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ROYAL : oI"rAWA HOSPITAL
HOPITAL ROYAL D'OI-i'AWA
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Dr. V,J. Kno~t,
Speciality Cllnics.
1145 CARLING. OTTAWA, ONTARIO KIZ 7K4 TEL. 613/722-6321
November 23, 1981.
Canadian Tobacco Manufacturers Council,
1808 Sherbrooke St. West,
Montreal, Quebec, H3H 1ES.
Dear CTMC Members,
In November of 1979, I proposed that CTNC fundinz of
my research be extended for an additional five year period so
that I could further my work on stress-reduction aspects of
tobacco smoking. Attached is a copy of the brief proposals
which I considered to be o~ critical relevance to the
motivstional understanding of the smoking habit. Of the projects
suggested, the lon~itudinal study ( which involved Year I0
Year II and Year V) was considered to be of greatest potential
in elucid~tin~ motivational mechanisms.
Attached is a research proposal which proviaes, in
addition to methodolo~, the theory, rationale, fr~,~cwork and
significance of this study. Specific details re<ardinc delails
of the methodology have purposely been left out so as to allow
the CTMC members a clear scope of the general procedures
without distraction by a myriad of detail. If however,
specific details of tests, re~arding procedures etc. are
required, this can be done on request.
Attached also is a list of budget requests and Zheir
rationale. My greatest concern and embarrassment here is with
the &mount of monies requested az it is the larges: budge~
(~89,789.00) I have requested to da~e. The greatest need of
course is technical assistance. I am in the laboratory from
9,00 a.m. - 5:00 p.m. and as such reading, summarizing and
.writing reports and papers is exzremely difficult. An additio-
nal member, at the technical level, would definitely relieve•
the pressure. The rationale for the additional requests is
attached so I will not elaborate here. The large reauest of
course pertains only to Year I of the five year plan. The 2nd
to 5th year budget requests will be greatly reduced as these
will only involve the two salaries and approximately $10,O00/year.
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BatCo document for PFSFC 1 March 1999
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As observed in the additional proposals, the purpose
of ~he protocols in Year III ~nd Year IV are t
Year III,
To determine whether the phyziological,
behavioral and psychological symptoms
experienced during tobacco abstinence are
indicative of a "return to an endurin~ .
psychophysiolo~ical makeup" or are indicative
of a temporary "withdrawal syndrome".
Yeaz'IV=
To determine whether tobacco smoking
alleviates attentionsLl deficits in psychia-
tric patients exhibiting such ,disorders in
the extreme (eg. anxiety patients, schizo-
phrenics etc.)
The written proposals for each of these stud'ies will be
submitted prior to each specific deadline date.
Thank you for your consideration of this research.
Your support and interest in my work over the past four years
is ~reatly appreciated,
Yours Sincerely,
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Verner J. FJ~ot¢, D.Phil.
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BatCo document for PFSFC 1 March 1999
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Rationale for Budget Requests, Year I, Jan_~82 - Dec/82.
This budget is the largest ($85,789.00) I have requested
¢o date and although I have tried to be very conservative in
my needs and expenditures for this longitudinal study, the
first phase (Year Z) just necessitates more staff and
equipment if a high quality product is desired in the fifth
year,
Salaries,
.Principal Investi£ators The salary request here is in lane
with the updated salaries of the ROK. For a Registered
Psychologist in the province of Ontario, the be~innin~
salary is $30,478.00 and the yearly increment is $1,378.O0.
As I now have 4 years of experience, the salary level is
$35,990.00. As CTMC kindly added additional monies to cover
my benefits last year, I included this 10% with assumption of
course that this is purely optional to CTMC.
Research Technician, Two full-time research technicians are
required for assistance in this study. One technician is needed
in the laboratory in assisting psychophysiological recordings
and a second technician is required in assisting, initiating
and maintaining sample records, and for codin~, storin~ and
analysing of data. As two full time salaries at a technical
level is a heavy expense, I have decided to take on only one
full time technician for psychophysiological records and to
spend less than half of the amount of the salary (to be used
for a second technician) in hiring a part-time computer
programmer to develop the software capacity of the micro-
processor in the laboratory so that it can take over the
major work and time involved in coding, storin~ and analysing data.
At the ROH, a full-time psycho-technician starts at
$14,382.OO with yearly increments of $?30.00. As the technician
I have in mind already has 9 months of relevant experience
elsewhere and will be available for a full-time position in
January, a salary of $15,000 would be appropriate for this
position. Salary for a computer programmer on a part-time
contract is estimated to run at $7,000.00. It should be made
clear here, that the salary for this part-time position would
only be required for one year and it would then terminate.
Major Equip: At present my Beckman polygraph houses four
amplifiers and this simply means I can only record 4 measures.
To go into a longitudinal study of such potential with this
restricted number of physiological measures would be a catastrophe
and it is proposed here that we at least double the number of
amplifiers to eight~ As Beckman prices have greatly increased
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BatCo document for PFSFC 1 March 1999
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with inflation etc. (i.e. to purchase 4 additional amplifiers
and associated couplers from Beckman would ~cost approximately
$10,000.00} I intend to purchase 4 separate stand-alone
amplifiers of similar quality which are compatible with my
microprocessor's A-D converter but are much less expensive
than Beckman, the price of these is $6,000.00.
In order to carry out some of the sophisticated data
acquisition and analysis of "attentional" and "cognitive"
components of brain event related potentials, specific
physiological filters are required to get rid of unwanted
electrical noise in order to examine the extremely small but
significant brain responses. The price of these 4 filters is
$4,000.00.
Up to this point I have been presenting auditory stimuli
via an external tone generator which is triggered .by.the
microprocessor. This has faltered several times and has
required repairs, probably because of its a~e. In addition,
in order to elicit specific brain potentials, high quality
control over auditory stimulus characteristics (eg. frequency,
duration, intervals, rise and decay time etc.) and this
necessitates a new sould generator which incorporates these
facets. The price of this is $2,500.00.
The impedance meter is required to ensure that electrode-
skin resistance levels are at a sufficiently low level so as
to ottain clean noise-free electrical responses. The price
of this is $300.00.
Supplies: The polygraph paper, ink and electrodes ($i,500.00)
are of course self-explanatory and the computer disks ($2,000.00)
are necessary for data storage.
Subject Payment, The biggest strategic problem facin~ this
investigation is gettin~ the family (both the parent for the
interview and the child for the recording) motivated to be
involved in the study. From past experience and in relating
to researchers who have done research within the school system,
monetary payment definitely enhances this probability. It
• is proposed here that a minimum of $I0,00.00 be paid to each
as both parent and child will devote two hours of his or her
time. Total cost is $6,000.00.
Miscellaneaous: Published questionnaires on personality and
psychological tests mus~ be purchased and the cost is estimated
to be $I,000.00. Mail is an essential process if contact is to
~e maintained with the sample pool and the cost here is
estimated at $I00.00. Filing cabinets are needed for physical
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BatCo document for PFSFC 1 March 1999
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storage of the questionnaires, polyEraph paper etc. ($600.00)!
A calculator is needed for mtnor descriptive tests and
assistance within the lab (cost is $200.00).
~, and as stated In the covering leter, I am aware
that th~s is a large financial request but I trust that CT~C
will keep in mind that this holds only for the demands of the
first year of the 5 year grant. The financial con,nittment for
the 2nd to the 5th years will be similar tnnature to what was
being requested in my lass ~ years, i.e. monies for salary
(In ~his case 2 salariess the principal investigator and
technician)'and approximately $10,000.00 extra for laboratory
demands.
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BatCo document for PFSFC 1 March t999
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Budge% Requestst YearlIt_~Jan~1982 - Dec/I~82
Salaries,
Dr. Y. Knott
(plus 10~ for benef£¢ coverage)
Research Technician
Sol%ware Development
$15,000.00
7,O00.00
Equipmentt Physiological Amplifiers
PhysioloEical F£1ters
Stimulators
Impedance ~e%er
6,000.00
~,000.00
.2,500.00
300.00
SuDDliest Polygraph paper, ink, electrodes
Computer Disks
Z,500.O0
2,000.00
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Ten doZlars~ subject and
Ten dollars/ parent interview
6,000,00
Miscellaneous,
Questionnaires
Bail
Filing Cabine%s
Calculator
Total
1,000.00
100.00
600.00
200.00
$85,789.00
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BatCo document for PFSFC 1 March 1999
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ROYAl. OTTAWA IIOSi'IFAI.
HOi'ITAI- ROYAl- O'OTTAWA -
Dr. V.J, i:n,~tt,•
5poolallty C] inicn
1145 CARTING, OTTAWA, ONTARIO KtZ 7K4 TEL. 613.';'22-S521
i;ovember 11. 1979.
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'~.h~.".':cienLLrit" 1. iLeratun: "h~ con.nL~tently r.-,Lnc, d
number of'(tuo.=ti3n..., in reference to .ratter',-, which both relate
1;o thc acquL.-i, ti,)'~ rye! ~,nLntenw~ce of smokLnr, behavior. Tt
Is my ,'trent h,.,1.ief bane,I on my o~m lnboratory findinKs and
,~.l;ud~e~ of "':uropo;a,•l, ~r~ti,~h and Amer~c:~l laboratoriec, that
the ~aechani::m:: ,m,lcrty~nF. ncq:~i,J;_tion-mRintonance processes
nre in p~rt h;'u,e,~ on the inherent or intrinsic p%,cho-
phycLolo~Lc~t "~u'=cu? of the indLv;-du.~~ croaker, fZore"
."necifi.coll..y, ~t L~ ;"~.t.hizl rearon to speculate ~h.~'c .~,nokers,
prio.- to n :'m.~:',h~." h~rtory, exhJ.b~.4; n p~,chophyr~oloFicnl
nrof~.l.n ~':hi.ch, rnl.nLiv.: to future non-nmokers, J.~ charncl:-
C,'J.~.~.!d ),y n rr:'~.".t'Tr vtll.t|ec-ab~lity tO ~;~;re.~.-. ~.-, refl.ected
~n cPntrnt, n'Jt,~,l't~ke m'~d skolct,~l-musculnr ~ystens m~d R
d~.f~c~cnt hchnvEnrat recponsiv~ty as reftected £n attentionRl
~Ln?O-.~', t| ~tt-,,,',)f'~.'='=inr ::n,! decicLon makinr functionn.
"It)1%!!.~. "l~,;,"l" [nhqrent1~' e=tn':)~i=hed, the enoc'mo'Js
:~t*,.,'~cl~.~n oF t~,:ncro I~c in it.". abLILty to "normnLine"
n~yciv~ph~,:~[o1-, i(.nl rq:::~op..':~vit.y ~%d thu~ nllow for "~ore
• "rf~c|,::it bnh',','i~,-.,l p,,rfor~n::ee and incrensed ~ubjectJ.ve
wn I i - h~. ] n ,:.
"~th r,-'-'..-~t, tn th.'re n.-~u,nntLqn';, ~.t Lr, su.=.P:e~ted
thrz~, the. ?otl.~:"}n'- h'.',~othe~en bc exam~n,:d:
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Int-inrir :~"::c;t~)phy"lolocic,n-I fnctoro o.n~rnt~ in ~om~.
~:~,li'.'~du~l"" t.~ l~,',;,li~po~e them to the acnu~n~t~.on of a
"',~..hqdt :, ,~,t•e~y or te,~:t.=. - pcychnl, hv~Lolo,-=.ical,
a,l~inknt.-~',,.' to y,,:~.~;: ch~1,1ren (8-9 yr',', of are) .~n,1
they ~'.'o'~ ! ,'- ?oL1.,v'e,l un over a h-5 year pcr£o,~ ('or
the p,~,',~..-., .;r ,,rl.;"~c;1,J.n~ the incidence of :'mokerr .~n,l
no-~--"~n4 ..... :, c~ ,..';nm~.nJ.n:' the re1.;ttLon~h~p o(" th(,~o tent
~,nt!.c,-~.,, • L', l..h,;~.~ .... nokin.'" - non-:'mnk~n,; ~t,~t,J.~. It, wout,l
~,,. :::~nec't.,.,! i.h:,t .:mo"er'; mr'l non-:',,~k,:rr. -;-oul,l be (luLte
• !~'l',,.Peltt v']l.', r'~'":~OCt to th,.,Lr ~nLttnl te=t re;;ul.t:.
A'I,'i tLonnl "~I 1.}~:-,~nn (5.ye.~r.~, 10, ] 5, 20 . •. ) could
b,: ~-,it~',t~.~ ,~.~ LIp..:~me -roup to (~et~.rmLne the ]on,:-term
.~m~::er n'r+ , nn-'9-~',~r s~.ntu= of thi~ r.nme rroup cample.
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BatCo document for PFSFC 1 March t999
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RL)YAL OTTAWA 1IOSrITAL
ItC)PITAt ROYAL I)'OTFAWA
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1145 CARLING. OTTAWA. ONTARIO KIZ 7K4 TEL.
813/122-6521
Alth,);J,'h :',.~,~k|n-" nh~t~nence [~ carrel:fLed i.:ith t~mporar~l
!l.~?/eho$,~ ;.",1 ,'.:/"~:~to-~.-., n= l,~ the dL.~co,~LLn'nation of"
• "itW ~.rr~i;-"h~l~it", t,h-, phv~Lolo,'icnl alteration~
OCCtJr"irl'" ;lt 1.tl~, ti.'l~, oJ" .'ll)~til~ence ore not transitory
~hn.~r~n~ i1.L~."- tel nted to a "smokin,~-wlth,lr.:.';:aL" nhenomena
whleh ret,arn to"nu:'mal" after an olnp::ed tLme period.
~t tn Cu,'F,,~L..:I h,.'r,J that the phy~Loto.=.Lcal alteratlono
are refl.'.cti',e of ~ returr~ to ~i en,lurin~, p~.vchophysLolo~.Lcal
=akeup which Lu charncterL~tic of =,,okern.
"'ethod: .:~n".,r': .r,-,J:n tobacro-nb=tillertce clinics will be
,~,~l,'tt~r~..l !,.e.~...,., :,i,l ~'or I year after (at 1 month ~ntervals)
:.'mm'-.Ln,." ce-:-:,~L~ ::'Lth re:::~rd~ to ;~ batter:! of tests
In~l,,.'ir;- p"ych,}phyniolorlca~, p~:Ichol,),:Lcal a~i,l
hehavio;..nl narnmoter.~. It v"),ild be expected that phym[o-
].o,oi.c~l ~h~:',:~. v'o.l],1 not ch,'m~e over time m~<! that
n~o':er.-., r,.t.~t.ive to non-.-.,nnkez's ~voula continue to exhLbi.t
vulrlqrnb~l.~t'., to -i,'en~ arid irlef£LcL.~nt perfol'mrmce evon
nf~cr I ','"'~". :'~.~p~rt of tlx~.~e fLndin:,r, c,o,itd di.-.mL.-,s the
rIP-r[ri,.ni.i,~,, ~lr ;,ohacco a.~ a "dopen,InliC¢'" 'lisor,ler as
• i ;;'i. th:lr:r';'.,1 -';,;idr'ime i.'; cr,ici.al, to the de!'inition of
• lrll- ~!~.llci,.l,',.i-.-,
~e
£;= toba,:c'~ "-n.~:Ln~. alleviate:: stre::~ hy (a) red,i~';-n.~ the
].~.".~Cl; O.~ ~--.:,..:~vr. rti',~,Jlnt~on ~I~,'.' by (~) [ncrea.-.Li;r'
i:~ r:):-lrl C i ,r ~. ,,....~ .¢, .... -. l hr. ,~n,i ntten t i anaL- f L l te-i.n:, c.~ na c t
t:/,
~LL i'. ,|'lil." ,-',:r',,'~:,ble I;o hvnothe~Lze that {t wo0.1].,t hove
aerial'it. ,:!i"~L"?L ,til Lty For p~ychintrLe patients who
.~'-.hLbL¢ -.,~,.h .:~-,q--1,~r.~ irl the e'{tremn. '[~h~ receive:;
~.-,l['-ect ,,.,-..,,~rt from the ":;or thnt nn:/chJatr[c nnttont.~
,.~:,:i[h[ ~ n ".'::-~:~,il" hi ~.hur connumpt.[c~ rate than the
li-~r~;il ;~)~'~l','.[orl ~;v! they ,:xhibit marked d~.~tre~.~ when
.-,u?~;~1[e.~. -~i'? 1"3":.
"..l.ll,rl i .I, "'~Oi ~l,hy':inlo~i('nl, p:,.;Ich,)lo~:icnl n,id i~ehavioral
~."':L:" w|ll '., -,.imi,,i:-L,,r~.,l t.o vari~'l.~ rltnlc:ll e,~t,.,.rories
( i . . ~ :-rhi ~',li."lr .... ii c,'l ljil .: i • I,),~ ~qll,1. ,I,,p.,'e';ncd p,-il~ient.~)
t,,f~ I,. i~4 ~" '*' i'~" ;'.ll,,l.~ll'r c1 i.lli.C;Ilj. Ryl'llltl'i,'n.': at',, egn,"t:ernl;ed
"ol.lo-:'i;1 1, ", i 'l~vr. cl~ ni,.'.ti.ne'~C," ~rld wh~l;her they
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BatCo document for PFSFC 1 March 1999
ROYAL OTT&~VA IIOSrlIAL
I IOPITAL ROYAL D'()IIAWA
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1145 CAIILING. OTTAWA. ON rA/~llO KtZ /K4 TEL. 6131722-6521
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?he comt'i::~.'t ,-~.~.nrch pr.~1~)~nl.-, could bQ c.nrried out
OVee n ~ yen.~ .-.n:m, ~h,., initi:~l lr;t ~ year~ wnu14 be foctl~ed
on proposal. :~o. 1 , [.e., c~] l•*rtLn.~, n lar,,e .~nm!~Le oJ"
chLldr~.n ~id acquirin,: nrofile.~ for fut~re reference Ln the
51;h y~.ar. The l;hL:'I nn¢l fo,.~rth yeara we,lid b,e focuned on 1;he
2rid anrl }rd p,-or.,~co~.~ (one year Eor each) nnd the 5~h year
wo,~Id h? :ledic:tl.~.,l t.o fnllowin-,p the ~nmple of ch~.idren
for 1:he ?i.nnl e,~ll..,etton of data.
.vt" ~.here ~-.:~nrch nro~oco]= are accepted for 'nupport it
L.-..~t~ctnn~.-,' r..h~t th"y ;':i11 n'~ inLtJ...nted follo",'in.= Pha~e Ill
o.r -,v ~,'c~cnt r,,:-~n~ch pro~ec~. on "Tobacco 3mo;,in~ m~d :~t;ress
':=¢~,~ct[on" v:i r.h ".P.:'.C. "~'!:e r,.,':enrch buc!zet per ,~nnum should
~.ppr~..~nCe tlw r:-, .~,:r0. -ate ;"ith m~nor alteraLLons to
CO,.a.rt.~|~-.~LQ f'Ot" ~:s¢:T.~,'l~e ] CLI.~':~.''.
\1 l,ho~ "!t -.n-.h '~ Lb., ~. pr3L.~,.'~Is m..:, :'enrel tow:~rd.~
,~.:nc:-al "h.',..-i~: -,:i,m:.;"i,'. eorr,,lnb~r'' of tobacco s'no;".in~~
|.~., .";hc~ a,'v '.h- ~.,~.:,, "lcinl or ~otivatla,~l .~ainc behind
~;hc'","l,*~l;.t.'~=,:'. ;. " "'." ,~r ~.l. -areLle .-.,.-.olin.it,° J..,>., ~,3r'kt
C].n.:,
~." "Ln hu:,e,l l!s'.L :~('~'"1':.;",':'" of .",he~e pz'opo~at.- .'*or ."u.nporl;
v:~L1 r,..~n~ i.t ,~ :n~-~, l~'cLd ~md-r':;t.nnrl~n= of nttr,~ctLon of
¢hn to~.~cco :',-'."::n," l~;O,it.
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BatCo document for PFSFC 1 March 1999
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IDENTTFYZNG PSYCHOPHYSTOLOGICAL PREDICTORS OF TOBACCO USE
IN CHILDREN: A F~VE-YEAR PROSPECTIVE LONGITUDINAL STUDY
Research Proposal
Dr. Verner J. Knott
Royal Ottawa Hospital
Submitted to Canadian Tobacco Manufacturers Council,
Nov/1981.
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BatCo document for PFSFC 1 March 1999
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CONTENTS
Introduction
Statistics
Psychosocial Factors
Individual Differences
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II.
III.
III.l.
III.2.
III.3.
III.4.
III.5.
State of the Organism
Etiology of Tobacco Smoking
Genetics
Morphology
Personality
Neurophysiology
Prenatal Mechanisms
IV. Empirical Integration
IV.I. Need for a Longitudinal Study
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V.1.
V.2.
V.3.
V.4.
Tobacco and Stress Reduction:
Affect
Performance
Psychophysiology
Neurophsyiology
An Operational Framework
VI. Summary, Rationale and Objective of Study
VII. Significance of the Study
VIII Methodology
VIII.l.Subjects
VIII.2.General Design and Procedures
VIII.3.Psychophysiological Test Battery
VIII.4.Statistical Analyses
Bibliography
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BatCo document for PFSFC 1 March 1999
IDENTIFYING PSYCHOPHYSIOLOGICAL PREDICTORS OF TOBACCO USE
IN CHILDREN: A FI~-YEAR PROSPECTIVE" LONGITUDINAL STUDY
Verner J. Knott, D. Phil.
I- INTRODUCTION
i. Statistics
The recent report of smoking habits of Canadian school
children by the Department of National Health and Welfare*
(1980) has shown that students start experimenUing with
cigarettes at an early age. The major conclusions regard/ng
prevalence of the habit were as follows:
- By age 12, one half of Canadian school children have at
least tried smoking;
- Regular smoking is established in the early teens by many
Canadian students;
- School aged boys experin~nt with cigarettes earlier than
girls, but girls begin r?gular smoking earlier than boys.
From the early teens, a hlgher proportion of girls than
boys smoke daily;
- By age 14, 15% of boys and 20% of girls are daily smokers
and by age 17 these figures have increased to 27% of boys
and 30% of girls. No significant change occurs in the
proportion of students who report daily smoking beyond
this age.
These figures are remarkably similar to the studies
reviewed by Russell (1971) in which it was found that of
those children who smoked more than one or two casual
cigarettes before the age of 19, 80% went on to become
regular smokers as adults. It is only the teenager who
never attempts, or who has attempted no more than once and
decided that he dislikes it and will not take it up, who
has much chance of being a non-smoking adult. The matter
is largely settled by the age of 19; if a person still is
a non-smoker at this age he is unlikely to take it up.
~a~E: see Sra~n, ~erry and Forbes [1980) for reference t~ ~ data
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BatCo document for PFSFC 1 March 1999
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2. Psychosocial Factors
But to establish the prevalence of cigarette smoking
in children and adolescents does not explain how it is
contracted. There is a general consensus that the motivating
factors mediating the onset of the smoking habit are distinct
from those factors maintaining the habit. This has been
discussed by Russell (1971) and the argument will not be
repeated here other than to say that after initiation to
smoking has been me.diated by various psychosocial motives,
the pharmacological effects of nicotine take over as prime
reinforcers. There is strong evidence that starting to smoke
is related to social factors, particularly the influence
of parents, siblings and peers (Mausner and Platt, 1971).
The effect of the behavior of parents, peers and siblings
on childhood smoking is presumably mediated partly through
increased exposure to cigarettes, partly through imitation
and example and partly through psychological and social
pressures to smoke. Evidence for social factors such as
parent's attitude and health education is to a great extent
derived from cross-sectional correlational studies which
give little insight into how these influences act on the
school-going child. Evans, Henderson, Hill and Raines' (1979)
review of the psychological factors reveals that smoking An
children is related to lower levels of perceived (and real)
academic achievement, to rebelliousness, anti-authority
behavior, low self-esteem and that children who begin to
smoke at an earlier age show a higher rate of sensation-
seeking behaviors than non-smoking peers.
3. Individual Differences
Although it is generally stated that social and
psychological factors are responsible for the initiation
of smoking, it is clear that no sharp line divides the
biological from the psychological and sociological. The
kinds of inner emotions that people experience in relation
to environmental conditions and events is at the same time an
expression of both psychological and biological factors. These
• emotions and the environmental situations that are perceived
as rewarding or aversive will determine, at least in part,
a wide variety of behaviors including one's response to
cigarette smoke (Jaffe and Jarvik, 1978).
Individual differences in personality- and particularly
in orientation towards the kind of psychological rewards
offered by smoking are considered to be of paramount importance
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in determining both smoker/non-smoker status and type of
smoking behavior. This is illustrated with respect to
early experimentation with cigarettes. The reasons most
people give for their first experiments with smoking are
~riosity, conformity, bravado or to appear grown-up
(Horn, Courts, Taylor and Solomon, 1959). The first
cigarette is almost invariably unpleasant. Nearly everyone
has experienced the shock of the first inhalation, often
accompanied by gagging and nauseousness - a physiological
response which presumably has a pharmacological basis.
On the other hand, nearly everyone who has continued
smoking more cigarettes can recall the pleasantness of
the light-headedness which followed inhalation, a sensory
experience that could be made to recur following a brief
time lapse between cigarettes. Tolerance is said to
develop to the unpleasant side-effects and skill is quickly
acquired to limit the intake of smoke to a comfortable level,
thus lowering the threshold for further attempts. Herein
lies a possiblQ cause of the virtual inevitability of
escalation after only a few cigarettes (Russell, 1971).
With curiosity satisfied by the first cigarette, the act
is likely to be repeated only if the physical discomfort
is outweighed by the rewards of smoking. If these motives
are sufficient to cause smoking to be repeated in the face
of unpleasant side-effects, there is little chance that
smoking will not continue as these side effects rapidly
disappear.
What then is the nature of these rewards and what
are their basis? There is a growing consensus that
organismic-dispositional factors contribute to the development
of the smoking habit but as to what extent such organismic
factors can be attributed to genetic biological influences
as opposed to acquired influences is as yet unclear
{Battig, 1980). The emphasis on organismic trait and state
factors in influencing smoking behavior has been expressed
in varying degrees by a number of reseachers. In attempting
to extract meaning from their highly variable data on
.students, McArthur, Waldron and Dickinson (1958) hypothesized
"...that starting to smoke J~; largely brought about by one's
social environment but that reactions to smoking ... seem
to depend in good part on the personal needs that the newly
established habit is able to gratify (p. 272)."
Seltzer {1962) paraphrased those observations in biogenetic
terms: "Rather than a superficial habit overlaid indiscriminate-
ly upon various persons, smoking appears to be a response
tO a wide variety of personality and behavioral characteristics
whlc~ have their origin, in part, in the biologic and genetic
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make-up of the individual (p. 43)." Dunn (1973) made similar
references to organismic variables with specific references
to early experimentation with cigarettes: "...it is likely
that we shall ultimately find that the critical mechanisms
involved, in smoking require the synergistic presence of some
other factor, such as anxiety or possibly some constitutionally
determined reactivity. The observation that only about half of
those w~o try smoking cigarettes go on to take up the habit
certainly suggests some kind of interaction process. Smoking
apparently is not sufficiently pleasurable among the
disinterested half of the tryers for the aversiveness of smoking
to be overridden. Smoke is smoke - whether its inhalation
is pleasurable is dependent upon what the individual brings
to the situation ... Whether or not the total experience is
judged by the smoker as positive or negative might in time
prove to be associated with biochemical, endocrinological,
or neurophysiological variables which are either constitutionally
fixed or shaped by experience prior to initial experimentation
with tobacco smoke (p. 101-102)."
If- STATE OF THE ORGANISM
The average pack-a-day smoker takes 8-10 puffs per
cigarette and absorbs approximately 50-150 ug of nicotine
per puff. Each dose of nicotine reaches the brain within
7 seconds and exerts widespread and varied central and
peripheral nervous system effects (both stimulation and
depression, all of which are potential reinforcers), via
its capacity to affect the actions of and release of
important neurochemical transmitters (Russell, 1976). For the
average smoker the behavior is reinforced approximately 50-70
thousand times a year and this consumption level would tend to
suggest that organismic factors of a markedly compelling
nature are operative in the inception and persistence
of smoking behavior. While environmental cues and contingency
factors play a crucial role in tobacco usage, a comprehensive
analysis of smoking also must take into consideration the
effects of tobacco in relation to organismic variables. The
mode of interaction between a pharmacological agent and
ongoing organismic state is of critical importance therapeutic-
ally but its study has also proved valuable in furthering an
understanding of target physiological systems by the known
actions of such psychoactive drugs (Irwin, 1968). A similar
approach can be taken in tobacco research, namely to determine
tobacco's effects on the organism, taking into consideration
ongoing states, so as to elucidate possible mechanisms and
sought for effects by the individual. Nicotine, as a chemical,
does not affect behavior directly but rather interacts with
other chemicals at a cellular level to produce changes in
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tissue, organ and systemic functioning. The resulting
alteration An physiological state then determines the limits
and manner by which the individual copes and interacts with
his environment. Thus the mode of action of nicotine at the
biochemical and physiological levels may provide useful
information of its possible dissimilar effects in smokers
and non-smokers that may result in differential behavioral
patterns of consumption. The issue is raised as to whether
smokers are unique in their reasons for selection of and
response to tobacco and hence consume this substance in
an effort at modifying or manipulating a target system
(or systems). Their consumption therefore would have ultimately
behavioral consequences that alter and possibly increase
coping capabilities (MAlls, 1978). Such an interpretation
of tobacco usage has an obvious teleological fla~or insofar
as it presupposes that smoking serves at least a potentially
adaptive purpose. As will be elaborated upon more fully
later, there is some indication that this may indeed be the
case for some smokers.
However, before proceeding further, a conceptual framework
is proposed so as to allow the reader to establish a context
or perspective for the position to be outlined. If, as pointed
out earlier, the organismic state is an important determinan~
of tobacco consumption, then it remains to be elucidated as
to what target physiological system or systems the person
seeks to modify and toward what altered state the individual
is striving. Irwin (1968) summarised some of the more salient
organismic conditions from psychopharmacological studies.
All of the factors - including wakefulness, arousal, activity,
endurance, biosocial drives, set, responsiveness to stimuli,
information processing and autonomic, neurophsyiological and
endocrine functioning have been investigated in tobacco
research and have been suggested as reasons for consumption
at one time or another (Dunn, 1973).
A person who voluntarily takes a drug often does so with
the intention of altering one or more of the organismic
.variables mentioned above.The point to be made here is that
the motivation for and effect sought can vary between
individuals and serve diverse functions in a given person
in different situations.
This fact is of paramount importance in the study of
smoking motivation. First, it emphasizes multiple causality
An the onset of the habit and illustrates how consideration
of organismi= states precludes unidimensional etiological
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mechanimsms as explanations for all smokers. A second point
is that in addition to motivational needs and sought for~
altered organismic states that tobacco can induce, another
factor for tobacco use may be intrinsic physiological
disturbance that is rectified by tobacco. Thus a pre-smoker
person who is defective in one aspect of physiological
functioning may seek tobacco with essentially medical intent,
much as a person with adrenocortical insufficiency craves
salt (Wilkens and Richter, 1940). Thus, the study of tobacco
consumption must incorporate into a comprehensive explanatory
system in understanding of the state of the organism which
under appropriate environmental circusmtances (cues and
contingencies) leads to experimentation and repeated use
of tobacco by an individual for its perceived and/or real
effects in modifying coping capacity through its mediating
action on target physiological systems.
III- ETIOLOGY OF TOBACCO SMOKING
From the preceeding discussion it is apparent that the
motivation for using pharmacological substance can vary between
individuals, and that a given chemical may also possess unique
effects for certain individuals, whose organismic state
dispositionally distinguishes them from others. Among the
results obtained in animal research in the last few years
there has been numerous indications that psychogenetic
inheritance can influence the mode of action of pharmacological
substances affecting the central neuropsychological systems and
of substances having other kinds of effects as well (Broadhurst,
1977). Although Battig (1980) has cited animal evidence
indicating response variability to nicotine as a function
of psychogenetic strains, the extent such a disposition in
man can be observed and attributed to genetic biological factors
is open to question. Of the limit-less number of organismic
variables that can lead to physiological and behavioral
disruption and thus possible use of tobacco, the concept of
disturbed arousal has probably received the most attention
(Thornton, 1978; Remond and Izard, 1979). Disturbances in
arousal mechanisms have been implicated in a variety of
~sychopathological conditions such as hyperactivity (Hastings
and Barkley, 1978), anxiety and depression (Lader, 1975),
sociopathy (Quay, 1965) and schizophrenia (Venables, 1977). Arousal
disturbance has been theorized to be an etiological factor
in children who as adults are at risk for these disorders.
The question is raised as to whether tobacco may also have
an arousal syndrome as an etiological substrate. The tentative
hypothesis advanced is that within a population of children
the=e exists a subgroup whose symptoms of arousal disturbances
is premorbidly extant. Such persons will exhibit higher probabi-
lity of acquiring the tobacco habit on the basis that
initial experimentation with oigar@ttes will result in
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alterations of organismic states which will be perceived
subjectively and behaviorally as reinforcing. The evidence
Implicating a premorbid difference in smokers and non-smokers
Is briefly reviewed below.
I. Genetics
Many studies that have implicated biological factors in
the initiation of smoking behavior attribute the behavior
to a genetic predisposition. Studies of tl~ins are among the
most popular means of assessing genetic factors. Initial twin
studies by Fisher (1958) showed thot monozygotic twins were
more concordant in their smoking behavior than dizygotic
twins, ctutn by Shields (1962) on monozygotic twins reared
apart indicated frequency of concordance in smoking status
which was significantly different from chance expectancy.
Subsequent studies however have both supported and denied
a significant genetic influence on smoking behavior (Jarvik,
1979} and an example of negative results is shown in a study
by Cederlof, Friberg and Lundman (1977) in which the results
of their monozygotic twin series speak strongly against the
constitutional hypothesis. The presence of a substantial
number of discordant twins in these studies indicates that
genetic factors do not operate exclusively to determine
smoking tendencies. As an example, an estimate of the amount
of variance with regard to smoking in Shields' (1962) sample
which can be accounted for by genetic f~ctors is somewhat
less than 33%. It seems reasonable to conclude that genetic
factors operate significantly, but by no means exclusively,
in the tendency to smoke; and they may do so in a wide
variety of modes, including personality characteristics,
and social and psychological needs and values, rather than
simply by producing an inborn craving or need which nicotine
satisfies (Kety, 1973). This line of thought parallels
Eysen~'s(1980) conclusions on his most recent twin studies:
"Our data do make us question the simple-minded exploitation
of the twin design and its conventional genetic interpretation
in relation to smoking. In particular, although we agree
that dizygotic twins are less alike than monozygotics in
aspects of the smoking habit, we are not so sure that the
similarity of twins for onset and consumption of tobacco
ks purely genetic... All in all, therefore, the picture
emerges from the whole body of data that the onset of smoking
and the consumption of cigarettes are governed by both genetical
and environmental factors (p. 281, 313).".
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2. Morphology
Although the above studies suggest the existence of genetic
mechanisms in the development of tobacco smoking, they give no
clue as to what they might be. They only indicate that the
smoker differs in some significant respect from his non-
smoking peers. Early morphological work by Seltzer (1963)
suggests that smokers differ from non-smokers on a variety
of anthropometric measurements (e.g. height, weight, head
oircumference, etc.). On every single measure e~amined,
smokers were found to exhibit larger mean, dimensions than the
non-smokers. As the measures involved a strong genetic component,
Seltzer concluded that smoking behavior may have a constitutional
basis. Although this data suffer from the fact that they may
have been affected in turn by the smoking habits of the
subjects investigated, this is not true of such studies as
Thomas and Cohen (1960) on ability to taste phenyl%hiourea
(PTC), a trait which has been demonstrated to have a genetic
basks; they found that heavy cigarette smokers showed a
significantly higher porportion of tasters than did non-
smokers. Although the functional significance of these findings
ks questionable, this is not the case with Seltzer's (1967)
most recent longitudinal work. Here, future smokers, compared
to future non-smokers, were found to have smaller tidal
air values, an increased frequency of sighs and swollows,
greater respiratory rate, a somewhat higher recumbent pulse
rate, more palpitations, more sinus arrhythmia, more constipation,
more loss of appetite, and a greater frequency of urination.
The future non-smokers, on the other hand, exhibited a consistent
lack of physiological reaction to stress, suggesting that smokers
are more prone to patterns of reducing anxiety which involve
physiological change. This is in good agreement with the
alleged tension-reducing properties of smoking (Gilbert, 1979}.
3. Personality
The possible existence of a constitutional difference
between smokers and non-smokers suggest a relationship between
personality and smoking. Of the numerous measures available,
the majority of research in the smoking area (Eysenck, 1980}
has focused on three major dimensions: extraversion-introversion ~E);
neuroticism-stabillty (N); and psychoticism {P). Each major
dimension is a combination of intercorrelations between traits.
Thus individuals with high scores E show traits such as
sociability, impulsiveness, carefreeness, activity, etc.
High N individuals exhibit such traits as worry, tenseness,
anxiety, emotionality, etc., and high P individuals exhibit
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such traits as emotional coldness, hostil~ty, egocentricity,
la¢k of superego control, etc. There is good evidence for the
geneti¢ determination of these major personality variables
and the behavioral manifestations of these personality traits
would seem to be mediated through various anatomical and
physiological features of the organism (Eyseck, 1967). In
arousal terminology, extraverts seem to be characterised by
low resting levels of cortical arousal, whereas introverts
have relatively high resting levels of cortical arousal;
these levels are presumably mediated by the ascending
reticular formation. Relative to extraverts who are hypothesized
as exhibiting strong inhibitory tendencies, low cortical arousal
and hypo-sensitive responsivity to stimuli, introverts are
hypothesized to exhibit weak inhibitory and strong excitatory
tendencies resulting in relatively high cortical arousal and
hyper-sensitivity to stimuli. Differences in emotio~ality,
characteristic of N, are governed by the visceral brain,
a limbic system, coordinating the activity of the sympathetic
and parasympathetic autonomic systems.
Physiologically, high neurotic/anxiety subjects tend to
respond more strongly to stimuli, show greater variability
~n response, and take a longer time to recover after the
response. As far as psychoticism is concerned, the evidence
suggests some degree of hormonal control, related to sex
hormones An general. Physiologically, individuals with high
P scores and individuals exhibiting psychopathic behavior
tend to exhibit low tonic resting levels of arousal and
concomitant hyper-reactivity to stimuli and stress situations.
Although inconsistencies are apparent, reviews of the
smoking literature are in general in agreement that smokers
exhibit higher scores on E, N and P dimensions (Matarazzo
and Saslow, 1960; Eysenck, 1973; 1980; Kozlowski, 1979), and
on average there seems to be a positive correlation between
these dimensions and the degree of smoking within the smoking
population. As with other studies and other variables however,
whenever differences are reported between smokers and non-smokers,
it is usually impossible to determine whether the differences
'reflect consequences of smoking or possibly have a causal
relationship to smoking behavior. This objection applies to
a lesser extent to studies on child smokers and to studies
where personality assessments were obtained prior to smoking
onset. Powe~l, Stewart and Grylls (1979) examined E, P, and
N dimensions on a sample of 808 middle-class children between
7 and 16 years of age. More than half of the boys and girls
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had tried smoking cigarettes by the age of 15 years. Of the"
children who tried, they were found to be-particularly
extreme on the P, N and Lie d/mensions and high on the E
dimension. The authors concluded that this pattern is
identical to that of children who misbehave and do not conform
in a general sense. Similar studies indicating that rebelliousness
and antisocial traits were correlated with smoking in children
and persisted into adult smoking (Jamison, 1978; Steward
and Livson, 1966).
Cherry and Kiernan's (1978) longitudinal study is of
particular interest in that their data pertains to personality
dimension pre-dating the smoking habit for those who took up
smoking after 16 years of age. It is clear from their data,
that those who become smokers are both more neurotic and more
extraverted than those who do not, and that the two personality
dimensions .are independent and additive in their effect on
the likelihood of becoming a regular smoker.
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4. Neurophysiolo~y
Although admittedly the scalp recorded electroencephalogram
(EEG) and the event related potentials (ERPs) observed in the
EEG are gross mcasures of brain activity, they provide the
best and most direct measure currently available for assessing
the functional state of the central nervous system. The
heritability of the EEG and ERPs has been firmly established.
Twin studies have indicated that there is a significant
genetic determination of EEG (Lykken, 1975) and of ERPs
(Dustman and Beck, 1965}. From these studies, it appears that
approximately half of the variance of the EEG and ERP is
genetically determined.
In relation to the preceeding discussion on personality
and its biological basis, there is evidence indicating that
variations along the various behavioral dimensions such as
extraversion-introversion (E} may be reflected in neurophy-
siology. Gale, Coles and Blaydon (1969) have reviewed the
literature on the EEG and have added their own important
.studies; they conclude that the evidence from the EEG is
fairly convincing. Introverts tend to have higher alpha
frequencies and lower amplitudes (i.e. higher arousal levels),
extraverts lower alpha frequencies and higher amplitudes
(i.e. lower arousal levels). Studies of ERPs have shown
shorter latencies and greater amplitudes (i.e. greater
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arousability) for introverts, longer latencies and lesser
amplitudes (i.e. lesser arousability) for'extraverts
($telmak, Achorn and ~lichaud, 1977).
The ability to monitor brain activity makes it possible
for researchers to examine the relationship between subjective
states, behavioral changes, individual differences, psychotropic
drugs and the electrophysiology of the central nervous system.
In the field of tobacco smoking, interest has focussed
primarily on investigations on the acute eEfects of tobacco
on EEG and ERPs (Thornton, 1978; R~mond and Izard, 1979).
Relatively few studies have examined the question of whether
smokers exhibit quantitatively distinct EEG and ERP characte-
ristics from non-smokers. If specific EEG and ERP activity
are characteristic of the smoker, those may point to a
possible predisposing neural mechanism underlying smoking
motivation. As is true in most research areas however, what
appears to be an easily answered question - do smokers show
distinguishing EEG and ERP characteristics - turn out to
be difficult to investigate. This question can break down
into a series of questions requiring investigation, some
of which present difficult methodological problems which make
clear-cut answers hard to obtain. For example, with respect
to EEG, one could make the g~neral question more complex
by asking whether the differences observed are (a) widespread
or predominantly localised in specific brain areas; (b) stable
during both resting and activated (eg. task oriented) conditions
and (c) related to the degree of smoking (i.e., light, moderate
and heavy smoking) and length of abstinence?
It is not within the scope of this section to consider all
the studies that have been carried out in this area. For our
purposes it is best to avoid the many controversies attendant
upon this area and we shall simply and briefly present two
studies on EEG alpha activity and two studies on visual ERPs
which reflect the inconsistency of the results to date.
Brown (1968, 1972) found that all active smokers and former
heavy smokers exhibited significantly higher resting alpha
frequenci~.s than non-smokers and former av~r;bge smoker groups.
• The abundanc~ of alpha activity present in the EEG was similar
for all groups except that for very heavy sn~kers who exhibited
significantly half the amount of alpha per unit of time. As
with Brown's findings on alpha abundance, Knott and Venables
(1977) observed no significant differences between smokers
and non-smokers, but in contrast to their data on alpha
frequency, these researchers found that non-smokers, in
¢ontrast to Brown's smokers, exhibited the higher resting
dominant alpha frequency. With respect to ERPs to visual stimuli,
Brown (1968) observed that smokers exhibited slower latencies
and smaller amplitudes than non-smokers. Knott and Venables
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(1978) however observed contradictory results in that smokers
showed faster latenci~s and larger amplitudes to visual stimuli
compared to non-smokers.
As with the previous studies on personality differences
An smokers and non-s~kers, these EEG and ERP findings are
based on a single testing of subjects with a long history
of tobacco smoking and th8 temporal or causal relation
between electrocortical findings and smoker vs. non-smoker
differences is unclear. Two rival interpretations may be
suggested: (i) the electrocortical patterns precede tobacco
smoking and may be related to possible neurophysiolgoical
and psychological states which predispose individuals to
smoking; or (2) the electrocortical patterns are a
neurophsyiologycal consequence of prolonged smoking. Again,
as with the preceeding personality studies it is.clear that
a longitudinal study is necessary in order to choose between
the rival hypotheses.
5. Prenatal mechanisms
The predisposing factors thus far discussed have been those
most possibly related to genetic inherited biological
mechanisms. There is, however, an additional and obviously
different possibility for predisposition i.e., the prolonged
exposure to the fetus to high levels of tobacco smoke in
utero. It is now widely accepted that maternal smoking in
pregnancy is associated with reduced foetal growth and therefore
with an increased incidence of infants who are small for
dates(SFD) (Simpson, 1957). As Scarr (1969) has observed
an association of low birth weights (less than 2,500 grams}
with deleterious effects in later brain and intellectual
development, there has been an .increasing research interest
on the long-term effects of smskinq in pregnancy on the
child. Whereas Hardy and Mellets (1972) found no difference
in intellectual functions up to the age of 7 years between
children of smokers and non-smokers, others have found significant
differences in reading, mathematics and general ability skills
. between the ages of 7-11 years, with children of mothers
who smoked exhibiting the slower development (Davie, Butler,
and Goldstein, 1972; Goldstein, 1972; Butler and Goldstein,
1973). These latter findings were confirmed more recently
in 7 year olds where children of mothers who smoked during
pregnancy exhibited: a higher (non-significant) frequency
of neurological abnormalities, including minimal cerebral
dysfunction and abnormal and borderline electroencephalograms
(EEG)~ lower scores in general on the Wechsler Intelligence
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Scale for Children (|qISC), and more specifically on sub-tests
of vocabulary, block d~sign and coding; higher adverse scores
on Haggerty-Olson-Wickman Behavior Rating Schedule scored by
teachers; Igram and Hunter, 1977). Denson, Hanson and
Me|darters (1975) have also noted an association between
hyperkinetic children and smoking in that mothers of
methylphenidate-sensitive hyperkinetic children were reported
as smoking two to three times as many cigarettes as the mothers
of normal controls. These studies are in marked disagreement
with Lefkowitz's (1981) recent findings which failed to find
any significant differences in the i0 year old offsprings
of mothers who smoked and did not smoke during pregnancy.
Measures of physical, intellectual, affective and personal
and social functioning were similar for both groups of children.
At this stage one can only speculate on the possible
biological mechanisms which may be operative in pregnancy and
thus responsible for the developmental differences observed
5etween children of smoking and non-smoking mothers. Carbon
monoxide (CO) crosses the placenta during pregnancy and the
CO concentrations of the fetus of smoking mothers is
significantly higher than in the fetus of non-smoking mothers.
As CO has a much higher affinity for hemoglobin than oxygen,
relative hypoxin may be a major biological factor operating
in the fetus. Nicotine may e:ert an effect at various levels.
For example, tobacco smoking is known to reduce appetite and
smoking mothers may exhibit reduced food consumption relative
to non-smoking mothers and this may impair the nutritional stake
of the fetus. Nicotine also causes vasoconstriction and may
constrict the uteroplacental vessels, thereby placing the fetus
in a state of relative hypoxia. Nicotine may also operate on
a more direct level by acting on neuronal systems within the
developing brain of the fetus.
Although all these factors may operate alone or in combination,
Yerushalmy (1971,1972) has raised the important question
of whether differences between the outcome of pregnancy in
smoking and non-smoking women might be due to the characteristics
of smokers rather than the smoking per se. For example,
Yerushalmy (1972) reported that the prevalence of low birth
weight infants was higher for non-smoking women who later
became smokers than for women who never smoked. This is
suggestive that the low birth weight was due more to the
smoker than to the smokin@, in accord with the genotype hypothesis.
Yerushalmy (1972) also observed that low birth weights were
significantly less prevalent among infants of smoking women
who later stopped smoking than among infants of regular
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continuing smokers. The birth weights of i'nfants of smoking
women who were to become ex-smokers were rather comparable
to the higher birth prevalence among infants of non-smoking
women. This is also compatible with the theory that low
birth weight is more a consequence of the smuker than of
smoking.
EMPIRICAL INTEGPATION
1. Need for a lonqitudinal study
The preceeding discussion has focussed on traits of
the organism as being important determining factors in
tobacco use. In searching for organismic conditions.that result
in a higher probability for tobacco use the ques6ion is
posed as to "what is given". Central to this is the suscep-
tibility of the individual. As poorly understood as are most
mechanisms involved in the development of smoking behavior,
the nature of increased individual susceptibility has been
perhaps the least adequately explored. As observed in the
previous discussions, this is probably true because of the
theoretical and methodological difficulties in such studies.
These difficulties revolve about the following points:
(1) there is evidence that increased susceptibility may be
genetic, neurophysiological, developmental, physiological,
psychologic, social or the consequence of prolonged tobacco
use~ (2) it is literally impossible to separate out the effects
of these various influences because they all operate concomitantly;
(3} the effects of prolonged tobacco use are particularly
difficult to parcel out because the characteristics of tobacco
smokers can only be determined in smokers who by definition
show the effects of prolonged consumption of tobacco.
These points emphasize the difficulty of developing etiological
findings from studies based on individuals who are already
smokers and they stress the long recognised need for the
implementation of a longitudinal study which carries out its
.measurements on a defined population prior to acquisition of
smoking behavior. In a "real time" prospective longitudinal
study where the goal is to examine predictors of specific
future events or behavior, the researcher selects an appropriate
aged child sample at time 1, examines its members for
frequency of the target behavior (eg. smoker vs. non-smoker
status), collects measures which are to be used as predictors
and then waits for a suitable follow-up period to measure
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again at time 2 the frequency of the target behavior. Then,
with appropriate statistical procedures, one examines the
relationship of the proposed predictors collected at time 1
with the presence or absence of the target behavior at time 2.
Robins (1980) has detailed the theoretical and technical
aspects of working within longitudinal studies of normal and
pathological development and it is obvious from their presen-
tation that there are certain methodological advantages in the
longitudinal approach in the tobacco area: (i) the subjects
are not yet smokers; they have not experienced the epiphenomena
of long-term smoking. Thus their reactions on tests and
measures are not heavily colored by these epiphenomena~ (2)
the researchers, relatives, and the subject himself do not know
that he will become a smoker. This relieves the data of a
certain part of the burden of bias; (3) the information
gathered is current, not retrosepctive; (4) the data. are
uniformly and systematically obtained. This is in contrast
to retrospective studies which make use of childhood records
concerning adult smokers; (5) one advantage of the longitudinal
method is that the ideal controls for the children who become
smokers are the children (matched for sex, sociocultural status,
etc.) who remain non-smokers. Such controls are an integral
part of the design.
In summary, we have criticized research into primaryetiology
based on smoker populations because the resulting observations
are so heavily contaminated by nonprimary phenomena. Research
on primary etiology is research into causes and the longitudinal
approach is one of the best approximations to this goal. This
is not to say that the prospective approach is without problems.
A long-term longitudinal study of a relatively large sample
faces certain problems including maintaining the sample, loss
of key personnel, appropriateness of measures, etc. In addition,
the longitudinal procedure yields correlative data and it is
extremely difficult to securely construct unequivocal causative
statements without experimental manipulation. Experimental
manipulation is the method of choice in research of the cause
of a behavior. With this in mind, of the masses of research
on the already smokers and the effects of tobacco on smokers
there is doubtless much which does relate to etiology. Information
on premorbid characteristics would be of great value in culling
these etiologically relevant findings. In this manner the two
methods may be mutually supportive.
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V. TOBACCO AND STRESS REDUCTION: AN OPERATIONAL FRAMEWORK
Having observed the need for longitudinal investigations
in researching etiological mechanisms in smoking behavior, one must
formulate a parsimonious scientific framework or theory of
susceptibility and proceed to test the hypothesis it generates.
The hypothesized increased response to tobacco smoke of the
susceptible individual can be designated as an element in the
development of acquisition of the habit, regardless of whether
that increased response is due to biochemical, physiological,
neurophysiological, or psychological mechanisms. In each or any
of these cases, the change is presumably from an aberrant state to a
more "normal" one or from a "normal" state to a more "pleasant"
one, and this change is translated into a psychologically
rewarding experience. Thus within this frame of reference
physiological processes are translated into psycholqgical
reactivities on which the principles of the reward conditioning
paradigm are fully operative. This may be conceptualized as a
psychophysiological paradiqm. Under these circumstances each
successive rewarding experience strengthens the conditioned response
(smoking) and the habit develops. Given a susceptible population,
the question still arises: Why specifically do they smoke?
Clues to the reasons why smokers smoke have been obtained by
investigating the acute effects'of tobacco inhalation on
psychological and psychophysiological functioning.
1. Affect
A key to the understanding of smoking behavior is to be
found in the management of affect. If you ask smokers why they
smoke, overwhelmingly they respond in sedational terms. In a
study by Meyer, Friedman and Lazersfeld (1973), smokers were asked,
"Why do you smoke?" The question could be interpreted historically
(How did you get started smoking?) or instrumentally (What do you
get out of smoking?). Of 126 respondents, 76 interpreted the
question instrumentally. Of this group, 64% answered in
sedational terms, that is, with such replies as, "It
relaxes me," "It calms me down," and so on. Not a single
respondent answered in terms that could be coded as indicating arousal,
such as "It stimulates me," or "It bucks me up." And these are
typical results. Aqu6 (1973) asked smokers to fill in a Mood
Adjective Check List before and after smoking a cigarette at
different times of the day. Although there were interactions
with time of day and test conditions, in general smoking was
found to increase feelings of relaxation and decrease feelingsl
of aggression, anxiety and tension. These effects were greatest for
high nicotine cigarettes. Tomkins (1962) has classified a number
of types of smokers in the smoking population. Many of the smokers
are "negative affect" or sedative smokers. They smoke when the
negative affect (distress, anger, worry, fear, shame, contempt, etc.)
gets to a certain intensity or when they feel that negative affect
is increasing to a high level or indeed when they anticipate negative
affect will increase in the near future. Russell, Pete and Patel
(1974} found that many smokers report smoking when anxious or angry;
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the proportions were 74% of hospital workers~ 93% of patients at
a smoking clinic and 88% of a group of university studnets "(War-
burton and Wesnes, 1978).
The outcome of these studies strongly parallel the findings
on individual differences which were discussed earlier and which
indicated that smokers tend to be characterized by higher neuro-
ticism (anxiaty} scores on personality tests than non-smokers.
Thomas {1978) found that smokers a,d non-smokers could be
differentiated on personality scores with smokers exhibiting
higher anxiety and anger scores than non-smokers. In addition
very heavy smokurs {over 60 cigarettes per day) have been found
to be more aggressive and anxious than heavy smokers (40-60 day)
and the latter felt greater negative affect than average (15-20
day) smokers. Non-smokers felt the least anxious and aggressive.
It is important here to keep in mind that these anxiety
differences do not seem to be a consequence of smoking as the
prospective study by Cherry and Kiernan (1978) showed that
young people with high neuroticism (anxiety) scores were more
likely to start smoking than more stable adolescents. This is
supported by McKennell's (1970) findings that situations of
"nervous irritation" were common occasions for smoking among
adults and ndolescents and by Henderson, Lewis, llowell and
Rayner's (1981) study of a secondary school population where
a significant positive association was found between the probability
of a neurotic disorder and use of tobacco. That this association
was significantly stronger in female adolescent smokers is of
particular interest in that it concurs with Frith's (1971)
observation that a greater proportion of female smokers than male
smokers reported a desire to smoke in high-arousal situations.
A common picture of smoking as a stress reducer emerges from
these studies and they are to a great extent supported by Lindenthal,
Myers and Pepper's (1972) study on the relationship between smoking,
psychological states and stress. Here, life crises were signifi-
cantly related to psychological impairment and a significant ....
positive association was observed between frequency and
intensity of life crises, degree of psychological
impa~rment and smoking intensity. These authors concluded that
t~eir data supported the notion that smoking served as an adaptive
behavior for coping with life's exigencies. Mills (1978) has
discussed the possible role of tobacco as a coping mechanism in
high-arousal situations and there is a growing consensus that
tobacco functions as a psychological tool in the attenuation
of stress (Stepney, 1979, 1980). Warburton and Wesnes (1979)
have suggested that tobacco (nicotine), like anxiolytics, acts
as a negative reinforcer by reducing the unpleasant emotional
experience of anxiety/arousal provoked by the internal or
external environment. Anxiolytics, however, do not exhibit
similar biochemical or electrophysiological actions as
nicotine and furthermore, anxiolytics are of little aid in
smoking cessation. In an attempt to elucidate specific mechanisms
of action, a great deal of research has focussed on behavioral and
physiological eoncommitants of tobacco-induced stress reduction.
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2. Performance
Studies on the effects of cigarette smoking on human
performance suggest that nicotine and smoking may enhance
behavioral efficiency on sensorimotor and cognitive functions
by increasing arousal. Improvements in sensorimotor tasks following
smoking or oral ingestion of nicotine tablets have been
repeatedly observed in long-term vigilance and signal detection
tasks which in Kahneman's (1973) terms, require sustained
mental effort (Frankenhauser, Myrsten, Post and Johansson, 1971;
Mangan and Golding, 1978; Tong, Leigh, Campbell and Smith, 1977;
Wesnes and Warburton, 1978; Myrsten and Andersson, 1978; Waller
and Levand~r, 1980}. These improvements are considerable, if
comparisons are made between deprived smokers and non-deprived
smokers. Typical non-smoker performances, however, usually
lie between these two extremes. Both Battig (1980)" and Stepney
(1979) have commented that it is difficult to interpret these
results as the observed differences may be attributed to a
performance reduction caused by nicotine deprivation, to a
performance improvement induced by the administration of nicotine,
or to both of them. Indications that improvement may actually
reflect on nicotine-enhancement effect is seen in Heimstra,
Fallesen, Kinsley and Warner's (1980) study which showed that
vigilance tasks were not affocted by smoking deprivation and
also by Wessnes and Warburton's (1978) study which made use
of nicotine tablets and found improvements in the performance
of non-smokers as well. Studies on cognitive functioning,
or more specifically learning and memory, have indicated that
smoking exerts adverse effects on short-term memory and improves
long-term retention as measuerd by delayed recall (Andersson and
Post, 1974; Andersson, 1975; Myrsten and Andersson, 1978;
Williams, 1980) .
As studies on learning and arousal agree that high arousal
during learning leads to improved ultimate memory (Kleinsmith
and Kaplan, 1963; Berlyne, Borsa, Hamacher and Koeing, 1966;
Walker and Tarte, 1963) but leads to detrimental effects on
immediate recall, the results of the above tobacco-learning studies
were interpreted on the basis of the arousal-increasing properties
of smoking. Although this proposed general arousal mechanism
seems to be an adequate hypothesis for these tobacco-induced
performance changes, an alternative second-order interpretation
based on Easterbrook's (1959) data suggests that increased arousal may function by narrowing the
focus of attention
(i.e., subjects sample a smaller range of potentially distracting,
irrelevant external and internal stimuli and focus selectively
on relevant stimuli). This increased ability to attend
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selectively to certain relevant aspects of "the stimulus field
whale simultaneously inhibiting responss to other aspects of
the field may account for Andersson and Hockey's (1975) findings
that smoking reduces the incidental learning of irrelevant
stimulus material. The results imply that attentional processes
are affected by cigarette smoking in the samu way as by other
arousal-increasing events. Easterbrook's hypothesis, proposing
that the range of cues are reduced in states of high arousal,
was supported by these findings. This increased selectivity of
attention by tobacco may well be the basis of the frequent
reports by smokers that smoking improves their concentration
and that not smoking results in extreme difficulty in concentration.
As with the cognitive studies, tobacco-induced improvement
in vigilance performancQ has frequently been interpreted within
arousal theory, and indeed there is a solid body of data supporting
relationship between arousal and vigilance (Mackwort~, 1969;
Tong, Henderson and Chipperfield, 1980). However, this data
may also be interpreted specifically within an attentional
framework as Mangan and Gelding's (1978) results indicated
conclusively that smoking improves vigilance performance by
decreasing the subjects errors of con~nission (false positive)
rather than by improving his detection rate.
The notion that the attraction of tobacco may lie in its
ability to screen or block out disruptive, distracting effects
nf irrelevant input on ongoing tasks and performance has been
forwarded by a number of researchers (Dunn, 1978; Knott, 1978,
1979; Warburton and Wesnes, 1978, 1979; Wesnes and Warburton,
1978). The empirical basis for this approach is based in part
on studies which have shown that tobacco does not appear to
have any consistent effect on short-term performance proficiency
under conditions conducive to good performance (Dunn, 1978;
Stepney, 1979), but it does seem to offer an advantage under
conditions likely to interfere with performance. Initial support
is forthcoming from studies which show that nicotine reduced
the distractibility on the Stroop task (Wesnes and Warburton,
1978) and that tobacco smoking .counteracts the decrement in
reaction time performance observed under distracting noise
conditions (Tong, Knott, McGraw and Leigh, 1974).
In contrast to Warburton and Wesnes (1979) who emphasize
the impact of tobacco on performance as being an enhancement
of signal or relevant target information, due to increased
arousal, both Dunn (1978) and Knott (1978, 1979) have emphasized
the inhibitory role of nicotine and tobacco in dampening down
the impact of hyper-arousal responsivity on task performance
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induced by disruptive, distracting input. An initial study by
Dun, (1978) on the disruptive effects of frustration on anger
~Id performance proficiency in a complex perceptual-motor task
supported this notion. Here, smokers and non-smokers displayed
the same increases in anger, but the performance proficiency
scores of the smokers were significantly superior to the scores
of both deprived and non-smokers during the anger-inducing period.
In Dunn's word's, "... the smoker is unwittingly triggering a
physiological response sequence when he smokes which has the
effect at the psychological level of improving his coping
efficiency in face of otherwise disruptive influences... I am
suggesting that ... the subjects emotional or affective arousal
had reached a level such as to impair ongoing task performance
and that the arousal did in fact impair the performance of the
non-smoking and placebo subjects. The smoking subjects, however,
were invoking protective physiological mechanisms that had the
psychological effect of insulating ongoing performance from the
disruptive influence of excessive arousal. Smoking .may be having
a negative or inhibitory effect upon the intrusiveness of excessive
affective arousal upon ongoing behavior (p. 22)." This data is to
a great extent supported by studies which clearly show that
nicotine can play a significant part in reducing the disruptive
effects of stress (electric shock) on behavior in animals
(Stepney, 1979, 1980).
Recently, based on his electrocortical findings which suggested
that tobacco "normalized" central nervous system activity of
smokers to a level comparable to that of non-smokers (Knott,
and Venables, 1977, 1978), a "filter model" was proposed by
Knott (1978, 1979) to relate the relative attentional deficits
in deprived smokers and improvement by tobacco to the frequently
reported sedational or stress-reducing effects of smoking
(Gilbert, 1979). The model hypothesized that (a) relative to
non-smokers, smokers deprived of tobacco exhibit an inefficient
central filtering mechanism for gating out irrelevant, distracting
stimuli and experience input more readily and more strongly and
as a result are characterised by a distressed state of relative
stimulus overload inappropriate for efficient performance and
(b) the attraction of tobacco smoking may lie in its ability
to normalize control of stimulus input thereby relieving distress
and improving performance and subjectivo well-being. The filter
mbdel runs parallel to findings of greater irritability to
intense stimulation and reduced pain thresholds, i.e., greater
sensitivity to pain, observed in smokers relative to non-smokers
and subsequent increasing pain thresholds and decreases in
stimulus irritability following smoking (Nesbitt, 1973;
Schachter, 1973, 1978; Seltzer, Friedman, Siegelaub and Collen,
1974).Initial behavioral support for smoker vs. non-smoker
differences on susceptibility to distraction effects was
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observed by Knott's (1980) finding that high intensity auditory
noise significantly impaired smokers performance on a choice
reaction time task but had no effect on non-smokers. A subse-
quent (1981~ study further indicated that female smokers, who
have been reported to have their greatest distraction induced
deterioration in choice reaction. Although this data is
colored by possible secondary phenomena such as long-term
tobacco effects and influences of deprivation, they may be
suggestive of predispositional factors relating ~o the onset
of the smoking habit.
3. Psychophyslology
All of the evidence from the performance studies provide
strong support for the notion that tobacco smoking reduces
perceived stress by inhibiting indiscrimate arousal responses to
disruptions bv internal and external input~his neatpicture is
complicated, however, by what is probably the least equivocal,
best established fact about the physiological consequences of
smoking - namely that it seems to lead to widespread increases
in nervous system arousal with the most obvious alternations
bei0g exhibited within the peripheral autonomic nervous system.
Larson, Haag and Silvette (1961) have remarked that there are so
many peripheral effects of nicotine that the central effects
seem to be obscured. Similarly, the Surgeon General's Report
(1964) showed that "Smoking I to 2 cigarettes causes in most
persons, both smokers and nonsmokers, an increase in resting heart
rates of 15 to 25 beats per minute, a rise in blood pressure of
i0 to 20 mm Hg systolic and 5 to 15 mm Hg distolic, and
an increase in cardiac output of about 0.5 I/min/sq.m. (p.318)."
In short, there are a host of transient increases in physiological
responses to smoke inhalation and they include elevated heart rate,
elevated coronary flow, elevated blood sugar level, lower cutaneous
temperature in the extremities, increased blood flow in skeletal
musculature, a reactive release of adrenalin and alterations in
electrical potential patterns of the brain (Dunn, 1973), all of
which are customarily associated with increased states of arousal
or activation or emotionality. As theories of emotion view
increased autonomic arousal as an essential component of emotional
processes, and as tobacco increases physiological arousal yet
freguently reduces behavioral effects of arousal and self-report
measures, an intriguing paradox pervades the motivational literature.
Recently, there have been an increasing number of studies and theories
(Gilbert, 1979; Schachter, 1973) that pertain to the resolution
of these apparently contradictory findings and there is a general
picture emerging which indicates physiological evidence for tobacco
induced arousal reduction as apparent in specific electrophysiolo-
gical measures and eliciting this response it is important to look"
at the effects of nicotine, not in isolation, but in conjunction
with the situation in which the nicotine is administered, and also
in relation to the personality of the subject. The combination of
these three factors (amount of nicotine taken in, arousal-
producing situations and low or high-arousal organism) determines
the outcome of any tobacco experiment.
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Neurophysiological studies in animals are in general agree-
ment that the effects of small and medium does of nicotine on the
central nervous system (CNS) aro biphasic, there being a marked
sequential effect, with a primary arousal phase being followed by
a secondary depression effect on electro corticograms (Schaeppi,
1967; Goldstein, Beck and Mundschenk, 1967). There is also
evidence that while small dose of nicotine increase arousal, larger
doses may decrease arousal. Thus, Armitage, Hall and Sellers (1969)
found that dosus of 2 mg/kg every thirty seconds for twenty minutes,
given intravenously to eats, caused desynchronization of the electro-
cardiogram indicating cortical activation, and an increase in
the release of cortical acetylcholine. However, a larger dose
given less frequently (4 mg/kg every minute for twenty minutes}
caused sometimes an increase and sometimes a decrease in cortical
activity, such changes being accompanied by an increase or a
decrease in cortical acetylcholine output. On this basis and
on the basis of the previously discussed distraction based stress
hypothesis, one would expect that the action of tobacco or
nicotine on the human EEG should mimic the action of anxiolytics
but the electrophysiological evidence does not strongly support
this notion. In a pioneering comparison of nicotine and an
anxiolytic (Murphree, Pfeiffer and Price, 1967), the means and
variance for the total energy increased across the spectrum of
EEG activity after the anxiolytic while there was a general
reduction in means and variance across the whole spectrum for
nicotine. It was concluded that the nicotine changes were more
typical of a stimulant drug than an anti-anxiety compound. Sub-
sequent EEG studies, reviewed by Conrin (1980) bare for the
most part focussed on 8-12 I1z alpha activity and are in general
agreement that tobacco smoking increases the dominant alpha
frequency. Knott and Venables (1977) observed a "normalizing"
effect of tobacco inhalation on dominant frequency. Analysis of
pre-smoking activity revealed a slower dominant frequency on
deprived smokers relative to non-smokers and non-deprived smokers
and the immediate effect of smoking was to increase dominant
alpha frequency in deprived smokers to a level comparable to non-
smokers and non-deprived smokers. Instead of relating these findings
:to an arousal phenomena, Knott and Venables cited a solid body of
literature which suggested that dominant alpha frequency reflected
a CNS scanning or gating process involved in stimulus-input and in
cognitive processing (Lykken, 1975). As this tobacco-induced
shift in EEG frequency may reflect improved cortical scanning and
• speed of cognitive processing, the authors suggested that smokers
may smoke in order to achieve the psychological state of increase~
vigilance and attention associated with this shift. On this basis
it would seem that this repeatable shift in dominant frequency induced
by smoking may have particular functional significance in relation
to both the distraction hypothesis discussed earlier and in relation
to predisposing electrophysiological factors to the smoking habit.
> The dominant rhythm appears to reflect CHS maturation, appearing
at 3 or 4 months of age at 3-4 Hz and increases to the adult
frequency of about 10 Hz at about 10 years of age. This rhythm,
although responsive to static factors, under normal circumstances
remains constant day in and day out and month by month(Lindsley
and Rubenstein, 1937). Is it possible, that the slower rhythm in
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deprived smokers represents a delayed CNS maturation, and hence
a relatively inherent perceptual deficit which may 'set up' a
need or predisposition for tobacco (or some other substance, or
activity) which is readily available and can specifically alter
the rhythm at any given time?
: As it is reasonable to suppose that the satisfaction of tobacco
smoking is ultimately dependent upon cerebral events, a number of
studies have focussed on the measurement phasic potentials which
sensory stimuli evoke (ERPs} in the cortex as a way of studying
cerebral processes. The initial study by Hall, Rappaport, Hopkins
and Griffin (1973) on visual evoked potentials showed that tobacco
smoking increased amplitudes of late components (more than 80 ms
after stimulus onset), changes which are consistent with the
contention that tobacco increases arousal. Later studies by
Friedman, Goldberg, Horvath and Meares (1974), and Friedman
and Meares (1980) suggested that the tobacco effect may be modality
specific, increasing late components of the visual evoked poten-
tial and decreasing late components of the auditory evoked potential.
The reduction in late auditory evoked potential components is of
interest in that Knott (1980) had shown that the performance of
smokers as compared to non-smokers, was significantly more affected
by high intensity noise. Knott and Venables (1978) observed a
"normalizing" ~ffect of tobacco smoking on visual cortical evoked
responses in that deprived smokers evidenced faster latencies and
larger amplitudes (i.e. more sensitive) than both non-smokers and
deprived smokers who exhibited comparable responsiveness. The
authors suggested that a possible attraction of tobacco smoking may
lie in its ability to function as a "chemical stimulus filter"
thereby reducing the distracting effect of irrelevant, adverse
stimuli on p~rformance efficiency and emotional tonus. Complimentary
results are provided by Vasquez and Toman's (1967) observation-of
a decrease in late E.R.P. amplitudes during smoking, an increase
during abstinence. These evoked potential studies r~ceive some
support from an animal investigation by Pradhan and Guba (1976) who
recorded from the auditory cortex of cats and observed that the
initial effect of smoking dosages of nicotine (12.5 mg/kg) reduced
~oth amplitude and area measures of late components of the auditory
evoked response. This appeared to be an apparent selective effect
as nicotine produced general CNS excitation at the same time.
A number of additional electrophysiological studies have
provided support for the notion that tobacco dampens CNS responsivity
to stimul input and therefore they are of particular interest
for the distraction hypothesis. Friedman, Horvath and Meatus (1974)
and Mangan and Gelding (1978) found that tobacco smoking increases
the speed of habituation of CNS (alpha blocking) and ANS (skin
Conductance responses) responding to repeated presentations of high
intensity auditory stimulation. These authors suggested that a
possible means of reinforcement of tobacco smoking may lie in its
ability to stimulate CNS inhibitory mechanisms (without simul-
taneous reductions in CNS excitatory processes) resulting in the
"screening out" of irrelevant and irritating sensory input into
consciousness. In this regard, it is interesting to note Mangan
and Gelding's (1978) observation that inhibition of momentary
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spontaneous imbalances in autonomic arousal may be a physiological
basis of tobacco induced improvement in vigilance performance.
During their vigilance task, it was observed hhat false positives
occurred most often immediately following a spontaneous skin
conductance fluctuation. As smoking reduced both spontaneous
fluctuations and false positives they inferred that performance
improvement was due to the increased stability of the autonomic
arousal system. The possibility that smokers may exhibit greater
autonomic responsivity than non-smokers was confirmed by Knott
(1980) who observed that smokers exhibited significantly higher
resting skin conductance levels, faster response latencies,
large response amplitudes and significantly faster and larger
cardiac accelerations to a high intensity auditory stimulus. More
recently Knott (1981b)has observed that female smokers relative to
male smokers and female and male non-smokers, exhibit significantly
higher resting skin conductance levels and larger skin conductance
responses to high intensity auditory stimuli. This is in line
with a previously discussed study which indicated that "female
smokers exhibit a more frequent craving in high arousal~anxiety
situations.
The contingent negative variation (CNV) is a small scalp-
recorded negative potential which slowly builds up between a warning
signal and an imperative signal (such as in a standard fore
period reaction time task) requiring the subject to carry out some
response, usually a motor response such as pressing a button.
This slow cortical potential occurs in an expectancy situation
is sometimes referred to as an expectancy wave. Tecce,
Savignano-Bowman and Cole (1978) have proposed that two pro-
cesses of arousal and attention become coupled under drug
administration, such that over increase in attentional demand
will increase arousal, but an over increase in arousal will
reduce attentiveness and so attenuate optimal CNV development.
The function of self regulated drug administration such as
smoking is thus presumably to adjust this distrachion - arousal
coupling to an optimal level according to task demand. As
Ashton and Watson (1970) and Ashton, Savage, Telford, Thompson
and Watson (1972) have shown that situational stress radically
affects smoking strategies (i.e., increases puff frequency and thus
nicotine dosage) this theory would predict that individuals differing
in @rousal levels would adjust their smoking parameters accordingly
(e.g. puff frequency, duration, volume etc.) so as to bring CNV
development to an optimal level. Studies on CNV, tobacco and
individual differences have on th~ whole supported this contention
and failure to take into account personality differences may have
been the basis for the non-significant tobacco effect on CNV
observed by Knott and Venables (1980). The initial study by
Ashton, Millman, Telford and Thompson (1974) and a subsequent
study by Eysenck and O'Connor (1979) showed that individuals
high in cortical arousal (introverts) exhibited consistent
CNV amplitude reductions (depression) following tobacco smoking
while individuals rated low in cortical arousal (extraverts)
showed consistent increases in CNV amplitude (stimulation)
following smoking. Estimates of nicotine intake (such as puff
volume, frequency, butt analysis) indicated that extraverts
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took in more nicotine than introverts. Subjects who said they
were relaxed by cigarette smoking tended to show a diminished
CNV and these results parallel reports of a greater desire to
smoke for tranquilization and stress-reduction in introverts
(Gilbert, 1980). Subsequent studies by Ashton, Marsh, Millman,
Rawlins, Telford and Thompson (1978) on effects of intravenous
injections of various smoking does of nicotine on the CNV
produced a dose-response relationship in which smaller doses were
found to have a stimulant effect and large doses a depressant
one. On commenting on these findings, Stepney (1979) stated
that smoking is capable of producing either stimulant or depressant
CNS effects, depending on the smoker's environment and the dose
of nicotine taken, and that the point at which the nicotine dose
crosses over from having a stimulant effect to having a depressant
one is within the range of dose that can be obtained from a
cigarette. This would give the smoker an extremuly useful tool
for arousal control. The notion that smokers may use cigarettes
to obtain a specific effect on arousal in the context 6f the
demands of a specific envirol~ment is supported by a study by
Myrsten, Andersson,Frankenhaeuser and Elgerot (1975). Here,
smokers who self-reported their strongest need to smoke under low-
arousal conditions (low-arousal smokers) performed and felt
better when smoking under laboratory tasks of low complexity and
smokers who self-reported their strongest need to smoke under
high-arousal conditions (high-arousal smokers), performed and
felt better when smoking under laboratory tasks of high complexity.
As with extraversion-introversicn, one may predict from the
above studies that under conditions of stress and overload, high
neuroticism scoring subjects should benefit more from smoking
than low neuroticism scoring subjects. Studies by Kucek (1975)
andWarburton and Wesnes (1978} bear this out. In the former
study, subjects were tested in an experiment under conditions
of information overload and smoking had a beneficial effect on
the performance neurotic subjects. In the Warburton and Wesnes
study, an attentional vigilance task was employed and it was
found that smoking helped high N scoring subjects, but not IQw N
scoring subjects. The correlation between improvement and neuro-
ticism was 0.68 which indicates the importance of personality
in evaluating the effects of smoking on performance and stress
reduction.
Finally, an additional target physiological system implicated
in tobacco-induced stress reduction is skeletal muscle activity.
A number of studies have reported on the effects of nicotine and
tobacco smoking on skeletal muscle tone in men. webster (1964)
reported a short-lived reduction in muscular tension in spastic
patients after smoking a single cigarette and Domino's (1973)
study showed a significant reduction of the patellar tendon reflex
(knee jerk) and associated clectromyographic (EMG) musculature
following tobacco smoking and oral administration of nicotine
arousal. Hutchinson and Emley (1973) established that deprived
smokers showed an increased frequency and force of spontaneous
masseter EMG contractions and found that 5 mg of nicotine in
water decreased the frequency and force of masseter EMG Jaw
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contractions to intense auditory stimuli in both smokers and
non-smokers. This consistent picture is disturbed, however by
Fagerstrom and Gotestam's (1977) study which showed that
resting EMG activity of the trapez~us neck muscle increased during
tobacco smoking. One must conclude that nicotine, or at least
tobacco smoking of varying nicotine content, has biphasic effects
as far as EMG activity is concerned. Stimulant and depressant
effects seem to be dependent on both the site of recording and
whether or not one is focussing on tonic or phasic components.
4. Neurophysio lopy
Up to this point, the neurophysiological mechanisms relevant
to the proposed filter model have not been discussed, and although
at this stage of research it is recognized that discussion is
purely speculative, some recent neurophysiological research is
worth mentioning. Jasper (1958) and other researchers IDemetrescu
and Demetrescu, (1962) have implicated the reticular formation
in controlling selective responsiveness to significant stimuli
by preventing general alerting actions to al~ incoming stimuli
and this focus parallels the findings of investigations which
found significant effects of nicotine on this CNS site (Domino, 1967).
However, as with recent empirical data which has focused on the
role of the limbic system in the control of attention, nuurophy-
siological investigations of nicotine action have also attributed
the effects of nicotine to changes exerted by the limbic system.
Here, employing electrophysiological measures, Nelson and
colleagues'(Bhattacharya and Goldstein, 1970; Nelson, Pelley
and Goldstei~, 1973) have provided evidence that the hippocampal
limbic system is a major target area for nicotine, in that cortical
activity under nicotine treatment is controlled more by the
hippocampus than by the reticular formation. Based on Routtenberg's
(1968) hypothesis that hippocampal activity inhibits the reticular
formation, Nelson (1974) hypothesized that the neurophysiological
mechanisms underlying nicotine-socking behavior lies in its ability
to counteract inappropriate responding by the reticular
formation, by its (nicotine) action on the limbic system. Support
for this hypothesis was observed in their animal investigation
in which nicotine treatment was found to counteract decreased
performance in selective attention which was induced by electrical
stimulation of the reticular formation. On this basis, these
authors suggest that a possible motivation underlying smoking
behavior is its ability to reduce reticular excitation which
is manifested in a hyper-stimulated anxious state inappropriate
for effective behavior and to engender what might be considered
a state of useful behavioral arousal. In relation to the filter
model, it is interesting to speculate here whether the often
reported relaxation smoking is related to inappropriate reticular
hippocampal filtering or inappropriate hippocampal limbic control
of reticular filtering' (or both) in deprived smokers relative
to non-smokers.
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Vl ° SUMMARY~ RATIONALE AND OBJECTIVE OF STUDY
An understanding of the etiological factors in the acquisition
of the tobacco habit has remained elusive despite intensive
study by researchers in the biological and social sciences over
the past several decades. While each discipline has contributed
important information on the factors which predispose an individual
to acquire the habit, the necessary conditions for becoming a
smoker have yet to be defined.
While psychosocial factors play a crucial role in habit
onset, the approach of this paper has been to examine the possible
role of organismic trait and state factors in relation to pre-
disposition to smoking. More specifically, the issue raised in
this paper was whether within a population of children there are
individuals who exhibit specific trait and trait arousal factors
which lead to experimentation with and repeated use of tobacco
for its perceived and~or real affects in modifying physiological
and consequent behavioral systems. In general, the ~i~erature
which relied primarily on studies of adult smokers, supported
an arousal interpretation in that:
I. in general, smokers tend to exhibit personality
profiles indicative of physiological hyper-responsivity and
there is evidence to suggest that these profiles pre-date
the smoking habit;
2. in general, smokers report that they smoke to reduce
hyper-arousal and experimental studies support the contention
that tobacco reduces both behavioral and subjective measures
of arousal;
3. in general, and in particular for smokers assessed
as exhibiting high-arousal profiles, tobacco smoking exhibits
a negative inhibitory effect upon the intrusiveness of
disruptive and excessive arousal upon ongoing physiological,
behavioral and cognitive processes.
A good portion oE this paper has been aimed at presenting
available evidence which may be indicative of disturbances in
arousal processes. From the studies cited, it appears that although
no .specific targct physiological system can be complicated in
smoking motivation, it appears that a host of CNS and ANS
irregularities in the direction of hyper-responsivity may
exist in smokers and thus may play a potential role in the
onset of the habit. Integrally linked with this picture is thQ
concept of defective filtering which implies certain characteristics
~f the individuals' attentional style that tends to augment the
intensity and impact of information both from the internal and
external world. For this type of individual the attraction of
tobacco seems obvious, The mechanism of action of nicotine
that has been proposed is not the same as negative reinforcement.
Negative reinforcement occurs when a drug terminates or reduces
a negative affect. Thus an anxiolytic is taken during aversive
events to enable the person to escape from the consequences or
before these events in order to avoid them. Alcoholics seem to
drank for this reason.
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In contrast nicotine enables the smoker to confront his
problems and perhaps overcome them. Thus we would paraphrase
nicotine's action by saying that nicotine is a drug of confronta-
tion and not escapism, a sharpening drug not a blunting drug.
In this way it is a unique anti-anxiety compound. It increases
clarity of thought and decreases distracting, disruptive input
as a consequence of its action on physiological systems
(Warburton and Wesnes, 1979).
In summary, the general trend toward hyper-responsivity
in smokers supports the contention of a "physiological susceptibility"
{acquired or inherited or both) for a coping behavior aimed at
arousal reduction.
Objective
To investigate predisposing psychophysiological parameters
in the acquisition of the tobacco habit by implementing'a 5-year
longitudinal investigation which will:
(a)
examine psychophysiological measures in a population
of children prior to the acquisition of the smoking
behavior; and
(b)
use these measures as a data base for subsequent
follow-up of the sample to identify predictive factors
antedating the onset of smokers status.
VII. SIGNIFICANCE OF THE STUDY
In general it will provide objective, quantified information
on motivationally critical relevant antecedant factors predisposing
to the acquisition of the smoking habit.
In particular, the study will provide objective information
on general "stress responsivity" profiles of smokers prior to the
onset of smoking and this will bc informative as to whether a
"stress-reduction need" is present prior to the acquisition
of smoking as opposed to being a consequence of long term effects
of smoking.
' The acquired data base, both psychological and psychophysiologi-
cal, will be an invaluable source of information for future studies
into (a) motivational mechanisms - e.g. to what extent are adult
smoking parameters, or difficulty in abstinence, etc. related to
pre-smoking characteristics, and (b) health-disease oriented
mechanisms - e.g. to what extent is pulmonary cancer in smokers
related to pre-smokinq characteristics and do certain individual
"stress response" individuals exhibit a higher probability of
cancer proneness regardless of smoking habit, etc.
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VIII.METHODOLOGY
1. Subjects
The study starts with a pool of children to be selected
from various schools of the Ottawa or Carleton School Board.
In order to obtain permission to conduct research withi~l the
schools, a formal proposal including a statement of the problem
area, theoretical framework, hypothesis to be tested, design
and details of the procedures and school resources to be used
will be submitted to the respective research committees. Following
acceptance of the research proposal, individual principals of
several schools will be approached for involvement and a study
protocol and necessary consent forms will be sent to the homes
foe parental consent.
Approximately 300 children (175 males) will be sampled at
II years of age at Year I. Because of the expected higher
frequency of daily smoking in females in the follow-up at
Year V, a larger number of males will be sampled so as to
ensure approximately equal outcome frequency distribution
across sexes. Based on the 1980 statistics of the Department
of National Health and Welfare, the composition of smokers, non-
smokers at Year I and V should be similar to that shown below
(Table I).
YEAR X: AGE Ii; M = 175; F = 125.
NEVER SMOKED TRIED SMOKING
M F M F
SMOKE DAILY OTHER *
M F
M F
N 97.5 80.6 50.4 31.3 2.5 l.l 24.7
12.0
* Other category includes unclassified cases, those who indicated
they had smoked but for whom other details were not known.
YEAR V: AGE 15; M ~ 175~ F = 125.
NEVER SMOKED TRTED SMOKING SMOKE DAILY
OTHER *
M F M F M F M F
N 66.3 37.5 53.2 31.8 36,7 33.8 36.2 21.9
* Other category includes unclassified cases, those who indicated
they had smoked but for whom other details were not known.
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The 300 children will conform to the following criteria:
[I) normal 1.0., i.e. an least 80 on either Verbal and~or
Performance scale of the WISC~ (2) living a~ home; (3) no
neurological or physical disease; (4) no psychiatric history;
{5) no currentmedication. In an attempt to control for socio-
economic factors, the parents occupational status will be
employed as a rough index to ensure a sample selection with
equal distribution across social classes.
2. General Design and Procedures
The five year longitudinal design will consist of 5 stages
as shown below:
YEAR I
-SMOKING ASSESSMENT AND TESTING
YEAR ZI
YEAR III
MONITORING IDENTIFIERS AND DATA ANALYSIS .I
SMOKING ASSESSMENT
YEAR IV
MONITORING IDENTIFIERS
YEAR V
SMOKING ASSESSMENT, RETESTING AND DATA ANALYSIS II
Year I will be concerned solely with the acquisition of
three types of data: (I) descriptors; (2} identifiers;
(3) .predictors.
Descriptors: In essence, the descriptors are variables which
are used as criteria for eligibility to enter the study sample,
and one in the sample, for classification within the sample.
I. this case, the purpose of the descriptors are to elicit infor-
mation on and factors related to the childrens' smoker vs. non-
smoker status. Descriptors will be based on a standard pre-
coded "smoking assessment" questionnaire which will elicit information
on~
0
- personal experience with cigarettes
- circumstances surrounding and reactions to first cigarette
- smoking habits of parents, siblings and friends
- personal attitudes to smoking and reasons for
and against, smoking
- personal attitudes of parents, siblings, friends and
school towards smoking
- knowledge of health hazards arising from smoking
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For the purpose of classification, children wall be cate-
gorized An Year I into one of four categories: non-smoker;
experimental smoker3 ex-smoker and regular &moker. In turn,
each of the smoker categories will be sub-divided to form
groups reflecting variations in frequency of usage.
In addition to these descriptors, all subjects will be
required to give a sample of expired alvealor air in order to
determine carbon monoxide levels. This measure will be used to
assess the validity of the self-reports of smoking behavior in
the children. Children categorized into any one of the
three smoker categories will also be given a "smoking motives"
questionnaire in order to assess the role of cigarette smoking
on psychological factors.
Identifiers: The sole purpose of identifiers is to allow ease
of--~o6-a-t-i-~0f target sample at follow-up. ~dentifier$ will be
established on initial contact with the sample via a pre-
coded standardised questionnaire which will elicit routine
descriptive data such as name, home address, phone, school,
parents work address and similar data for the closest relative.
Predictors: Although the primary predictors in this study are
psychophysiologically based, it is obvious from the literature
review that there is significant interplay between physiological
processes and psychological, social, behavioral and personality
factors in detormining future smoker vs. non-smoker status. On
this basis, the test assessment of the entire sample will
include the following procedures all of which will be obtained
with appropriate consent:
- Standardised psychophysioloqical testing of central,
autonomic nervous system and behavioral reactivity.
- Standardised pre-coded interview with parent having
the major rearing responsibility.
- Standardised personality testing with specific form
on extraversion and neuroticism dimensions.
- Standardised coding of scholastic records and teachers
behavior rating.
- Standardised coding of school medical health records.
- Standardised coding of obstetric records.
Years If, III and IV will involve contact with the
school and/or home to ensure identifiers are updated. Year
III will also involve contact with the sample pool for a
repeated smoking assessment. This will involve the presentation
of the identical pre-coded questionnaire and carbon monoxide
sampling employed for identifying "descriptors" in Year I.
This repaated measurement will form the basis of a more detailed
analysis of early vs. late onset factors in the developmental processes
of ~e tobacco habit.
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Year v, the follow-up period, wili again involve presentation
of the standardised "smoking assessment" questionnaires and carbon
monoxide sampling, flaying obtained this information on smoker vs.
non-smoker status, sub-samples of clearly defined non-smokers,
ex-smokerse experimental smokers and regular smokers will be
retested on psychophysiological measures in an attempt to relate
change in smoker status to changes in physiology.
3. Psychophysiolo~ical Test Battery
The abundance of research procedures in psychophysiology
reflects the popularity of these techniques as a means of testing
models and underlying mechanisms of behavior. In comparison
to clinical judgements and, for that matter, other biological
measures in the clinic, psychophysiological measures aru non-
Invasive, methodologically simple, make few demands on the
subject and have the advantage of providing data that may not
be directly observable. In a similar vein, the covert nature
of the psychophysiological measurement is of potential and
unique value in longitudinal studies of predictors in that,
in contrast to more overt measures, it enables the investigator
to examine aspects of dysfunction possibly before they become
apparent to the outside observer, and even perhaps before they
become apparent to the subject himself.
The choice of target physiological response systems and
procedural paradigms is to a large extent based on previous research
and on the stance of the investigator. As there is no
published psychophysiological data which can be used as a direct
basis for a prospective study on smoking the battery of response
measures and procedures to be employed are chosen on the criteria
that they have been shown to be sensitive to {a) smoker vs.
non-smoker differences and (b) effects of tobacco smoking.
In addition to behavioral reactivity, the physiological response
systems will include tonic and phasic components of:
a. Skeletal muscular activity
I. Electromyographic (EMG) activity
b. Autonomic nervous system activity
Io
2.
Electrodermal (SC; skin conductance) activity
Cardiovascular (HR; heart rate) activity
c. Central nervous system activity
i. Electroencephalograms (EEG; power spectrum)
2. Event related cortical evoked potentials (ERP's)
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Each child will attend the ROI! laboratory for one session.
It is proposed that the measurements of ANS, CNS and skeletal
muscular activity will take place during the .one recording
session so as to offer the possibility of inter-relating and
integrating these variables. The total session will be divided
into five sections preceded and followed by time allowed
for the placement and removal of electrodes. The total testing
time will be approximately 2.0 hours.
Section I: Examination of ANS and EMG Orienting (OR) and
Defensive (DR] Responses
Task:
This will involve the presentation of a series of
low and high intensity auditory stimuli for the purpose
of eliciting peripheral physiological features of
"intake and rejection" to simple non-signal stimuli.
Measures:
Analysis will focus on both tonic and phasia
(temporal and amplitude] components of SC, fIR,
EMG and EEG alpha (8-12 Hz] responses.
Section II: Examination of Cortical Augmenting and Reducing
Ta sk z
This will involve the repeated presentation of auditory
stimuli over four stimulus intensities for the purpose
of examining the relative tendency of the CNS to
"augment or dampen" the perceived impact of incoming
stimuli.
Measures :
Analysis will focus on latency and amplitude measures
of late components of the averaged cortical evoked
response. Measures of SC, HR and EMG will also be
examined as general indicators of tonic arousal.
Section III: Examination of EEG During a Cognitive Stress Test
Task:
This will involve the I minute presentation of the
Stroop Colour Word Test preceded and followed by
1 minute of rest. The purpose here is to elucidate
correlates CNS processing during a task with inherent
disruptive and distracting properties.
Measures:
Analysis here will focus primarily on power spectrum
analysis of EEG from 0-20Hz and measures of SC, HR
and EMG will also be examined as general indicators
of tonic and task-induced arousal.
Section IV: Examination of "Slow" Component Correlates of Cortical
Potentials During a Choice Reaction Time Task: Effects
of Distraction
Ta sk:
This will involve the presentation of two sets of i0
three-choice reaction times. One set will be
~raiontod al~nn anrl ~ uo=ond SOt will be pr,~,entod
n combination with an additional distracting task. i
Each trial will consist of a presentation of a warning i
stimulus followed in 6 seconds by an imperative (go) stimulus. ,
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Measures:
Analysis will focus primarily on the slow cortical
negative potential (contingent negative variation)
elicited between the warning and imperative stimulus.
In addition to reaction time, latency and amplitude
measures of evoked potentials to each stimulus will
be examined and tonic and phasic components of SC,
HR and EMG will be examined for the effects of
distraction.
Section V: "Attentional and Coqnitive" Components of Cortical
Potentials During a Divided Attention Task
Task -
This will involve the presentation of a multi-channel
divided attention task in which subjects will listen
to a sequency of tones (3 types) delivered at a high
presentation rate and at one of three spatial
locations (channels), left ear, right ear
and an apparent position midway between left and right
ears. Subjects will be instructed to monitor one and
two channels and detect slightly louder target tones
in the monitored channel.
Measures:
Analysis will focus primarily on latency and amplitude
measures. . of early (NI) attentional, and late (P])
cognatlve components of the cortlcal evoked responses
to attended (relevant stimuli) and non-attended
(irrelevant stimuli) channels. Behavioral measures
of reaction time and detection will also be examined
and testing measures of SC, HR and EMG will be
examined as measures of tonic arousal.
General Psychophysiological Analytical Method
It is proposed to acquire data from the polygraph channels
in three steps: paper record; analogue tape; and computerised
digitization. An analogue tape recorder is available from the ROH
and a microprocessor is now set up for analyogue-to-digital
conversion of eletrophysiological signals. Software programs
will have to be developed further for easy-to-handle data
acquisition, storage and analysis stages.
J
4, Statistical Analysis
The data from the initial phase (Year I) of the study will
be subject to multivariate analysis, in particular (a) principal
component analysis - to determine the characteristics of the
oveEall sample (and to compare the sample with currently
available norms), and (b) discriminant function analysis with
9rouping on non-smoker vs. experimental smoker status so as to
determine the characteristics of each group.
Upon completion of the final phase (Year V), multivariate
analysis will be performed. The data from the first phase of
the study will be subject to a discriminant function analysis
with grouping as per smoking status as determined in the final
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phase En order to elucidate variables particularly relevant to
the etiology of smoking. Principal component profilus of each
smoking status group will be drawn from initial and final data
in order to investigate the role of the various measures in the
development of the final smoking status.
Further multivariate and univariate analysis will be
performed as necessary to "explain" the data.
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REFERENCES
AGUE, C.= Smoking patterns, nicotine intake at different times
of day and changes in two cardiovascular variables while
smoking cigarettes. Psychopharmacologia, 30, 135-144, 1973.
ANDERSSON, K.: Effects of cigarette snaking on learning and
retention. Psyc.hopharmacologia, 41, 1-5, 1975.
ANDERSSONt K. and HOCKEY, G.: Effects of cigarette smoking on
incidental memory. Reports from the Department of Psychology,
University of Stockholm, no. 455, 1975.
ANDERSSON, K., POST, B.: Effects of cigarette smoking on verbal
rate learning and physiological arousal. Scandinavian Journal
of Psychology, 15, 263-267, 1974.
ARMITAGE, A., HALL, G. and SELLERS, C.: Effects of n~cotine on
electrocortical activity and acetylcholine release from the
cot cerebral cortex. British Journal of Pharmacology, 35,
157-160, 1969.
ASHTON, If., ~RSE[, U., MILL~U~N, J., R~qLINS, M., TELFORD, R. and
T}IOMPSON, J.: The use of event-related slow potentials of the
brain as a means to analyse the effects of cigarette smoking
and nicotine in humans, in: Smoking Behaviour, Physiological
and Psychological Influences, R. Thornton (Ed.), 54-68,
New York, Churchill Livingstone, 1978.
ASHTON, H., SAVAGE, R., TELFORD, R., THOS~SON, J., and WATSON, D.:
The effects of cigarette smoking on the response to stress in
a driving simulation. British Journal of Pharmacology, 45,
546-556, 1972.
ASHTON, H. and WATSON, D.: Puffing frequency and nicotine intake
in cigarette smokers. British Medical Journal, 19, 679-681, 1970.
BATTIG, K.: The smoking habit and psychopharmacological effects
of nicotine. Activ. Nerv. Sup. (Praha) 22, 274-288, 1980.
~ERLYNE, D., BORSA, D., HAMACHER, J., KOEING, I.: Paired associate
learning and the time of arousal. Journal of Experimental Psycho-
iogy, 72, 1-6, 1966.
BHATTACHARYA, I., and GOLDSTEIN, L.: Influence of active and chronic
nicotine administration on intra-and inter-structural relation-
ships of the electrical activity in the rabbit brain.
Neuropharmacology, 9, 109-118, 1970.
m
O
Co
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BatCo document for PFSFC 1 March 1999
BROASHURST, P.: Pharmacogenetics. In: Handbook of Psychopharmacology,
Vol. 7, L. Iversen, S. Iverson, S. Snyder (Eds.), Plenum
Press, New York, London, 1977.
BROWN, B. : Some characteristic EEG differences between heavy smoker and
and non-smoker subjects. Neuropsychologia, 6, 381-388, 1968
BROWN, K°, CHERRY, W., FORBES, ~.: Smoking Ilabits of Canadian
• School Children: A summary Report, Health Promotion Directorate
Department of National Health and Welfare, 1980.
BUTTER, N., GOLDSTEIN, H.: Smoking in pregnancy and subsequent
child development. British Medical Journal, 4, 573-575, 1973.
CEDERLOF, A., FINBERG, L., LUNDMAN, T.: The interactions of
smoking, environment and heredity and their implications for
disease etiology. Acta Medica Scandinavia. Supplement 612, 1977.
CHERRY, N., KIERNAN, K.: Personality scores and smoking behaviour -
a longitudinal study. British Journal of Preventive and Social
Medicine, 30, 123-131, 1976.
CHERRY, N., KIERNAN, K.: A longitudinal study of smoking and
personality, In: Smoking Behaviour: Physiological and Psycho-
logical Influences, R. Thornton (Ed.), 12-18, Edinburgh,
Churchill Linvingstone, 1978.
CONRIN, J.: The EEG effects of tobacco smoking - a review.
Clinical Electroencophalography, ii, 4, 180-187, 1980.
DAVIE, R., BUTLER, N., GOLDSTEIN, H.: From Birth to Seven.
London, Longmans. 1972.
DEMETRESCU, M., and DEMETRESCU, M.: Ascending inhibition and
activation from the lower brain stem: the influence of
pontine reticular stimulation on thalamocortical evoked
potentials in the rat. Electroencephalography and Clinical
Neurophysiology, 14, 602-620, 1962.
DENSON, R., NANSON, J., McWATTERA, M.: Hyperkinesis and
Maternal Smoking. Can. Psychiatr. Assoc. J. 20, 183-187, 1975.
DOMINO, E.: Electroencephalographic and behavioral arousal effects
of small doses of nicotine: a neuropsychopharmacological study.
Annals of the New York Academy of Science, 142, 216-244, 1967.
DUNN, W.: experimental methods and conceptual models as applied
to the study of Motivation in Cigarette Smoking: In:
Smoking Behavior: Motives and Incentives. W. Dunn (Ed.),
93-111, Washington, D.C., Winston& Sons, 1973.
o.
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BatCo document for PFSFC 1 March 1999
DUNN, W.: Smoking as a possible inhibitor of arousal. In:
Behavloural Effects of Nicotine, K. Battig (Ed.} 12-25,
Basal, S. Karger, 1978.
DUNN, H. McSURNEY, A., INGRAM, S., HUNTER, C.: Maternal cigarette
cigarette smoking during pregnancy and the child's subsequent
development: II. Neurological and intellectual maturation
to the age of 6} years. Canadian Journal of Public Health,
68, 43-50, 1977.
DUSTMAN, R., BECK, E.: The Visually Evoked Potential in Twins.
Electroenceph. Clin. Neurophysiol. 19: 570, 1965.
EASTERBROOK, J.: The effect of emotion on cue utilisation and
the organisation of.behaviour. Psychological Review, 66, 183-201,
1959.
EVANS, R., HENDERSON, A., HILL, P., RAINES, B.: Smoking in Children
and Adolescents: Psychosocial Determinants and Prevention
Strategies. NIDA Research Monograph 26, 69-96, 1979.
EYSENCK, A.: The Biological Basis of Personality. Springfield:
C.C. Thomas, 1967.
EYSENCK, H.: Personality and the Maintenance of the Smoking Habit.
In: Smoking Behavior: Motives and Incentives. W. Dunn (Ed.)
113-146, Washington, D.C., Winston & Sons, 1973.
EYSENCK, H.: The Causes and Effects od Smoking. Great Britain,
Maurice Temple Smith, Ltd., 1980.
EYSENCK, H. and O'CONNOR, K.: Smoking, arousal and personality,
In: Electrophysiological Effects of Nicotine. A. R~mond and C.
Izard (Eds}, 147-158, Amsterdam, Elsevier, 1979.
FAGERSTROM, K., GOTESTAM, K.: Increase in muscle tonus after
tobacco smoking. Addictive Behaviors, 2, 203-206, 1977.
FISHER, A.G.: Cigarettes, cancer and statistics. Centennial
Review, 2, 151-166, 1958a.
FRANKENHAUSER, M.MYRSTEN, A., POST, B., JOHANSSON, G.: Behavioral
and physiological effects of cigarette smoking in a monotonous
situation. Psychopharmacologia, 22, 1-7, 1971.
FRIEDMAN, J., GOLDBERG, J., HORVATH, T. and MEORES, R.: The
effect of tobacco smoking on evoked pc~ntials. Clinical
Experimental Pharmacology and Physiology, I, 3, 249-58, 1974.
FRIEDMAN, J., and MEORES, R.: Smoking and cortical evoked potentials=
an opposite effect on auditory and visual systems. Clinical
and Experimental Pharmacology and Physiology, 7, 609-615, 1980.
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FRITH, C. : Smoking behaviour and its relation to the smoker's
immediate experience. British Journal of Social and Clinical
Psychology, 10, 73-78, 1971.
GALA, S., COLES, M., BLAYDON, J. : Extraversion-Introvcrsion and the
EEG. British Journal of Psychology, 60, 209-223, 1969.
GILBERT, D.: Paradoxical tranquilizing and emotion-reducing effects
of nicotine. Psychological Bulletin, 86, 643-661, 1979.
GILBERT, D.= Extraversion and self-reported reason for and =imes
of urge for smoking. Addictive Behaviors, 5, 97-99, 1980.
GOLDSTEIN, H.: Human Biology, 43, 92, 1972.
GOLDSTEIN, L., BECK, R. and MUNDSCHENK, D.: Effects of nicotine
upon cortical activity of the rabbit brain: quantitative
analysis. Annals of the New York Academy of Sciences, 142,
130-180, 1967.
HALL, R. RAPPOPORT, M., HOPKINS, H. and GRIFFIN, R.: Tobacco
and evoked potential. Sciences, 180, 212-214, 1973.
HARDY, J., MELLITS, E.: Does maternal smoking during.pregnancy
have a long-term effect on the child? Lancet, 2, 1332-1336,
1972.
HASTINGS, J., BARKLEY, R.: A review of psychophysiological research
with hyperkinetic children. Journal of Abnormal Child
Psychology, 6, 413-447, 1978.
H'EIMSTRA, N., FALLESEN, J., KINSLEY, S., NARNER, N. : The effects of
'~'doprivation of cigarette smoking on psychomotor performance.
~/~ono.,~.cs, 23, 1047-zoss, 1980. ' '
•.~ ~.~~ .~" . ~!, .
~
• ~.~/<~uERSON, S. LEWIS, I.C., HOWELL, R. H. and .~AYNER, K~J.: .
"" ~': M ' '"
~"" "'" '
:~..:~ Menta~ Health and the use of alcohol, tobacco, analg...eg~cs and
" '~"~q'~':.~tam/ns..,,~- .in 4 secondary school population.-Acta Psych'i:~trica
186- 89, 1981 ....
• ... .- ...:
..,R:~ ~,= O., COURTS, F., TAYLOR, R., SOLOMON, E.: Cigarette smoking
-~on9 high school students. American Journal of Public Health,
• -'.'~4~, 1497, 1959.
~ CHINSON,. R., EMLEY, G. : Effects of nicotine on avoidance,
• "j , °
: :~.onditaoned suppresszon and aggression response measures in
i~im~is and men. In: Smoking Behavior: Motives and Incentives.
. Ounn (ed.), 171-196, Washington, Winston and Sons, 1973.
IRWIN, S. : Rational framework for the development, evaluation and
use of psychoactive drugs. American Journal of Psychiatry,
124, 1-19, 1965.
~.;
!
,....,l.b,
0
r,o
cr,,
c::D
BatCo document for PFSFC 1 March 1999
JAFFE, J., JARVIK, M.: Tobacco use and tobacco use disorder. In
Psycho~harmacology: A Generation of Progress. 1665-1677,
Raven Press, New York, 1978.
JAMISON, Ro: Personality, antisocial behavior and risk perception
in adolescents. London: University of London, unpublished
Ph.D. thesis. 1978.
JARVIK, M.z Biological imfluences on cigarette smoking. In:
Behavioral Aspects of Smoking, M. Kragengor (Eds), NIDA Research
Monograph 26, 7-45, 1979.
JASPER, H.: Reticular Formation of the Brain, London, Churchill
Livingstone, 1958.
KAHNEMAN, D.: Attentlona and Effort, Englewood Cliffs: Prentico-llall,
1973.
KETY, S.: The motivational factors in cigarette smqking: a summary.
Zn: Smoking Behaviour: Motives and Incentives. W. Dunn (Ed.)
287-295, Washington, D.C., Winston & Sons, 1973.
KLEINSMITH, L., KAPLAN, S.: Paired associate'learning as a
function of arousal and interpolated interval. Journal of
Experimental Psychology, 65, 190-193, 1963.
KNOTT, V.: Smoking, EEG and input regulation in smokers and
non-smokers. In: Smoking Behavior: Physiological and Psychological
Influences, R. Thornton (Ed), 115-130, Edinburgh, Chruchill
Livingstone, 1978.
KNOTT, V.: Psychophysiological correlates of smokers and non- smokers: studies on cortical,
autonomic and behavioral
responsivity. In: Electrophysiological Effects of Nicotine, A.R~mon~.
C. Izard (Eds), 99-116, Amsterdam, Elsevier, 1979.
KNOTT, V.: Reaction time, noise distraction and autonomic
responsivity in smokers and non-smokers. Perceptual and Motor
Skill% 50, 1271-1280, 1980.
KNOTT, V.: Reaction time,distraction and sex differences in smokers
and non-smokers, 1981a (In preparation).
p
KNOTT, V.: Electrodermal reactivity to high intensity stimuli:
sex differences in smokers and non-smokers. 1981b (in preparation).
KNOTT, V., VENABLES, P.: EEG alpha correlates of non-smokers,
smokers, smoking and smoking deprivation. Psychophysiology,
14, 150-156, 1979.
KNOTT, V., VENABLES, P.: Stimulus intensity control and the cortical
evoked response in smokers and non-smokers. Psychophysiology, 15,
186-192, 1978.
O
r~O
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GO
--.j
CD
CO
BatCo document for PFSFC 1 March 1999
KNOTT, V., and VENABLES, P.: Separate and combined effects of
alcohol and tobacco on the amplitude of the contingent negative
variation. Psychopharmacology, 70, 167-172, 1980.
KOZLOWSKI, L.: Psychosocial influences on cigarette smoking. In:
Behavioral Aspects of Smoking, N. Kresenger (Ed.), NIDA
Research Monograph 26, 97-125, 1979.
KUSEK, P.: Effect of smoking on performance underload. Studia
Psychologia, 17, 204-212, 1975.
LADER, M.: The psychophysiolog of anxious and depressed patients.
In: Clinical Applications of Psychophysiology, Fowles, D.F.
(Ed.) 12-41, New York, Columbia University Press, 1975.
LORSON, P., HOAG, H., and SILVETTE, H.: Tobacco: Experimental
and Clinical Studies. Baltimore, Williams and Wilkins, 1961
LEFKO~qITZ, M.: Smoking during pregnancy: long-term effects on
offspring. Developmental Psychology, 17, 192-194, 1981.
LIMENTHAL, J., MYERS, J. and PEPPER, M.: Smoking, psychological
status and stress. Social Sciences and Medicine 6, 583-591, 1972.
LINDSLEY, D., and RUBENSTEIN, B.: Relationship between brain
potentials and some other physiological variables. Proceedings
of the Society of Experimental Biology and Medicine 35,
558-563, 1937.
LYKKEN, D.: Psychometric applications of the EEG, In:
Clinical Applications of Psychophysiology, D. Fowles (Ed.)
• 139-166, New York, Columbia University Press, 1975.
MAC~ORTH, J.: Vigilance and Habituation. Middlesex, Penguism,
1969.
MANGAN, G., GOLDING, J.: An enhancement model of smoking maintenance.
In: Smoking Behavior: Physiological and Psychological Influences.
R. Thornton (Ed.), 87-114, New York: Churchill Livingstone, 1978.
~4ATARAZZO, J., SASLOW, G.: Psychological and related characteristiou
of smokers and non-smokers. Psychological Bulletin, 57, 493-513,
1960.
MAUSNER, B., PLATT, E.: Smoking: A Behavioural Analysis. New York:
Pergamon Press, 1971.
McARTHUR, C., WALDRON, E., DICKINSON, J.: The Psychology of Smoking.
Journal of Abnormal Psychology, 57, 267-275, 1958.
CD
Co
O
~4D
BatCo document for PFSFC 1 March 1999
McKENNELL, A. : Smoking motivation factors. British Journal of
Social and Clinical Psychology, 9, 8-22, 1970.
MEYER, A., FRIED~%N, L., LAZERSPELD, P. : Motivational conflicts
engendered by the ongoing discussion of cigarette smoking. In:
Smoking Behavior: Motives and Incentives, ~4. Dunn (Ed.),
243-254, Winston and Sons, Washington, 1973.
MILLS, I.: Coping Mechanisms in the Brain. In: Smoking Behavior
Physiological and Psychological Influences, R. Thorton,
(Ed.), i-ii, Churchil Livingstone, Edinburgh, 1978.
MURPIiRER, H. PFEIFFER, C. and PRICE, L.: Electroencephalographic
changes in man following smoking. Annals of the New York
Academy of Sciences, 142, 245-260, 1967.
MYRSTEN, A., ANDEI{SON, K.: Effects of cigarette smoking on human
performance. In: Smoking Behavior: Physiological a~d Psychological
Influences. R. Thornton (Ed.), 156-167, New York: Churchill
Livingstone, 1978.
MYRSTEN, A. A'~DERSSON, K., FRANKENHAEUSER, M. and ELGEROT, A.:
Immediate effects of cigarette smoking as related to different
smoking habits. Perceptual and Motor Skills, 40, 515-523, 1975.
NELSEN, J.: Neurophsyiological and Behavioral consequences of
chronic nicotine treatment. In: Drug Addiction Vol. 3,
Neurobiology and Influences on Behavior. J. Singh and H. Lal
[Eds) 375-386, New York, Strotton Zntercontinental, 1974.
NELSON, J., PELLEY, K. and GOLDSTEIN, L.: Chronic nicotine treanmenu
in rats: 2. Electroencephalographic amplitude and variability
changes occurring between and within structures. Research
Communications in Chemical Pathology and Pharmacology, 5,
674-704, 1973.
NESBITT, P.: Smoking, physiological arousal and emotional response.
Journal of Personality and Social Psychology, 25, 137-144,
1973.
POWELL, G., STEWART, R., GRYLLS, D.: The personality of young
. smokers. British Journal of Addiction, 74, 311-315, 1979.
PRADHAN, S., and BUGA, D.: Studies on gross behavior and electrical
activity of the brain during various environmental and pharmaco-
logical states. Research Communications in Psychology, Psychiatry,
and Behavior, I, 257-268, 1976.
QUAY, H.: Psychopathic personality as pathological stimulation
seeking. American Journal of Psychiatry, 122, 180-183, 1965.
~O
Cr~
OO
O
CD
BatCo document for PFSFC 1 March 1999
REMOND, A., IZARD, C.: Electrophysiological effects of nicotine.
Elsevier/North-Holland Biomedical Press, Amsterdam, 1979.
ROBINS, L. : Longitudinal methods in the study of normal and
pathological development. In: Psychiatrie der Gegcnwart, Band 1
"Grundlagen und Methoden der Psychiatrie" K.P. Kisker, J.E.
Meyer, C., Muller, E., Stromgren (Eds), Heidelberg Springer-
Verlag, 1980.
ROUTTENBERG, A.: The two arousal hypotheses: Reticular formation
and limbic system. Psychological Review 35, 51-80, 1968.
RUSSELL, M. : Cigarette smoking: natural history of a dependence
disorder. Br. J. Med. Psychol., 44, 1-16, 1971.
RUSSELL, M.: Tobacco snaking and nicotine dependence. In: Resen~
Advances in Alcohol and Drug Problems, vol. III, R. Gibbins
(Ed.) 1-47, New York: Viley & Sons, 1976.
RUSSELL, M., PETO, J., PATEL, V.: The classification of smoking by
factorial structures of motives. Journal of the Royal
Statistical Secrety, 137, 313-346, 1974.
SCORR, S.: Effects of birth weight on later intelligence. Social
Biology, 16, 249-256, 1969.
SCHOCHTER, S.: Nesbitts paradox. In: Smoking Behavior: Motives
and Intentives. W. Dunn (Ed.), 147-155, New York, Winston and
Sons, 1973.
SCHAEPPI, V.: Effects of nicotine administration to the cat's
lower brain stem upon electro-encephalographic and autonomic
system. Anals of the New York Academy of Science, 142,
40-49, 1967.
SELTZER, C.: Why people smoke. Atlantic Monthly, 211,
41-43, 1962.
SELTZER, C.: Morphologic constitutions and smoking. The Journal of
the American Medical Association, 183, 639-645, 1968.
.SELTZER, C.: Constitution and heredity in relation to tobacco
smoking. Annals of the New York Academy of Sciences, 142,
322-330, 1967.
SELTZER, S., FRIEDMAN, G., SIEGELAUB, A., and COLLEN, M.: Smoking
habits and pain tolerance. Archives of Environmental Health, 24,
170-172, 1974.
SHIELDS, J., Monozygotic Twins. London: Oxford University Press,
1962.
CD~
~o
Co
CD
BatCo document for PFSFC 1 March 1999
SIMPSON, W.: A preliminary report on cigarette smoking and the
incidence of prematurity. Amer. J. Obstet. & (;ynec., 13,
808, 1957.
STELMAK, E., ACHORN, E., MICHAUD, Ai: Extraversion and individual
differences in auditory evoked response. Psychophysiology, 14,
368-374, 1977.
STEPNEY, R.: Smoking as a psychological tool. Bulletin of
the British Psychological Society, 32, 341-345, 1979.'
STEPNEY, R. : Smoking behaviour: a psychology of the cigarette
habit. British Journal of Diseases of thu Chest, 74, 325-344,
1980.
STEWARD, L., LIVSON, N.: Smoking and rebelliousness. Journal of
Consulting Psychology, 30, 225-229, 1966.
TECCA, J., SWIGNANO-BOWMAN, J., and COLE, J.: Drug effects on CNV
and eye blinks: the distraciton arousal hypothesis. In:
Psychopharmacology: A generation of Progress, H.Lipton, A.
DiMACCIO, K. KILLMAN (Eds), 745, New York Raven, 1978.
THOMAS, C.: Personality differences between smokers and non-smokers
Maryland State Medical Journal, 114, 84-87, 1978.
THOMAS, C., COIIEN, B.: Comparison of smokers and non-smokers. I.A.
preliminary report on the ~ility to taste phenylthiourea
(P.T.C.). Bulletin of the Johns Hopkins Hospital, 106,
205-208, 1960.
THORNTON, R.: Smoking Behavior Physiological and Psychological
Influences. Churchill Livingstone, Edinburgh, 1978.
TOMKINS, S.: Psychological model for smoking behavior. American
Journal of Public Health, 56, 17-20, 1962.
TONG, J., HENDERSON, P. and CHIPPERFIELD, B.: Effects of ethanol and
tobacco on auditory vigilance performance. Addictive Behaviour
5, 153-158, 1980.
TONG, J., LEIGI~, G., CA~BELL, J., SMITH, D.: Tobacco smoking,
personality and sex factors in auditory vigilance performance.
British Journal of Psychology, 68, 365-370, 1977.
US Public Health Service. Smoking and Health: Report of the Advisory
Co,~nittee to the Surgeon General of the Public Health Service
(USPHS Publication No. 1103). Washington, Government
Printing Office, 1964.
VOZQUEZ, A.' and TOMON, J.: Some interactions of nicotine with
other drugs upon cnetral nervous system function. Annals of
the New York Academy of Sciences, 142, 201-215, 1967.
CD
~o
c~
CO
~O
BatCo document for PFSFC 1 March 1999
VENABLES, P.: The electrodermal psychophysioloqy of schizophrenics
and children at risk for schizophrenia= controversies and
developments. Schizophrenia Bulletin, 3, 28-48~ 1977.
WALKER, E. and TARTE, R.: Memory storage as a function of arousal
and time with homogenous and heterogenous lists.
Journal of Verbal Learning and Verbal Behaviour, 2, 113-119,
1963.
WALLER, D., LEVANDER, S.: Smoking and vigilance. Psychopharmacologia,
70, 131-136, 1980.
WARBURTON, D., and WESNES, K.: The role of electrocortical
arousal in the smoking habit: electrophysiological effects
of nicotine, A. R~mond, S. Ezard (Eds), 183-199, Amsterdam:
Elsevier, 1979.
WEBSTER, D.: The dynamic quantitation of spacticity with automated
integrals of passive motion resistance. Clinical Pharmacology
and Therapeutics, 5, 900-908, 1964.
WELKENS, L., RIQITER, C.: A great craving for salt by a child with
corticoadrenal insufficiency. Journal of the American Medical
Association 114, 866-868, 1940.
WESNES, K., WARBURTON, D.: The effects of cigarette smoking and nico-
tine tablets upon human attention. In: Smoking Behavior:
Physiological and Psychological Influences. R. Thornton
(Ed.) 131-147, New York: Churchill Livingstone, 1978.
WILLIAMS, D.: Effects of cigarette smoking on immediate memory
and performance in different kinds of smokers. British Journal
Psychology 7, 83-90, 1980.
MERUSHALMY, J.: The relationship of parents' cigarette smoking to outc,
outcome of pregnancy - implications as to the problem of inferring
causation from abserved associations. Am. J. Epidemiol. 93:
443, 1971.
YERUSHAL~, J.: Infants with low birth weight born before their
mothers started to smoke cigarettes. Am. J. Obst. Gynecol.
112: 277, 1972.
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BatCo document for PFSFC 1 March 1999
