© The Au ho 2017. Published by Ox o d Uni e si y P ess on behal o Zhejiang Uni e si y P ess. 131
Food Quali y and Sa e y, 2017, 1, 131–137
doi:10.1093/ qs/ yx011
Re iew
Ad ance Access publica ion 26 May 2017
Re iew
Exposu e o Kenyan popula ion o a la oxins
in oods wi h special e e ence o Nandi and
Makueni coun ies
E. K.Kang’e he*, M.Ga wi i*,**, A. J.Si ma*,***, E. O.Ouko*,***,
C. K.Mbu ugu-Muso i*,**, P. M.Ki ala*, G. J.Nduhiu*, J. G.Nde i u*,
J. K.Munga u**, V.Hie aniemi****, V.Jou sjoki**** and H. J.Ko honen****
*Depa men o Public Heal h, Pha macology and Toxicology, Nai obi, Kenya, **Jomo Kenya a Uni e si y o
Ag icul u e and Technology, Nai obi, Kenya, ***Minis y o Ag icul u e Li es ock and Fishe ies, Ve e ina y
Labo a o ies Kabe e, P i a e Bag Kabe e, Nai obi, Kenya and **** Na u al Resou ces Ins i u e Finland, LUKE,
Jokioinen, Finland
Co espondence o: E. K. Kang’e he, Depa men o Public Heal h, Pha macology and Toxicology, Box 29053– 00625 Nai obi,
Kenya, E-mail: [email p o ec ed]
Recei ed 19 Feb ua y 2017; Re ised 8 Ma ch 2017; Edi o ial Decision 9 Ma ch 2017.
Abs ac
A la oxins cause acu e and ch onic heal h and p oduc ion e ec s in humans and animals,
espec i ely. This s udy epo s on he exposu e o he Kenyan popula ion o he wo myco oxins in
wo coun ies (Nandi and Makueni) using child en younge han 5yea s as he p oxy. Aques ionnai e
was adminis e ed, which cap u ed knowledge o he incidences o acu e a la oxin poisoning, ood
consump ion pa e ns. Analysis o a la oxin in samples o u ine, b eas milk, maize, so ghum, and
mille was done using cELISA and HPLC. Maize and so ghum a e used in he weaning o mula o
child en. The di e ence in consump ion o maize- and so ghum-based die s in child en be ween
younge han 1 and be ween 1 and 5yea s was signi ican wi h P=0.037 and P=0.002, espec i ely,
in Nandi and Makueni. In child en younge han 5yea s, he consump ion o maize anged om
0.1 o 0.25kg pe pe son pe day in Nandi and Makueni wi h an a la oxin exposu e a e o 0.011
and 0.49µg pe kg body weigh (bw ) pe day, espec i ely. The exposu e o a la oxin h ough milk
o child en younge han 5yea s was 4×10−4 and 1×10−4 µg pe kg bw pe day in Makueni and
Nandi, espec i ely. The exposu e o nu sing child en h ough b eas milk was 6×10−3 and 1×10−6
µg pe kg bw pe day in Makueni and Nandi, espec i ely. Child en younge han 30mon hs in
Makueni had 1.4 imes highe le els o a la oxin M1 (AFM1) in u ine han hose o he same age in
Nandi. The s un ing and se e e s un ing a es in Makueni and Nandi we e 28.7%, 18.5% and 30.7%,
16.5%, espec i ely. Thus, he e is need o u gen mi iga ion measu es, a cons an su eillance
p og am, s ic egula ions, and awa eness c ea ion di ec ed a poo households o educe die a y
exposu e o myco oxins.
Key wo ds: A la oxins; Con amina ion; Exposu e; Kenya.
In oduc ion
A la oxins equen ly con amina e s aple oods o many Kenyans.
A la oxins a e p ima ily p oduced by Aspe gillus la us and
A. pa asi icus. Humans a e exposed o a la oxins om consump-
ion o ce eals, nu s, pulses, oo s, and animal sou ce oods om
li es ock ed con amina ed eeds. In Kenya, maize is he majo s aple
This is an Open Access a icle dis ibu ed unde he e ms o he C ea i e Commons A ibu ion Non-Comme cial License
(h p://c ea i ecommons.o g/licenses/by-nc/4.0/), which pe mi s non-comme cial e-use, dis ibu ion, and ep oduc ion in any
medium, p o ided he o iginal wo k is p ope ly ci ed. Fo comme cial e-use, please con ac [email p o ec ed]
132 E.K. Kang’e he e al., 2017, Vol. 1, No. 2
ood and i is es ima ed ha annual pe capi a consump ion s ands
a 97kg (FAO, 2000) compa ed o 76kg pe capi a consump ion in
Eas and Sou he n A ica, espec i ely (M’mboyi e al., 2010). Maize
con amina ion wi h a la oxins in Kenya has been epo ed by Lewis
e al. (2005), Mu u e and Ogana (2005), S osnide e al. (2006),
P obs e al. (2010), Daniel e al. (2011), and Mu homi e al. (2012).
Human exposu e om milk ob ained om animals ed wi h con-
amina ed eeds has been epo ed by Kang’e he e al. (2007) and
Kang’e he and Lang’a (2009).
Long- e m exposu e (2–3mon hs p io o sampling) o a la ox-
ins in humans can be assessed by analysis o albumin adduc s (Wild
and Tu ne 2002; Gong e al., 2002, 2004) and p esence o a la oxin
M1 (AFM1) p oduc s o AFB1 b eakdown in u ine o sho - e m
exposu e.
This s udy aimed a es ablishing he exposu e le els o house-
holds o a la oxins and e ec s o a la oxin exposu e exempli ied by
g ow h indices in child en younge han 5yea s in he Nandi and
Makueni coun ies o Kenya.
Ma e ials and Me hods
Si e and household selec ion
The coun ies Nandi and Makueni in Kenya we e pu posely selec ed
based on his o y o human acu e a la oxicosis in Makueni (Lewis
e  al., 2005) and high incidences o esophageal cance in Nandi
(Wakhisi e al., 2005). The sub-loca ions we e iden i ied by a eam
o esea che s oge he wi h e e ina ians, ag icul u e ex ension
o ice s, and heal h o ice s a he coun y and wa d o ices. The
selec ion c i e ion was based on dai y and maize p oduc ion. In
he i s ins ance, he sub-coun ies we e selec ed ha i ed he c i-
e ia based on he eco ds a he coun y le el. Th ee sub-coun ies
we e selec ed in each coun y. A he sub-coun y headqua e s, he
wa ds we e selec ed using he same c i e ia o dai y p oduc ion and
maize g owing. A he wa d le el, he ex ension o ice s ( e e ina -
ians, ag icul u e, and public heal h) selec ed he sub-loca ion ha
bes i ed he c i e ia used o selec he wa ds. The households
in he sub-loca ion we e lis ed which i ed he c i e ia o ha ing
dai y animals, g ew maize and o so ghum and mille , had a child
younge han 5yea s, and/o i he spouse was p egnan a he ime
o lis ing.
Based on he popula ion and numbe o households in he sub-
loca ion and he households ha i ed he c i e ia, a p opo ion o
he households was andomly selec ed o sampling (Ma in e al.,
1987), and he household sample size was co ec ed o ini e popu-
la ion acco ding o Daniel (1999).
Nandi alls wi hin he ag o-ecological zones o lowe humid
highlands o uppe midland and uppe highland zones ((LH2, LH3,
UM3 and UM4, Jae zold e al. 2006). I lies be ween 1300 and 2500
m abo e sea le el and ecei es abou 1200–2000mm o ain pe
yea . Nandi is bes sui ed o ea cul i a ion, dai y p oduc ion, and
g owing maize, whea , and ba ley. Makueni alls wi hin he lowe
midland ag o-ecological zones LM3, LM4, and LM5. I ecei es
be ween 200 and 1200mm o ain all pe yea , which is un eliable
a imes wi h equen d ough s esul ing in c op ailu es.
Sampling o u ine
U ine samples we e collec ed om child en younge han 5yea s in
all he households. Clean bo les we e supplied o he mo he s o
collec ing he u ine. The samples we e ozen a ದ20°C un il analysis
wi hin 3mon hs.
Sampling o b eas milk
Nu sing mo he s we e gi en clean bo les in o which hey exp essed
milk om hei b eas s. The samples we e ozen a ದ20°C un il hey
we e analysed wi hin 3mon hs.
Tes ing o a la oxin M1 in u ine using c-ELISA
(helica es ki )
To de e mine a la oxin M1 in u ine, 5ml o u ine was cen i uged
a 743× g o 10min. Nine hund ed and i y mic oli es o dis illed
wa e was pipe ed in o ska on (SKATRON AS LIER, No way.
CAT. No 7071) ubes and 50µl o s anda ds o supe na an -u ine
was added in o 950µl o dis illed wa e in he ska on ubes and
mixed by p iming pipe ing a leas i e imes. Two hund ed mic o-
li es o he assay bu e was added in o he mixing well pe pla e
and 100µl o he dilu ed s anda ds ( anging om 0 o 40 pp ) and
u ine samples was added in o wells o he mixing well pe pla e.
The con en s o he mixing well we e shaken using a mic o-shake
(DYNATECH) o 2min. One hund ed mic oli es o he mix u e
was ans e ed o he an ibody-coa ed Reac ion-Assay Pla e (a la-
oxin M1 assay o u ine, Helica Biosys ems Inc, 1527 W. Al on
San a Ana, Cali o nia, USA). The samples we e mixed by shaking
o 1min (DYNATECH Shake ) and incuba ed a oom empe a u e
in he da k o 1h. The pla e was washed h ee imes using phos-
pha e-bu e ed saline–Tween-20 (0.05%) bu e using he well-wash
(The mo Scien i ic, Finland) machine wi h 3-min in e als be ween
he washes. A e d ying, 100µl o conjuga e was added in o each
well, mixed gen ly by apping, and incuba ed a oom empe a u e
o 15min in he da k. The pla e was hen washed and 100µl o sub-
s a e eagen ( e ame hyle hidine) was added in o each well, mixed
gen ly by apping, and incuba ed a oom empe a u e o 15min in
he da k. The eac ion was s opped by adding 100µl pe well o s op
solu ion and he op ical densi y (OD) ead a 450nm wi hin 15min
o s opping he eac ion. The le el in each sample was de e mined
using he p og am om he ki manu ac u e , which allowed calcula-
ions o he le els based on he abso bance eadings.
Tes ing o a la oxin M1 in b eas milk using cELISA
(Ridasc een es ki )
The analysis o milk o AFM1 was ca ied ou using he com-
pe i i e ELISA me hod acco ding o manu ac u e ’s ins uc ions
( -biopha m, Ge many) wi h modi ica ion adop ed om EVIRA
(Finnish Food Sa e y Au ho i y). Analysis was done wi hin
3mon hs o sample collec ion. Fi e millil es o milk sample was
wa med and cen i uged o 15min a 1011× g.The uppe c eam
laye was emo ed and 2.5ml o he de a ed milk ans e ed o
a es ube and 5ml o e hyl ace a e (88.1 g/mol; mel ing poin
ದ83.6°C) added. This was o exed o 1min and he mix u e cen-
i uged a 1011× g o 15min a oom empe a u e. Th ee mil-
lil es o he e hyl ace a e laye we e ans e ed in o a clean es
ube and e apo a ed o d yness using a s eam o ni ogen. The
sample was dilu ed wi h 250μl o he sample dilu ion bu e and
30μl o 70% me hanol:wa e , o exed, and analysed o AFM1
using a compe i i e ELISA acco ding o manu ac u e ’s p ocedu e.
The limi o de ec ion was 5ng/l. Le els below his limi we e es i-
ma ed using a company p og am ha de e mined quan i ies by
ex apola ion.
An h opome ic measu emen s
Heigh , weigh , and age we e he an h opome ic measu es aken
om he child en en olled in he s udy. The heigh was measu ed
Exposu e o Kenyan popula ion o a la oxins in oods, 2017, Vol. 1, No. 2 133
using a measu ing ape o he nea es whole cen ime e while he
weigh was measu ed o he nea es g am using a Sal e weighing
scale. Weigh o age Z-sco e (WAZ), heigh o age Z-sco e (HAZ),
and weigh o heigh Z-sco es (WHZ) we e calcula ed acco ding o
he median alue o he in e na ional e e ence popula ion ecom-
mended by he Na ional Cen e o Heal h S a is ics (NCHS) and
Wo ld Heal h O ganiza ion (WHO, 1986).
Household ood sou ces and consump ion
A ques ionnai e was adminis e ed o he esponden s o 547 house-
holds in o al. The esponden s, mainly spouses, we e asked o
indica e o each household membe he ype o ood ea en (maize,
so ghum, and mille ); sou ce o he ood ype whe he i was home-
g own, ma ke sou ced, gi , o elie ; amoun s ea en and equency
pe day. The amoun ea en was indica ed by he wi e who dished ou
ood o e e y household membe om a empla e displaying a pho-
og aph o he ood quan i ies; she would selec he amoun which
closely es ima ed he amoun se ed.
Da a analysis
The da a we e en e ed in sp eadshee s and analysed in SPSS Ve sion
19.0. Explo a ion o he da a was by nume ical summa ies oge he
wi h g aphics. Rela ions and associa ions in bo h he opinion/pe -
cep ions and expe imen al da a we e u he examined using chi-
squa e and - es o he le el o signi icance a 5%.
Resul s
Food consump ion
Ce eals
The la ges quan i y o maize, so ghum, and milk consumed by
households was home p oduced. Maize is he main s aple ood in
Nandi and Makueni. The majo i y o he households (60–90%)
elied on homeg own maize excep in Makindu loca ion in Makueni
and Kap umo loca ion in Nandi whe e homeg own maize con ib-
u ed abou 40% o he household needs. Maize and so ghum was
consumed as ugali o po idge and mu hokoi ( adi ionally dehulled
maize, cooked oge he wi h beans o pigeon peas). Maize and so -
ghum in he o m o uji, gi he i, and ugali we e used o weaning
child en. Child en younge han 1yea and be ween 1 and 5yea s
a e mo e so ghum uji in Makueni, compa ed o hose o he same
age (Figu e1) in Nandi. The di e ence in consump ion be ween he
wo age g oups was signi ican wi h P=0.037 and P=0.002 o
younge han 1yea and 1–5 yea s, espec i ely. Makueni house-
holds we e gi ing uji made om maize o olde child en (1–5yea s)
while in Nandi his s a ed wi h child en younge han 1yea .
Consump ion o maize in he o m o lou pe pe son pe day
di e ed ac oss he si es and wi hin age g oups. Fo child en younge
han 5yea s, consump ion anged om 0.1 o 0.25kg pe pe son
pe day in Nandi and Makueni, espec i ely. The o e all a e age
consump ion o maize in he o m o lou in Nandi and Makueni
in e ms o kg pe pe son pe day was 0.18, 0.36 and 0.4 o peo-
ple younge han 5, 6–60, and olde han 60yea s, espec i ely. The
mos ulne able indi iduals o a la oxin poisoning (younge han
5yea s and olde han 60yea s) in Makueni we e consuming 0.22
and 0.41kg o lou pe day, espec i ely, bu his was no he case
in Nandi whe e hose younge han 5 and olde han 60yea s con-
sumed 0.13 and 0.37kg, espec i ely.
Consump ion o milk
Households in bo h Makueni and Nandi had an a e age o 5.9 pe -
sons and consumed on a e age 0.38 o milk pe pe son pe day in
he wo si es. The a e age consump ion in Makueni and Nandi was
0.32 and 0.44 o milk pe pe son pe day, espec i ely. The annual
pe capi a consump ion was 117.9 and 161.9 in Makueni and
Nandi, espec i ely. Six y- h ee pe cen o child en less han 1 yea
old we e consuming milk as esh, 16% consumed milk mixed wi h
po idge, while 3.4% d ank milk wi h ugali and 8.7% ook milk in
he o m o e men ed milk, especially in Nandi.
A la oxin M1 inu ine
A o al o 377 and 362 u ine samples we e collec ed om chil-
d en younge han 5yea s in Makueni and Nandi, espec i ely, and
analysed using cELISA o AFM1 in u ine. Resul s showed ha
79% and 83% o he u ine samples we e posi i e in bo h Makueni
and Nandi, espec i ely (Table1). The e was a signi ican di e -
ence ( =12.64, P alue=0.00) in he mean o a la oxin M1 le -
els in he u ine samples collec ed om he wo coun ies, hough
he e was no signi ican di e ence in he alues be ween u ine
samples om child en younge han 30mon hs and hose be ween
30 and 60 mon hs wi hin he coun ies. U ine samples (posi i e
and nega i e) om Makueni had a highe mean le el o AFM1
(910.56 [721.31, 1099.78] pa s pe illion (pp )) han hose om
Nandi (518. 60 [400.58, 636.62] pp ). The child en younge han
Figu e1. Consump ion pa e ns o die s based on maize, so ghum, and mille by child en younge han 60mon hs in Makueni and Nandi coun ies. Ugali, hick
po idge p epa ed om maize lou ; Uji, po idge p epa ed om lou (so ghum, mille , and maize singly o in combina ions).
134 E.K. Kang’e he e al., 2017, Vol. 1, No. 2
30 mon hs in Makueni had e y high le els o AFM1 in u ine;
being 1.4 imes highe han ha ound in he u ine o child en o
he same age in Nandi. Fo child en be ween 30 and 60mon hs in
Makueni, he le els o AFM1 in u ine we e 2.3 imes highe han
hose omNandi.
A la oxin M1 in b eas milk
A o al o 67 and 98 human milk samples we e collec ed om
Nandi and Makueni, espec i ely, and 86.7% and 56.7% o hese
samples we e posi i e o a la oxin M1 in Makueni and Nandi,
espec i ely (Table2). The e was a signi ican di e ence ( =30.75,
P<0.001) in he mean alues o a la oxin M1 in he b eas milk
om Nandi and Makueni. The Makueni samples had a highe
mean o 8.46 [8.24, 8.68] pp compa ed o 0.02 [0, 0.061] pp
in Nandi. The mean le el in b eas milk samples om Makueni
was 423 imes highe han he mean le el ound in he b eas milk
samples omNandi.
Exposu e h ough maize andmilk
Table 3 shows he exposu e o a la oxins in Makueni and Nandi
among he a ious age g oups. Makueni households had a highe
exposu e a e han he households in Nandi. This is a e lec ion
o highe a e age le els o a la oxins in oods om he wo si es.
Exposu e a es o a la oxins h ough lou in child en younge han
5yea s in Makueni we e 44 imes mo e han in hei coun e pa s
inNandi.
G ow h indices
S un ing
S un ed g ow h is a educed g ow h a e in human de elopmen . I
is a p ima y mani es a ion o malnu i ion in ea ly childhood. The
s un ing and se e e s un ing a es in Makueni and Nandi we e 28.7,
18.5 and 30.7, and 16.5%, espec i ely. The na ional a e age o
s un ing is 26 and 11% o se e e s un ing (KDHS, 2015). The le els
o a la oxin in ce eals om households wi h s un ed child en di -
e ed signi ican ly be ween he wo coun ies (Table4). The AFM1
le els in u ine om he s un ed child en was no signi ican ly di e -
en be ween Makueni andNandi.
Unde weigh
Weigh - o -age is a composi e index o heigh - o -age and weigh -
o -heigh . I akes in o accoun bo h acu e and ch onic malnu i-
ion. Child en whose weigh - o -age (WAZ) is below –2 s anda d
de ia ions (SD) a e classi ied as unde weigh . Child en whose
weigh - o -age is below ದ3 SD a e conside ed se e ely unde -
weigh . The unde weigh (WAZ) child en we e 2.9 and 14.6%
in Nandi (n = 102) and Makueni (n = 103), espec i ely, while
Makueni and Nandi egis e ed a p opo ion o 3.9% each o
se e e unde weigh . The na ional a e age o unde weigh is 11
and 2% o se e e unde weigh (KDHS, 2015). The es ima ed
le els o unde weigh a e 10.2 and 11% in Makueni and Nandi,
espec i ely.
Discussion
The p esence o AFM1 in u ine indica es ecen exposu e o child en
o a la oxin-con amina ed ood because he AFM1 is easily exc e ed
om he body. Child en younge han 5yea s we e in oduced o
ce eal-based die s a di e en imes in he wo coun ies and hei
consump ion o maize-based die s anged om 0.1 o 0.25kg pe
pe son pe day in Nandi and Makueni, espec i ely. Lowe con-
sump ion o maize-based die s in Nandi is due o consump ion o
al e na i e oods om so ghum and inge mille . Nandi compa ed
o Makueni is iche in o he ypes o oods. The p opo ion o
maize con amina ed wi h a la oxin om bo h coun ies was 68.3 and
80.4% in Nandi and Makueni, espec i ely (Kang’e he e al., unpub-
lished da a), wi h Makueni ha ing 24.5% o posi i e samples wi h
a la oxin le els abo e 10 ppb le el. So ghum was equally con ami-
na ed wi h a la oxin, 66.7 and 88.9% o he samples we e posi i e
and 37.1 and 29.9% exceeded he limi s in Nandi and Makueni,
espec i ely. Feeding on such con amina ed oods explains he high
le els o AFM1 in u ine samples om child en in bo h Nandi and
Makueni coun ies. This inding ag ees wi h Gong e al. (2002, 2004)
in Benin who no ed ha he le els o a la oxin–albumin adjunc
le els we e app oxima ely wo imes highe in ully weaned chil-
d en compa ed wi h hose ecei ing a mix u e o b eas milk and
solid ood.
Human b eas milk samples om Makueni had highe AFM1 le -
els han he le els in Nandi samples (mean 8.46 [8.24, 8.68] pp in
Makueni compa ed o 0.02 [0, 0.061] in Nandi). The p opo ion o
samples wi h le els abo e he 25 pp EU limi was 10.2% in Makueni
bu none exceeded his limi (25 pp ) in Nandi. This is a u he e lec-
ion o he highe le els o a la oxins ound in ce eals consumed in
hese wo a eas whe e mo e samples exceeded he 10 ppb limi in
Makueni (25.05 [18.48, 31.62]) han in Nandi 0.98 ([0.86, 1.10]).
In Nige ia Adejumo e al. (2013) epo ed 82% o he b eas milk
samples we e posi i e and 16% exceeded he 25ng/kg (pp ) limi
o AFM1 by he Eu opean Union. The socioeconomic s a us o he
mo he s o he child en in he Nige ian s udy was ound o in lu-
ence hei die a y exposu e and also ha o he in an s b eas eeding
on hem. Abdul azzaq e al. (2003) epo ed ha in he Uni ed A ab
Emi a es 92% o he b eas milk samples es ed we e posi i e, while
Sadeghi e al. (2009) epo ed a p e alence o 98.1% posi i e in he
b eas milk samples aken in Teh an bu only one sample exceeded
he EU/USA limi o 25ng/kg limi . The majo sou ce o AFM1 in
b eas milk, like AFM1 in child en u ine, is he ecen consump ion
o a la oxin-con amina ed oods by he nu sing mo he s.
Homeg own maize cons i u ed 75 and 59% o he household
consumed maize in Nandi and Makueni, espec i ely. The home-
g own maize had mean a la oxin le els o 0.98 [0.86, 1.10] and 25.05
[18.48, 31.62] o Nandi and Makueni, espec i ely (Kang’e he e al.,
unpublished da a). The o he sou ce o high le els o AFM1 in b eas
Table1. A la oxin M1 in posi i e u ine samples om child en unde 30mon hs and younge han 5yea s in Makueni and Nandi coun ies.
Coun y Age g oup Mean (pp ) (95% CI) - alue P- alue
Makueni Younge han 30mon hs (n=34) 1182.894 (±637.99) 0.562 0.46
30–60mon hs (n=47) 1546.257 (±662.65)
Nandi Younge han 30mon hs (n=42) 857.279 (±625.09) 0.481 0.49
30–60mon hs (n=54) 667.294 (±299.06)
Exposu e o Kenyan popula ion o a la oxins in oods, 2017, Vol. 1, No. 2 135
milk is consump ion o cow milk con amina ed wi h AFM1. The p es-
ence o AFM1 in cow milk is a esul o eeding AFB1 con amina ed
eeds o he animals. Spoil maize was used as animal eed ac oss he
wo coun ies (23.9% in Makueni and 77.6% in Nandi, Kang’e he
e al., unpublished da a) and his ac ed as an exposu e ou e o ani-
mals o a la oxins and e en ually exposu e o b eas eeding mo he s
and child en weaned on o cow milk o his myco oxin. A la oxin M1
mean le els in he home-p oduced milk we e 22.3 [16.89, 7.67] pp
in Makueni and 2.7 [1.92, 3.50] pp inNandi.
Conside ing ha a child consumes 776±141g pe day o b eas
milk (WHO/UNICEF, 1998), and aking an a e age o 776g pe day
and a mean o a la oxin con amina ion o 10.83 and 0.06 pp o
b eas milk ob ained om Makueni and Nandi, espec i ely, de e -
mined using HPLC, exposu e h ough his ou e would be 6×10−3
and 1×10–6 µg pe kg body weigh (bw ) pe day in Makueni and
Nandi, espec i ely. The le els a e lowe han he allowed limi o
19 400 pp pe day in ake conside ing a maximum limi o 25 pp
and 776g o milk in ake pe day (Ghiasian and Maghsood, 2012).
A la oxin in ake in child en om his ou e would be exc e ed
h ough u ine and is consis en wi h hese in ake le els.
This s udy con i ms ha malnu i ion is a p oblem in he wo
coun ies; Makueni shows a highe pe cen age o child en unde -
weigh , 14.6%, and equa ed o Nandi, 2.9%. Makueni also had a
highe pe cen age o s un ed child en (28.7%) han Nandi (18.6%).
These igu es, al hough lowe han hose epo ed o Kenya (16.4%
o unde weigh and 36.2% o s un ing; WHO, 2010), he Makueni
(in Eas e n p o ince) igu es a e lowe o s un ing and highe o
unde weigh han hose epo ed o he Eas e n p o ince (30.1%
s un ing and 12.2% unde weigh , KDHS, 2015). Again, he Nandi
(Ri alley p o ince) igu es a e highe o s un ing han he igu es
gi en o he en i e Ri alley (14.9%) bu less han he unde weigh
igu e (7.3%) o Ri alley p o ince (Kenya Nu i ional p o ile,
FAO, 2005), al hough hese alues a e high enough o cause conce n.
These igu es a e also compa able wi h he p e alence eco ded by
Gong e al. (2002) in Togo and Benin o 33% o s un ing and 29%
o unde weigh . Al hough he e idence linking a la oxins o causal
o s un ing is s ill weak, a la oxins a e known o con ibu e o s un -
ing. I was no ed in a s udy in Togo and Benin (Gong e al., 2002)
ha he deg ee o s un ing and unde weigh in child en younge han
5yea s was co ela ed wi h high a la oxin–albumin adduc s ound in
he se um o 99% o he child en. In Nandi, child en younge han
30mon hs had highe le els o a la oxin M1 in u ine han hose o e
30 bu less han 60mon hs old, bu his was he e e se in Makueni.
The di e ence in he a la oxin M1 le els in u ine o child en younge
han 30mon hs and olde han 30mon hs in Makueni and Nandi
coun ies was no s a is ically signi ican (  = 0.562, P = 0.456;
= 0.481, P = 0.49, espec i ely). The e was no signi ican di e -
ence o he AFM1 in u ine o child en younge han 30mon hs in
Table2. A la oxin M1 in b eas milk samples (cELISA and HPLC) om b eas eeding mo he s in Nandi and Makueni coun ies.
Sample Si e % Posi i e % >25 pp Range o posi i e (pp ) Mean (pp ) [95% CI] - alue P- alue
cELISA
B eas milk Makueni (n=98) 86.7 10.2 0.215–47.5 8.46 [8.24, 8.68] 19.96 <0.001
Nandi (n=67) 56.7 0.0 0.003–3.7 0.02 [0, 0.061]
HPLC
B eas milk Makueni (n=18) 22.2 11.1 1.4–152.7 10.83 [6.86, 14.8] 1.4 0.183
Nandi (n=21) 9.5 0.0 0.5–0.8 0.06 [0.043, 0.077]
Table3. Exposu e o a la oxins om consump ion o maize and a la oxins in milk in Makueni and Nandi coun ies.
Food ype Age in yea s A la oxins
Makueni Nandi
A e age consump ion
(kg pe day)
A e age exposu e
(µg pe kg bw pe day)*
A e age consump ion
(kg pe day)
A e age exposu e
(µg pe kg bw pe day)*
Maize lou <5 0.28 0.49 0.17 0.011
6–59 0.59 0.26 0.48 0.008
O e 60 0.60 0.26 0.48 0.008
Milk <5 0.27 0.0004 0.55 0.0001
6–59 0.36 0.0001 0.73 0.00004
O e 60 0.33 0.0001 0.72 0.00004
*The a e age body weigh was based on median measu ed body weigh o 16 500 men and 19 969 women in 13 EU s a es a e applying g ow h ac o s. Fo
less han 5yea s, he a e age body weigh was he mean o a e age body weigh o child en less han 3yea s and a e age body weigh o child en be ween 3 and
6yea s ( an Buu en e al., 2012).
Table 4. A la oxin le els in ce eals om households wi h s un -
ed child en and A la oxin M1 con en in u ine samples om he
s un ed child en in he same households in Makueni and Nandi
coun ies.
Coun y Food ype Mean a la oxin le els
in ppb (±95% CI)
Nandi Maize (n=37) 0.97 [0.67, 1.27]
So ghum (n=9) 27.8 [0, 63.88]
Mille (n=6) 1.50 [1.06, 1.94]
U ine AFM1 (n=41) 997.3 [0, 17638.82]
Makueni Maize (n=98) 41.5 [26.65, 56.35]
So ghum (n=46) 20.43 [6.94,33.92]
Mille (n=1) 2.00
U ine AFM1 (n=106) 1336 [925.33, 1746.67]
AFM1,A la oxin M1 in pa s pe illion.

136 E.K. Kang’e he e al., 2017, Vol. 1, No. 2
Makueni and Nandi ( =0.67, P=0.415), bu he e was a signi ican
di e ence in he AFM1 le els in u ine samples o child en olde han
30mon hs and younge han 60mon hs ( =6.126, P=0.015) wi h
hose in Makueni ha ing highe le els and double hose inNandi.
The a la oxin le els in maize, so ghum, and mille om house-
holds wi h s un ed child en and AFM1 in u ine o s un ed child en
om he same households we e compa ed o Makueni and Nandi
(Table4). Households wi h s un ed child en bu whe e no samples
we e analysed o a la oxins we e no aken in o accoun . The mean
a la oxin le els in maize om households wi h s un ed child en
we e signi ican ly di e en be ween Makueni and Nandi ( =10.75,
P<0.01) whe eas a la oxin le els in so ghum and mille om house-
holds wi h s un ed child en and u ine om s un ed child en we e no
signi ican be ween he wo coun ies. The likelihood o child en who
we e s un ed and being exposed o a la oxins (p esence o AFM1 in
u ine) was 6.8 imes mo e likely o occu in Makueni compa ed o
2.1 imes in Nandi (OR=6.8 and 2.1, espec i ely) while he p ob-
abili y o unde weigh child en being exposed o a la oxins was 2.4
imes mo e likely o occu in Makueni compa ed o 1.9 imes among
child en in Nandi (OR=2.4 and 1.9 espec i ely).
Conclusions
The exposu e o people o a la oxins (o myco oxins) consequen ly
s a s ea ly and con inues in o adul hood. The esul s o his s udy
emphasize he need o be mo e igilan on a la oxin and con ol. I
is impo an o educa e he a me s on be e ca le eeding p ac ices
and mo he s on he need o eed he amily wi h good-quali y ce eals
o a oid ch onic exposu e o a la oxin h ough he eed-milk chain.
Mo he s would be a good a ge o hese capaci y building messages
as p epa a ion o he amily ood is he mo he ’s main esponsibili y.
Acknowledgemen s
We hank he Minis y o Fo eign A ai s o Finland o p o iding inancial
assis ance ha enabled his s udy (MFA 24819801); he communi ies in Nandi
and Makueni o allowing us o ca y ou he s udy and Go e nmen o ice s
in bo h coun ies o hei acili a ion. The iews exp essed in his pape a e no
necessa ily hose o he unding agency o ins i u ions aking pa in he s udy,
bu hose o he au ho s.
Con lic o in e es s a emen . The au ho s decla e ha hey ha e no con lic o
in e es wi h he publica ion o his pape .
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