Document 2JX9LMpyXaY5q0aJXpBxbeJDR
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I- Europtm Jolnnolof Gmcm Revenha 1995.4 3 1 4 3
REVIEW
919-g66-1 537
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T-222 P.002/014 F-034
P Epidemiological evidence on hair dyes and the b .risk of cancer in humans
C La Vecebia'3, A T a d '
(Receiwd 25 July 1994; accepted 23 September 1994)
Introduction
Hair colouriry products (hair dyes) an widely used, and it has bear cotimatcd that in Europe, North America and Japan over one third of women above the agc of18 aad over olOm ofmen above the age of40 use some type of hair dye,perm&t dyes accounnng for about three quarters of global use. This wide
-*
spread personal use implies considcrabIeprofcesional
exposure by haitdresras andbarbns,sinocthereirn about two millian professional hairdnosas, harbcrs and beauticians in North Amaica and Europe done (Cosmetics, Toiletry and Fragr~ce Aurociation,
undated).
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Tabk 1. Campoawrs of hair coloring products that have been evaluated in the IARC Monograph Series
Compound
Product in which found
MI evrl~atimor
cudnopnici~to hurmnr
URCmonographs
VOlUmC M.
57
57 16 48 52 57 27 16 16
n
51 57 57
Hair dyes conrain components that ~IE mutagenic
in vitro ( A r m er ai, 1973, some arc &ogenic in anhals, and several have beep evaluated by working groups of rht Inkrnarional Agency for Rcscarcb on
Cancer of the World Health organizadon (IARC/ -0, ' d in IARC, 1993) for their carciuogmkityb hurnaus, A summary tabulation of Lhest components is given in Table 1.
Epidsmiologicaldata on cancer risk amongsubjects occupad~dlye x p ~ s e dto, and 10w-kmp e n 0 4 UELC~Sof hair dyes have been mrudat least since rhc
1960% but only during rhe last two decades has Lhe
issue attracted widespread attention in the scientific
and lay pms. Af" a sum~llsvynvicw of experimental data on cancer in animals, rhc present ovcrvicw will wnsider and discuss epidemiological
data in humans with reference IOvarious CSIzIccr sites, and with spccific focus on two goups of neoplasms whose assodation with hair dyes has been widely debated in the last few years, ie bladder cancer and
lymphoid w o p l a L m o .
Evideace of carciuogenichy in experimmtal
animals
In at kast three sNdics which investigated skin
applications of pumanent (Burnen et ui, 1975) or
sani-pumaacnt( S e d 8 and Jouc6,1977; J m b s et d,
1984) hair dye fonndauous m mice, no skin tumour
wai-obscnnd, and no s-ti
diairaacc emerged
for l u g carurn.lymphomas or any other neoplasm
.%onsidered.However, the number of afiimnls in each
'-&camemgroup was small (appmximarely 20-60),
a d this precludes any codusion. '
In three studiea also comprising 20-60 animals per
treatment p u p , and byed 011 skin applicanons in
rats (Kinkel and Hokmann, 1973: Rojanapo ez d,
1986; Bunnsrt and Guldenrhal, 1988). again no skin
rumour was observed at the Site of application.
Likewise, there was no sigaificant difference in body
weight or sumival rim. One d y (Rojanapo er al,
1986) found an exccss of mammary tunours
(fibrorucomu, adenoman and fibroadenomas) in the
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Hair dyes mrd cancer
treated group, and a n o k (Burnerr and Ooldcnhal,
1988), an elevated incidmce ofpinr;rarY adenomas in
f d c s . No excess risk ac any other cancer sire was
reported.
A smaIl study (based on 10 male and IO female m
per ueauncnt group), cwpidmd subcurancous injec-
tion of mem-phenylene diamine wcry other week for
18 months. Thre was a0
ofmammary lepions
(d-`a and admo&), and two sarcomas and two
lymphomas ame at rhe site ofinjection (Rojanap et
uf, 1986). However, the snall absolute numbers of
animals again prccludt any C ~ l u s i o n .
Thus, cvidmce of the carcinogcniciry of hair dye
cornpaneats in.rodentp i s limittd an& from several
methodological aspens, it can be criticizd for
instancc, m most experiments only SJeCtcd organs
wen:exarm*ncd htologically. Although a r d c
amines act W y , tbe urinary bladder and
liver o b king their targets (hence skin KumOuII)
may not be their predomi~nttarget), the general
atmeace of skin tumours at the sites of application is
wonh noting. Some excess cancer incidence has b a n
reported bur, as a whole, the data am largely
inconclusive and offcr no clear focus for epidcmiolo-
gical studies in humans.
E p i a e m i o l ~data in bmnnlnr
Lymphoid neop&nw
At least nine cohort studies reported some dam on
OccupBtioIAal exposure to bair dyes and rmbSEqumt
risk Oftymphoid neoplasms(Alderson, 1980; Kono et
al, 1983; Teta et al, 1984; G u h et al, 1985;
McLaughiin et d,1988; Shibara at d,1989; Skov et
al, 1990; pulrkala et 4 1992; Hnrkc er d,1992).
Theirmain d t s are rcponedin Table 2.All studies
were based on very small absolute numben of cases
(1-22 ob-);
still, -t RR estimates WCR close to
unity, and all wen within the rrlsxivdymrrowmngc
of 0.4-2.5, with no dear exceptions.
This means that any subscantially elevated risk can
k Confidmtly excluded. when all the data were
pooled, a total of 100 lymphoid Iztoptasrm, was
observed vs 84.4 ex+ (mrmrmy,RR = 1.2). The
corresponding figures WCR 35 observed vs 31.3
expoctcd (RR = 1.1) for leuksermas, one obsmnd
vs 0.7 urpened for Hodgkin's disease, 17 obsemd vs
11.2 ;expected for nm-Hodglrio's lymphomas
(RR= 1.9, 24 obsavcd vo 20.1 expected for
lymphomas unspeded (RR = l.Z), and 19 obaerved
vs 16.8expected for multiple myeloma (RR = 1.1).
T.bL 2. Summary results fnuD selectcd cohort szudits providine information on occupational exposure to hair dyn and lymphoid neoplasmr
A h , yar, -ly
kx No.of
sub-
Lymphoid neoplpnnr
R&UW risk
Type
Obrrrnd
Exp&ted
Aldaon. 1980 (UK)
K m n rl. 1983 ( J a w Tep el ai. 1984 (USA)
Gubbrncr ul, 1985 (sllircerlmd) Mchghlia cf ul, 1988 @weden)
!#ihar 41989 (ftpm)
Sov er d, 1990 Okmark)
RJJrrl. cr d.,1992 (PinLd)
M F F
MSF
M McF
.M+F F
M
M+F
T o d (all hidogiu)
MtF
1.83 1 7,736
11,845
1,380
3,067 016 14.371
3.637 740
Y923
52,923
LEU LEU LEU Mh4 LYM All RAM
LEU,
LYM. N?lL LEU MM 'W H L HD
MM
LEU
LEU
HD NM LYU MM
All
3 6
14
3 22 4
I1 3
2 13 4 1 4 1 4 5
35 1 17
24 19
I00
2.7 1.1 4.4 1.4
11.6 1.2
4.3 0.7 17.1 1.3 4.3 0.9
8.5 1.3 . 3.8 0.8
3.0 0.7
8.1 1.6
4.2 1.o
24 0.4
3.1 1.3 0.7 1.4
1.6 2.S
4.6 1.1
31.3 1.1
0.7 I.4 11.2 I.5 20.1 1.2 16.8 1.1
84.4 1.2
%Eu. lairkarmiu: MM.mukipla mvdonu: LYM. IymDhhOmu (unplrcificd);HD. Hodgldn'm diwure. NHL.non Hodgkin's IpPhOmu.
~ur0p.n~ o u r n so~rc a m-tion.
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116 78 59 131 128 54
106 256 607
622 360
-321
2
5 1 0 1 0 1
I 2 I
13
I 12
--
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0 3.3
4 27 2.2 0.1 0.7 2.4 1.5
-1-3
Thus, froma staljsrical and biological viewpoint, the data on occupational exposure from cohort
studies am compatible both with a moderatelyincreassd risk (parucularly of non-Hodgkin's lymphomas) and with the absence of association.
However, since v a y littk is known about the
aetiology of these neuplasma, no plausible sugwstian can be made 011 the priorities for identification or allowance for potential confoundingfactors.
Data on o c c u p t i d exposare to hair dyes and rhe risk oflymphoid acoplasms from casbconuol sNdics
arc given in Table 3. At lcast eight SNdieS wen micwed (Gilaer at,1984)Fl& er al, 1987; Boffetm et 01,1989; PeMon et d, 1989; Eriksson and Kalspon,
1992;Pottern et d,1992; Blair et al, 1993; Heningtnn cr al. 1994). Of these, five (Gilcs et ol, 1984, Flodm cr
d, 1987; PeMOn er d, 1989; Blair et d, 1993; Hmiogtoa et d, 1994) showed some incrrascd ris4
although most RR esdnufes were d y modcratcdy
above unity, and none of them was signihmt. Tho rtmaioiLLg three (Eoffctta er of, 1989; Eriksson and
Karlsscm, 1992;Pottun et d,1992)found no evidence of usociauon. Only two studies (persson er al, 1989; Blair er al, 1993) includeddata and risk estimrteS on non-Hodgkds lymphamss, for a total of 14 exposed
axd a RR of around 2.4.
Case-conaol studies of occupational exposure to hair dyes and lymphoid ncoplssnu have at lam two major limitations: the extremely small number of
exposed cascs (only a),and the fact &at none of
them was spedfically d e s i p d to address this issue.
Thus, no iirm conclusions can be drawn, although,
taken together with cohort d e s , the results arc
~mpatiblewith some moderate assochuon between past employment as a hairdrrsser or b a r k and
lympboid neoplasms a6 a group, and p a r t k ~ h l ynmHodgb's lymphomas.
These epidrrmological hiding gain plausibiliry in
-thc light of the Ialwldge that urposurr to s c l e c r e d chemicals may increase tbe risk of 1eUkaemraJ W &
1985) and perhaps other lymphoid ncoplasms (za Vccchia er 01, 1989). Our knowledge of the aetiology
of these neoplasms in humans is, however, roo scanty to allow any mon precisc inference to be drawn on
potential pathogenic links. In any case, it musf be strclsed that any infmncc is b a d essmtislly on exposure to hair dyes (or otha potcnrial risk factors) by- rs and bprbtrs in thc distant past,
considaing the long duration (latency) of the process
of cardnogenesis. sin# even tht presence of any iwociation is open to discussion, it is not possible to formulaze any more prrcitc inference on latmcy,or any other dmt time faccor in tho process of
-lymphoid carcinogenesis. Additional information on the occupational expo-
surcs KO hair dyes of haitdrsssers, beauticians or
barbuy and the risk of lymphoid neoplasms can be derived from several descriptive suuiits on poputa-
tians. A report for the office of Population Censuses and Sumys (1986). covering occupabal exposure in England and Wales in 1979-80and 1982-83, found uon-Simrifirantlyincreased ramfor Hodgkk's disease and leukacmias in males, based, bowever, on five cascs or fewer. A larger CXCCSP was observed for lung cancer (21 deaths observed vs 7.9 expected), again suggesting elevated smokiug prevalma in rhost
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T-222 P.O06/014 F-034 Haw dyes and cmtxr
T.bk A Summary mults from sclccrcd cohort studinr providing infomarion on pasonal arposun to hair dycs and
lymphoid ncoplanar
Hcnnrlccns er ul. 1979 (USA) Thun ez ai, 19w (US4)
imsn
ny6e
LYM
NHL HD
Mu
LLEU
umu
LEU
All
10 0.6 (0.3-1.1,)
37 1.O (0.7-1 2)
6 0.6 (0.2-1.4)
SI
16
1
1.1 (0.8-1.S) 0.8 (0.61.4)
49 0.9 (0.6-1.3)
18 1.0 (0.61.8)
227 a9 (0,s-1.1)
occupational categoies in rhe past. For females, only breast cancer was in CXCCSII (seven obscrvd, 1.6
expected). This, however, might be refated tu ditrixeaces in reproductive factors or otha conrlafes of breast cancer risk (Boyle, 1988) between hair-
drrssm and the general populaTion.
In a Danish study (Qcmmcsm, 1977, 1981), no ex- risk ofall cancer sites was obsavtd for males (477 naalignant cancrrs observed vs 512.4 expectad), w h data for females wcrc diflidt to interpm due to difcrences in the dcfinirion of the azupational categories in thc census and cancer registranan data.
Some cxoc56 of multiple myeloma or lymphomas was also observed in descriprivc occupational studies from Los Angel- County (Cuidotti et 01, 1982), Washington State (Milham, 1983) and British Columbia (Gallagher et ul, 19891, but the ligures were geneally b a d on small absolute numbers and
the results wm o h inconsistcnr betaretn rhe two
sexes. otha snrdiesshowed no or link evidence of
mwiatim( ~ s s t Hk 4,ign;~ e u b e r egz ~d,~1991).
lnfoimntion on peusoml use of hair dya and tha risk of lymphoid ncoplaanu can k obrained from at leas two cohort studies ( H eer al, 1979;Thm cc ui, 1994)and fivc case-conuol sNdies (Smvraky er
d,1981;cantorer 4 1988;zahm et tal, 1992;Moms
Brown er 01, 1992;Herrinum et u l , 1994). Data fim cohort studin arc summand in Table
4.Among 120,557 fmralr nurses acdw in 1972 and
recruited in the Americln Nurses H d h Srudy (Hmnefrens et d, 1979), 10 lymphomas were
re&tered up to 1976 among hair dye USCIS vs 15.7
expected, correspondinpto a RR of 0.6.
The American cancer society cancer prrvention Study 11 (CSS II) included 573,369 people who wezc
followed-up between 1982 and 1989 (Thun er ai,
1994). A total of 941 hawratopoa'tic cancaa wore
observed overall, and 227 smong ever USQS of hair
dycs. The overall RR for all lymphoid neoplasms was
0.9 (95% CI 0.8-1.1) and thar of non-Hodgkin's
lymp&om was 1.0 (95% CI 0.7-1.2), and 110 excess
was observed for any other type of neoplasm.
Likewise, thcn was 00 iadicatian for the RR to
increase w i b increasing duration ofexposum, and the
only strata of elevated risk wcrc for long r n m use of
black dyes in relation u) mm-Hodgkia's lymphoma
(RR= 4.4, based on three cases), and multiple
myeloma (RR= 4.4, based on two cases). Taken as
a whole, thcrdore, the~tdata provide reassuring
evidence on the ab- of risk of lymphoid canerain
uscrsof hair dyes, even for 20 or mare years (Thun et
ul, 1994;Colditt, 1994).
Thc summary renrlb of the fivecascumtml S N d i e S
an given in Table 5. An earlier study from Canada
(Srawakyer d, 1981),comidaing 70casesofall types.
of lymphoid neoplnsmr, showed no evidence of risk.
Some modcratesspociarion, however, was appuentin
thctblW~~tCtMMODQOlstudisr,~
in varioqi areas of thc United States (Cantor et uf,
1988;Zahm er d,1992; M o d s Brown et ul, 1992).
maltchaow.u*ugghfuolnnlyumfobrernsoonf-Hc oxdgplind'scalsyemspahvoamilaabsleweforer
analysis.
A population-basedstudy c d u c ~ c idn 1980-83 00
malts from Iowa and MinncsoCs (Cantoret ul, 1988)
found an a v d RR of 2.0 (9P?confiAcncr inttrval
(a)1.3-3.0) for non-Hodgkin's lymphomss, and
showed some indication of duration-risk relatianship.
The risk esrimamwere adjusudfor smu of tcsidonce
and age only in two groups.
Another popuhcion-based -0nrrOl
d y was
cod& between 1983and 1986in Nebraska (7nhm
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Table 5. Summay resultsfram selectedcasscoarrol smdics of lymphoid neoplasms providing infoxmationon personal use of
hair dyer
Aurhan. year. country
sa
Typed
No.of
No.of
a n d uree crrpord-
odds d o
slavraky r. d, 1981 (Canada)
F
All
m
NR 0.9
C.nror et ul, 1988 (USA)
M LEU 578
43 1.8
NEIL
622
53 2.0
zphm CI at I992 (USA)
M NHL 201
I1 0.8
F "L
184
106
1.5 (1.7 pumancllr. p)
M BD
35
3 I .7
F HD
35
I6
1.7 0.0 -5
F)
M MM
32
4 I.8
P MM M CLL
40 37
24 1.8 @.a Pam--tS F) 3 I.o
F cu
19
9 1.0 (0.8 pamoamt, F)
Monir B m et a/, 1992 (USA)
M
MM
I73
14 1.9
Heninton el 4 19% (LISA)
M NM
360
17 13
F MM 319 114 1.1
`HD. HadJan'r d i m , MHL, ma Hod&Ss lymphornu; MM,multiple mydomr: LEU, Ieukramir. NR,aot rrpoMd
`et al, 1992), d included 201 mea and 184 women ., on the Surveillance, Epidemiology, and End Results
with histologicallyconfinned non-Hodglin's lympho- program found no material asodariw in women
mas: 11 m~aand106womtnhadevcrustdhairdyts, (RR=1.1) and only a modest nondlgnificant associa-
the RR estimates being 0.8 and 1.5 (significant), tion inmar (RR=1.3)
nspccdvely. The RR in women was 1.7 for use of In a leuex dimming the results on non-Hodgkin's
permanent hair dyes. Although this study c o M d lymphomas, no assadation was reported between
idomatiou OR several risk factors. these risk ocnrparional exposure to hair dyes and lymphoma
estimates werc adjusted for age only. Whcn total risk in people with acquired immunodcficitncy
hair dye use w89 considered, no relationship was syndrome (AIDS)(Cort er al, 1993).
evident with duration (RR1.2 for rhelo-t durahon A popularion-based caso-can~olstudy of multiple
caegory, 1 21 years), age at first use, or frequency of myeloma conducted benuem 1977 and 1981 in four
use (RR 1.4 for the most frequent category, 2 52 anas participating in the Surveillance, Epidemiology
times per year). Some association with duration was and E n d - R d m Programme (Seattle, Urab. Detroit
apparcnt in the subgroup of black, browrJbnurerrc or and Arlanra) included infomuon on occupational
nd dyes only, but this can be cons&red an a and personal exposure to hair dyes (Heninton et ai,
parreriori subgroup andysis, if not due to selection 1994). Among womm employed as haitdrrssap far 6
and confounding bias, since greyiug hair might be a months or more, the OR waa 1.3, in rhs aboeace,
correhzc of both hair dye use and lymphomas risk. however, of any duraumrisk rclattonship(ORfor >
Howmr,eveah tbis subgroup Chaewasnoevidence s,ycan (xpomre-0.7). only one man rcportcd
of a fqucuc-risk relationship. The same study occupational exposure. The ORs for personal use of
reported data 011 32 male and 40 female cases of hair dyes were 1.1 for womco and 1.3 for men when
muhiple myeloma The RR &marcs
were 1.8 (not ~
all data were cowidered,and 1.0 and 1.3 when all sclf-
significant) for both sacs and, again, rhae was no -. rtspondents were coasidsnd. None ofthcw Csrimates
evidnrce of any relationship with duration, latency or was signidarnt and tho auhors concluded that the
hqaency of use. The data were scanty on Hodgkin's study provided littie evidence rhat exp0sure.mhair
disease, and there was no evidence of BsSociatioawith dyca incream myeloms risk.
- 1 The results of epidemiological studies on hair dyes
Another srudy of 173 ma& cases of multiple should be discussed With reference to our knowledp
myeloma f m Iowa (Moms Brow et d, 1992) of the aetiology of lymphomas and myeloma. The
suggested a moderate assodadon (RR = 1.9,950/aCI beat recognized risk factor for nou-Hodgkids lym-
1.O-3.l), but proVided no details Ot the type of colour phomas is severe immunodqmssion, sincs the risk is
u9c4 and made no allowance for any covaxiate, substantially increased afkr (kidney) rransplanmdon
except age and vital status. A canconml study based and in subjtcul wirh human imxnun-
virus
36 EUMP.~Joumrl of evnCer Rmnrion. Val 4 iWS
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Hair &es a d mar
I (HIV)infedon (Kinlmer ai, 1979; La Vecchia et ai, mas and orhu lymphoid ncoptaansmay be of intenst
r 1992; Hangc and Dcvcm, 1992; Rarce and for fum eprdaniologkd stpdics, but available
Berhwairc, 1992). Myeloma is related u) ionizing evidence is inadequate for any public health or
)I radiation (Cuzick, 1981), but link is knownabout the regulatory implication.
role of infections, autoimmune diseases, immunode? prwion or other potential risk fanors ( G r a m 4 cz B M G Tcancer
al, 1991).
At least seven cohort studies based on 10 d B " t
D C&d incidence and mortality for both types of popuIati003 provided informadon on occupatiaaal
ncoplapms have substantially increased over the last exposure to hair dyes as bairdrcssns1 b a h t 3 P few decades, airhougb it is not clear how much of the beauticians and cosmet4logisu, and sub8cquent
h a # is real and how much is due to improved bladder cancer risk (Alderson, 1980; Koa0 cr ui,
b instrumemandcriteria for diagnosis and certification 1983; T- e?d,1984; Gub- et ai,1985; Skov et ai,
(Doll and Peco, 1981; Harts and D c v a 1992). A 1990; Hrubec et d,1992; Pukkala et al, 1992). The P recent and@ and quantification of the role of main finding arc summana zsd in Table 6. Fourstudies
various risk f a a m on time trends for non-Hodgkin's wen from Europe (one was a c4opcfBfive study from
lymphoma incidcncc concluded that about 80% of four Nordic counnics), two from the USA and ODC
these trends rrmain u1Iu[p18iI1cd (IHartgc and Devesa, h m Japan, for a total of over 81,OOO subjccrs(63,828
P 1992).
females and 17,247 males). In seven o m of 10 studiw,
z
In panicular, there is no clear evidence of any some moderate assodap;on was reponed. A total of association bctwcen exposure 10 chemicals and the 183 cases of bladder cancer were o k e d us 129
risk of disease, even at rhe relatively high doses found expected, conespondingto a summary RR of 1.4. 'Ihe
in the occupational environment. Thus, it is diKcult association waa apparcndy, though not omrifiunrly,
10 draw any inference on the roles of the chemical SUO&= in mlcs (RRa1.6) than in female
b
constimu of hair dyes, particularly in the a h a of (RR = 1.1). Thus the results of cohort studies arc
reliable -ts
of exposure a d of allowance for compatible with some moderate association between
indimon of socioeconomic status, which is o h a paa professional exposure to hair dyes (or other
correlate in hair dye use. There is also no information subsrancts in the working envinmmcnt) by hair-
on the doscs, biadionibution and bioavailabiliry of dressers and barbers and subsequent bladder cancer
potential carcinogens in hair dyes, with particular risk.
D reference to thcir conccnrrations in lymphoid tissues. There is,however, some indication that, at least in
In cmclusion, therefore, two studies (Cantorer ai, the past and in selected populations, rhe prevalence of
1988; Zahm er ul, 1992) reported a positive, though cigarette smoking, a recognized risk factorfor bladder
moderate, association bctwccn personal use of hair cancer (US Depanmmt of Health and Human
dyes and non-Hodgkids lymphomas, and two d e r Services, 1982). w h@er in rhcsc occupaKiod
datasets mggested a linlr with multiple myeloma groups thau in &e gcneral popularion, and cohort
(Zahm et al, 1992; Moms Brown ez al, 1992). The studies were g c n d y unable to allow for this major
d m howma, h an be criticized a epidemiologi- confounding factor in the anaIysM. It is thus possible
caI grauads, prtidarly because no allowance was that at least part of the apparent ZLuOciafion is due to
made far potenrial confounding facton, and the confounding by tobacco spoldD& as olso rugocsted
d t s lackad a plau6ibk biological inmpmation. bYbwwF- * 'oninmab,whowatmorr
In addition, epidemiological evidence rnay be influ- frequently 9mbJecR,than females.
enced by sclmilm publication- of positive resula Some mdication on the smoking issue can be
('publication bias'), since, panicularly in the absence duiucd from casbcoatroi studice, which p e r a l l y
of plausible biological hypotheses, there was little inclbdui information on smoking, and could therefore
rationale for publishing negative studies, ie those allow for this variable in the d y s i s . The main
hding no &tion.
findings from casbconuol sfll(iicsam mmmarkedin
since thc -on
was appaxmtly stronger or Table 7. Out of 11 sfudies (Wyndm et a1, 1963;
r e d 4 to subjects using black hrmnm/brunetta or Dunham et ai, 1968; Anthouy and Thomas, 1970;
red dyes, it is also at least theoretically conceivable Cole er d, 1972; Viadana et ai, 1976; H o w er d,
that gnying hair m a y be a corrclatc both of hair dye 1980; Vieis and Magnani, 1985; Morrison et d,
usc and of the subsequent risk of lpphoid 1985; Risch er 01, 1988; Silvumau et ai, 1989, 1990),
ncoplarms.
seven showed some assodation between occuparid
Thus, suggestions of a positive association between exposure to hair dyes and bladder cancer risk. Most
hair dye use and the risk of non-Hodgkin's Iympho- estimates, however, were around or only slightly
37f2-n Journal of aWefPRVmWOn. vOl4 1995
* .0.6-2,0-2001
12 :5 7 ~ a F rom-UNC HEALTH L IBRARY CLa Vecchh, A Tovani
Auzhom yar. -w
.al- 1980 (UK)
KOM 81 4 1983 (Japan)
Tstr CI a& I984(USA)
09#rrm 8I d. )-s(
slrav er a/,1990 (Norway)
srrcdg
FirJIld
DemMlk PlrldFllr 81 Id, 1992 (FinlraQ)
Hrpbcert d. 1992 (USA) Td
srm
M F F P M P M F M P M F M
Q
M
F M FtM
916-966-1 537
1-222 P.000/014 F-034
Na of
-9
1.831 7,736 11,845
m
m3 4,356
16942 -2 9,138
&a
9,497 4374 3,637
740
63,828 17,247 81,075
~~
Blrdderancsr
~-
Okmcd
p-'ilwcud
7 5.6
0 1.o
14 10.3 2 1.5 11 5.3 11 7.2 23 15.1 6 13.5 54 36.6 3 1.8 0 0.3 7 4.0 41 20.0, I 2.5 3 4.3
44 41.8 139 87.2 183 129.0
kluiw
*.
1.3 0
1.4 1.3 tl 1.5
IS 0.4 I .S
1.7 0
1.B
2.1 0-4 0.7
1.1 1.6 1A
A4 M
M
M
P M M F M
M M
M
M+F M F
300 265 812 356
105
NR 480
152 512 430 399
116
836
2.100 652
4-
4 2.8
4 4.1
4 0.6
1 1.1
-5
3
1-.s
2
9 0.9
7 1.0
2 I.3
1 1.0
2o 0.8 *
28 1.3
17 1.4
abow unity, and not statidcally signilkant. Still, tbc
gmaal evidcnce from -mol
S is in
agreement with that fmm cohort investigations, and
is cornpatable With a moderately incrrascd bladder
c r n c o r r i s k i l m o n g a~nd barbas.
Some excess risk of bladder amd other urinary Sites
cancers was also obscrvod in descriptive occupational
d i t s From New ztslond (peua and Howard.
38 buapmnJ o d of-
R u e a h . Vol4.199J
1986) and hfassachusetrs pubrow and Wcgman, 1984). but thc figures were b a d 011 srmller absolute numbm, snd are incoasr*sttnrwitharherscudia
(Mcnck cr aZ, 1977; Ncuhcrgcr et uZ, 1991).
It must be secssed that most inFdnnarion Fmm
descriptive, cohort and casecontrol studies c o o c ~ ~ l l l
exposure in the nlativcIy dhtant past, when there wlls
lesa strict control of carcinogenic substanas in hair
06-20-2001 12:58pm From-UNC HEALTH LIBRARY
91 g-g66-1537
1-222 P.010/014 F-034
su
H w e er ai. 1980 (Canada)
F
M
152 NR 480 8
0-.7
Hart# ez ul, 1982 (USA) f 733 443
0.9
M 2,249
172
1.1
Ohno er ai, 1985 (Japan)
F
65 42
1.6
Claude cl ul, 1986 (Gumany)
F
91 NR No associalion
M 340 NR
Nmm a ul, 1989 (USA)
F
66 41
1.5
M 195 15
1.3
m.IWCrrporrcd;--,M~parsdcOnEO~
dyes and of the working conditio^^ and activities of tionconductedby the US NationalCancer Institutein
hairdrtsocrs. There is therefore a reasonable biologicaI 10 US states (Harts et ul, 1982). The study was
backgmuadfor the obsmved amciation, which could originally focused on anificial SwcttePQs, but
also be compatiblewhh latency and other limc-nlated included adequate infomation on hair dyes, tobacco
facrors in the process of bladder ca.rcino@
smoking and other major covlviatcs of inuzcst. There
@ecarli et al, 1985). Thus, a m n t IARC working was no evidence of an asrcocizrdon between hair dyes
group (IARC/WHO, 1993) stared that `occupationas and bladder cancer risk,the RR estimates bdng 0.9 in
hairdnsser or barber entails exposures that arc f d t s (based on 443 exposed cases) and 1.1 in males
probably carcinogenic'.
(based on 172 exposed cases), nor wen there any
However, rhe cstimsfedrelative risks, as well as the mds in risk with fhquency or durationineither sex.
o v d p l c d estimam, arc only moderately above The other four 9Ndios were much smaller, and thus
unity, and hence compatible with m n and biases in were ks infonnauve, iududing only a few dozen
observational epidaniol0,gical studies. A major open exposed subjects, but the RR esham were again
quntion, moitovct. is whaher current cxposurc to clocle to wily.
modem hair dyes is still related tp some excess risk, or Thus, the O V &~ hf- cohort and c=-
w h e b the selective elimination of carciaogenic conuol eeudics consistbzrrly exciudes any appreciable
compounds (Table 1) over FeccnK y t m has reduced and measurable rislr of bladder cancer from penonal
any such risk m nonmcasursblc lcvels. Only further usc of hair dyes.
srweiuance and futurr studies will provide answers.
personal hair dye use in relation to bladder a~cs!r Other neoplannr
risk was considemi by at least one cohort and five
other
ius, rhc bieast has bem most
taswxmml studies. The cohm study ( H e n n a el exreooively smdicd, bccause of rhe high incidum of
al, 1979) was &e Nunu' H d t h Study, based on the disaasc in women and thc report $a dstan-td Y 120,557 fcmafe Amencan n q active in 1972 and elevated'RR of breast cancer from a small study
followed-up for incidence of d i s e k until 1976. Five published in the 1970s (Wkrand Shafer, 1976). Of cases of bladder cancer wen rcgisurd vs 7.4 100 paticnu f m a dirrical praaiOe in New York, 87
mpecred, comsponding to a (nonsislificatit)relative had-bcen l0ng-m USCIS of hair d m
risk of 0.6.
wirh 27% of a COmpLuiso~group, with a RR estimate
?.he main fbdings from case-conml mdies are elevated over IO-fold.
31' d in Table 8. Five d e s were considered At lean scvm caswxmrrol ONdibs (Kiden ut ai,
(Howe et al, 1980; Hmgc et Ol, 1982; Ohno et 41, 1977; Shore e: al, 1979; Stavxaky et a& 1979; Nasca et
1985; Claude et ai, 1986; Nomura et al, 1989). two d,1990, 1992; Wyndcr and Goodman, 1983; Kou~ig
from the USA and m e each from Canada, Germany et 01, 1991) and one cohon study (Hennehs cr a4
and Japan. By far the l a q m srudy, and hence &e 1979) wen subsequently published, including a total
mOSf hfOrIIlaUVC O m , includin6 O W thrCC fOUrLhS O f of over 3,200 breast cancer cases. Some of these wcrc
the cases and of thc ex&
subjms, was a specificauy designed to address thc hair dye issue.
multiccntsc population-bd, casccontrol investiga- N o ~ efound evidence of an assodation. and it is
~ ~ a morrcl.ncrr~eventioa.Val 1.19~s39
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C& Vecchk A Tavani
therefore now established that hair dye use is not a risk factor for human breast cancer.
Same accuparional cohort studies (eg Teta et a!, 1984;Osorio cr al, 1986; Skov et al, 1990; Hnrbec et ul, 1992) nponed an excess lung cancer rare in cohorts of subjects occupatidy exposed to hair
dyes. The m)ults,however, were not consistent acroI studies and oftea not even within studies (eg
Were Observed bOKweCn d C S and
females). Most sNdies, mol#)vct. were unable to allow for Qnoking, by far rbe most impOnanr risk
factor for hang canccr (Doll and Peter, 1981; US Dcpacnnent of Health and Human Services, 1982),
and chmfore the most reasonable intezpreCarion of &e associauon obsmed in a few studies is a
somewhat elevated prcvalance of smoking among hairdressers and barben in rhc past. Likewise, no s i p i h m association with lung cancer was observed for personal use in a small sNdy (60lung cancer cases,
Stavraky GI ai, 1981). An cxcm of laryngeal cancer rates in barbers
(Viadana er ai, 1976) can be interpreted along tbe
same lines, although in that study the RR Cstimare
(2.8 based on 10cases) was not materiallymodified by allowance for smoking.
The results for other neoplasms am scarered. An elevatedrisk ofcancers ofdu:cervix and of the ovary was reponed among hair dye users in a multi-aite
ca8e=controlstudy conducted in Canada (Stavraky et al, 1981). Then may have been some confounding by
sexual and rrproducuve factors, w h i art known comlatcs of the risk of h a c neoplasms (Brinum and Frammi, 1986; Pamahi et al, 1991) and, wnceivably, of hair dye use. However, a most careftdly
designed and conducted c a s b c o n ~s~nlrdy of ovarian cancer from Atheos, Greece (Tzonou et ai, 1993) found a sigdcant association, with an RR of 2.2 for frequent hair dye users.
Two studica from Awrrrli;r (Hohnoa rad Annsmug, 1983: Annstrorrg and Hoknan, 1985) and Denmark (Osrerlind et ai, 1988) found no association
benveen hair dye use and ski0 melamma. ' Data are inadsrent for thc relationship between
hair dye usc and brain cancer (Ahlbom er d, 1986; Burch af al, 1987). as well as for some rarer neoplasms, such as salivary ghad cancers (Spitz er d,1990), and childhood neoplasns in tbc oflspling (Ktamcr et al, 1987; Bunin e?ai, 1987; Kuiljun el d, 1990), particularly since some scattered positive findings may be influenced by publication bias.
Thus, thcre is at present no convincing evidence
that occupational or personal exposure to hair dyes is
related to the risk of any ~ l ~ p l i ~ samt ssiw orher tban the bladder and the lymphoid tissue.
C O ~ ~ ~anOd iIdcEations for tbrther
teselveh
A substantial amount of epidemiological evidence is available on the possible assodation between hair
dyes and smraf cancer sites, permitting a number of wdlcstablished conclusia Occupationnl exposun KO hair colouraxxrs or pasonal bair dye use is not related to breast cancer, nor ia it c a d y relaud to lung cancer. Likewise, r,ture is no convincingevidence lialdng hair dye use to cancers d t h e skin, brain,
fdegtnitaltrad,stomachandorhcrdigcsrivesites. Further, personal use of hair dyes docs not enrail any measurable excess bladder cancer risk.
Thc two remaining opca queshns art the possible relationship between bladder cancer and (past) OCOUpQtionat exposure by hnitdr#sen, barbw and
beauticians, and between bair dye sxgos~re and
lymphoid neoplas;ms, with rrfmncc to bath bccup8-
t i 4 and persoaal me. g e association between past occupuonal expo-
sure to hair colourants and bladder cancer risk is
reasonably consistent on epidedological data, and
plausible on biological grounds oriand
Elliott, 1981). The question arises whether the risk has been eliminated, following selective nmoval of carcinogens from hair dyes and improvements in working conditions over the last few decade, or whether some exccso iisk is still idenrifiablc. Thus, furehKmonitoring on more rrctllt cohorts will be an issue of scientific inttrcst and public health r t l a ~ ~ n a .
An associauon between p o d hair dye use and non-Hodgkin's lymphoma and multiple myeloma wag nccntly reporred from rhrcc csse-conuol studies (Cantor et d,1988;Zahm et d,1992;Mom6 B m et ai, 1992). The dative risk estimsreswere moderate, ~ d belowy a facror of two, and theFc wa9 no
clear evidence ofduration or a doJbrisk relatiomhip.
on spirlam;rlogicol grauart, tbedkKC9 IlmJBbdiagS
require fwllcr mdy, paniculalrly since rhcy may be
i z l f l d by StlCctiMpublication ofposidve fbdhlgs.
This publicauon bias is plausible, considering the ;hence of any rdiabk idenrificarion and measure of
potential carcinogcos in hair dyes which could have reached& bonc marrow or thelymphoid tissue,and hencc of any ooavindng biologhl link for these
epidemiological observations. These cautious notwithstanding, repow from
unpublished investigations and from fbrthcr casecouuol studies of lymphoid neop&sms and hair dye use would be of interest, wbenas cohort studies are unlikely SO provide m~aningfdi n f o d o n ~1 such rare diseases. These ca-onuol smdics, eveu if
&aped to invcsdpre; s c d potcnujl rids f-ra
40 Europan Joumrl of Cancer Pmranlim. V o l 4 199s
ri
,
L
b
06-20-2001 12:59pm From-UNC HEALTH LIBRARY
919466-1 537
1-222 P.O12/014 F-034
Hair d,vcp and cancer
for lymphoid ncoplagns, considerkg thc lack of definite knowledge on their aetiology, should none-
theless include a suuctured and, ideally, an (externally) validated d o n on &e history ofhair dye use. They should also include further informadon 031 poscible confounding faaors, and hmct adcquau allowanceshould be made in the analysis for the main covariatcs of potential interest.
Ref-=
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OD time umds in non-Hodgkin's
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