING ON PP SECRETION
BEFORE A~ AFTER MEAL INGESTION
10oo
500
T~me (M~n)
Figure 5 shows the comparison of D- and L-nicotine cigarette smoking on
motilin release. The intermittent fluctuation in the fasting state and the
peak_mor_ilin_lev.~af~- ~ndd__to~e ~educe& by-J~nico~zJme_ciga-
rette smoking when compared to D-nicotine cigarette smoking. We found also
that the suppressive effect of L-nicotine cigarette s~oking on PP release
after meals is much stronger than D-nicotine cigarette smoking, as shown in
Figure 6.
TI08350892
