PCB concentrations in breast-feeeding mothers and their infants

Chemosphere. Vol. 37, Nos 9-12, pp. 1731-1741, 1998 Q 1998 Elsevier Science Ltd All rights reserved. Printed in Great Britain 004%6535/98 $19.OO+O.OU

PII: SO0456535(98)00238-O

TIME COURSE OF PCDDIPCDFIPCB IN BREAST-FEEEDING

MOTHERS

K. Abraham, 0. Ptipke*, A. Gross, 0. Kordonouri,

Children’s Hospital, Charite-Virchow

CONCENTRATIONS AND THEIR INFANTS

S. Wiegand, U. Wahn and H. Helge

Klinikum, HU Berlin, Augustenburger

Platz 1, 133 53 Berlin, Germany

Geierstr. 1, 22 305 Hamburg, Germany

*ERGO Forschungsgesellschaft,

ABSTRACT

PCDD/PCDF/PCB lactation)

concentrations

were measured

in samples from four mothers

(at delivery and during

and their infants (at birth and the end of first year of life). For two of these mothers it was the

second delivery and breast-feeding

period, and additional data were available from first lactation period and

the first-born infant at the age of 11 to 12 months. Five of the six infants were tblly breast-fed weeks. In four of them a distinct PCDD/PCDF/PCB life: concentrations Due to decreasing

for at least 17

accumulation was observed at the end of the first year of

in blood fat were 1.5 to 3.6 times higher than maternal levels measured at the same time. maternal body burdens during lactation, PCDD/PCDF

concentrations

at 11 to 12 months

of life were only about half as high in the second infant as in the first one at the same age. During second pregnancy, no important change of the concentrations

was observed in maternal blood.

01998 Elsevier Science Ltd. All rights reserved

KEYWORDS

Polychlorinated

dibenzo-p-dioxins

biphenyls (PCBs); toxicokinetics;

(PCDDs);

polychlorinated

dibenzofurans

(PCDFs);

infants; mother’s milk, prenatal transfer, breast-feeding.

1731

polychlorinated

1732 INTRODUCTION

Infants are exposed to PCDDs, PCDFs and PCBs prenatally [l] and via mother’s milk [2,3]. With a longer duration of breast-feeding with a decrease

an increasing body burden of these compounds

in the maternal

body burden.

can be expected in the infant, along

After six to seven months

of nursing the concentrations

measured in blood fat of infants were distinctly higher than those of their mothers. In contrast, concentrations measured

in formula-fed

breast-fed

infants [3].

infants at the end of the first year of life were less than one-tenth

In order to get more information

about PCDD/PCDF

mother and her children, concentrations

toxicokinetics

of these compounds

during pregnancy

of those in the

and lactation in the

were measured in samples of four mother/child

pairs.

EXPERIMENTAL

CONDITIONS

Samples were collected from four mothers (at delivery, and about 5 and 12 months later) and their breast-fed infants. Two of these children were second-born, the first-born following

and samples of the mothers before second delivery and of

child were also analysed. Basic data of the mothers

and their children is presented

in the

table (for time course of mothers’ body weight see Tables 1 to 4). All infants were born after

pregnancies without major problems. They were healthy and had a normal weight gain during the first year of life. With exception

of mother/child

Mother/child

pair III, all infants were Mollybreast-fed

pair 1 a+b

pair n a+b

for at least 17 weeks. The time

pair III

1

pair IV

Mother: age at first delivery Height body weight before1”prepay body mass index

34 ys 172 cm 58 kg 19.6 kg/m2

31 ys 174 cm 65 kg 21.5 kg/m2

31 ys 164 cm 57 kg 21.2 kg/m2

31 ys 176 cm 76 kg 24.5 kg/m2

First child: born, gender Gestational age, body wt Fully breast-fed/weaning at equiv. full breast-feeding Blood sampling age/body wt

1 l/92, male (B-l)* 40 wks, 3.88 kg 18134 wks 26 wks 49 wks, 10.4 kg

4/93, male (B-2)* 40 wks, 3.74 kg 17147 wks 30 wks 50 wks, 11.9 kg

12/94, female 39 wks, 3.30 kg O/18 wks 7 wks 56 wks, 9,2 kg

3/95, female 41 wks, 3.15 kg 26135 wks 30 wks 51 wks, 9.7 kg

Second child: born, gender Gestational age, body wt Fully breast-fed/weaning at equiv. fully breast-feeding Blood sampling age/body wt

1 l/95, female 40 wks, 3.32 kg 20134 wks 29 wks 48 wks, 8.9 kg

l/95, male 40 wks, 3.80 kg 26148 wks 32 wks 52 wks, 12.3 kg

* First-born children participated in a PCDD/PCDF balance study [3]: names of the children in parentheses

1733 of equivalent full breast-feeding milk corresponds At delivery,

was estimated from nutrition records: the total amount of ingested mother’s

to this duration of till breast-feeding

samples were taken from placenta,

mother’s blood (mother/child

pairs

Ib, IIb,

with abrupt weaning.

umbilical cord blood,

III, IV). Mother’s

obtained at the end of the first year of life, together with-a’blood milk of mothers

untersuchungsamt

Oldenburg),

Ia and IIa was analysed

stool and

Ib

and IIb. In all six children, blood was

sample of the mother.

4 weeks

after first

delivery

(by Lebensmittel-

and one month later in mother Ia and shortly before weaning in mother IIa.

Whole blood was drawn by venipuncture and collected in heparinised

transitional

milk was collected 4 weeks later and again at

the age of about 5 months, together with a blood sample in mothers

Additionally,

meconium,

(15 to 20 ml in the infants, 40 ml in the mother) before breakfast

vials. Cord blood was also taken by venipuncture

with a large lumen needle. All

these samples as well as those of placental tissue (about 100 g) and mother’s

milk.(about

frozen at -18°C until analysis. Meconium and transitional stool as collected in pre-extracted

100 ml) were

diapers [2,3] was

frozen and later lyophilised. The birth of second newborn Ib occurred unexpectedly collection was impossible

(within one hour at home), and the planned sample

(no cord blood) or not optimal (meconium

pre-extracted

cotton

diapers

leading to contamination

2378-T4CDF,

but probably also with other PCDDs/PCDFs/PCBs).

PCDDs and PCDFs were analysed as described elsewhere for PCDDs

and PCDFs

were calculated

and transitional

stool not collected in

with non-2,3,7,%substituted

[l-3]. 2378-T4CDD

PCDDs/PCDFs

toxicity equivalents

using I-TEFs not taking PCBs into account

and

(I-TEq)

[4]. Concentrations

below the limit of detection were recorded as one half of the minimum detectable value.

RESULTS

Concentrations

AND DISCUSSION

of the main PCDD/‘PCDF/PCB

congeners

children are listed in Table 1 to 4 (for mother/child PCDD/PCDF/PCB concentrations

analyses’ performed

measured in . the samples of the mothers and their

pairs I tti IV). To our knowledge,

to this extent in mother/child

these are the first

pairs, allowing comparison ,. in the mothers anBtheir children longitudinally. The main aspects are the following:

of the

.

PCDD/PCF/PCB concentrations in maternal samples PCDD/PCDF/PCB

levels in maternal blood and milk sample were found to be within the typical range

measured in other samples from Germany (1994 in 134 blood samples: median 17.3 pg I-TEq/g fat, range 5.2 to 43.9 pg I-TEq/g fat, median age 36 years) [5].

na. Ii.8.

PCB 126 PCB 169

PCB 138 PCB 153 IPCB 180

115

71

190

n.a. n.a.

14.6

6.0

1.9

24.2

2.4

0.7

3.8

3.6

1.1

na. na. na. na. na.

111 209 107

105 111

12.3

1.9 8.6 4.1 4.0 3.7 Cl.9 4.1 18.9 2.1 13.3 21.8 189.3

2.4 17.0

79.8 98.0

16.3

2.1 14.8 5.7 4.0 3.2 1.1 4.2 22.2 2.3 4.4 11.0 56.1

na. n.a. na.

n.a. na.

287 270

29.2

9.8 8.1 4.4 7.8 43.0 7.1 13.1 24.3 148.7

11.1

3.7 23.1

66.4 128 99.4

4.1 18.6

na. n.a.

10.3

11.7 118.2

1.7 7.1 3.5 4.6 2.3 2.5 3.6 12.9 2.8 na.

1 l/95 72 kg

* snalyscd by LebensmitteluntersuchungsamtOldenburg [3] m = maximum value, due to possible contribution of a contaminant

I

b&i

19.1

I-T&

PCB 105 PCB 118

63.6

1.9

19.9

compound Wg) 2378-T4CDD 23478-P5CDF 12378-P5CDD 123478-H6CDF 123678N6CDF 234678N6CDF 123478N6CDD 123678-H6CDD 123789-H6CDD 1234678-H7CDF 1234678-H7CDD OCDD

l/93

mother

Oligil1r notber Mother mother 1” child @seIIIno.) 10/93 10193 58 kg 10.4 kg

blood

matrb‘ milk*

milk blood

Before 20d pregnancy blood

I

21.8 m 262 m

26.9m 701 Ill

25.2 42.2 28.2

2.3 14.6 48.4 92.4 72.4

49.7 95.5 62.61

34.9 67.5 62.9

1.2 7.4

59.0 60.6

11.2

1.2 7.8 3.9 5.2 4.0 1.6 3.6 15.9 2.7 33.3 22.1 202.6

4196

n.a. na. n.a.

n.a. n.a.

52.6 66.6

10.1

1.3 6.5 3.6 4.5 3.3 c2.0 3.1 14.7 2.3 32.4 21.6 202.9

13.9 16.7 10.71

n.d. 3.0

47.5 13.7

10.8

2.8 6.1 3.2 4.7 2.9 1.5 2.5 10.6 2.6 8.3 28.8 230.2

na. = not analysed, n.d. = not detected (no signal in the relevant time window)

“.a

n.a.

ma

11.8.

8.8.

2.9 7.0

47.3 14.9 1.8 7.6

75.7 81.7

68.6 78.9 UP. “.8.

11.0

11.9 12.5 m

1.2 9.3 3.7 4.6 3.1 1.7 3.1 14.6 1.7 19.3 13.3 77.7

4196 60 kg

1.6 10.1 4.3 3.4 2.2 1.1 3.5 15.4 1.9 10.1 8.5 42.4

12195

blood

notber mother

milk

5 mo. after 2* birth

14.5

14.5 m

3.9 m

1.8 m

3.5 m

5.3 m

3.1 m

7.8 m

2.3 m

1.5 m

1 l/95 3.3 kg

transit. milk stool 2* child mother

39.3 m

meconimn

15.8 m

cord blood

2.2 11.7 5.7 2.2 3.0 1.4 3.4 9.8 2.2

1 l/95

placenta

at or shortly after 2”d birth

Concentrations of PCDDs, PCDFs and PCBs in samples of mother I and her first (a) and second (b) child, based on lipids extracted. Bold face: childrens’ samples. Empty rows: sample not available.

date: 12192 body weight

Table 1

5 g

PCB 126 PCB 169

230

PCB 138 PCB 153 PCB 180

4.8 21.8 111 145 92

4.6 23.9

194 254 138

85.8 52.3

4.3

298 362 1741

121 143 93

3.4 21.4

374 148

11.0 63.5

11.9 88.4 58.0

2.7 7.4 3.8 3.6 2.8 1.6 3.1 14.9 2.4 4.2 28.6 210

37.5

236

9.0 58.1

47.5 11.3

13.4

9.7 3.5

11.2

31.5 13.8

* analysed by Lebensmittelunters~hungsamt Oldenburg [3] m = maximum value, due to possible contribution of a contaminant

160 115

La. n.a.

PCB 105 PCB 118

(r&g

105 166

n.a. *.a.

10.5

12.8

22.2

1.8 7.1 3.6 3.1 3.0 1.7 3.5 12.7 2.7 5.0 28.0 205

1.5 9.7 5.4 3.6 2.6 1.0 4.2 18.5 3.3 3.2 12.1 111

I-T&

36.2

2.9

4.0

21.3

3.0

1.0

4.1

4.4

8.9

21.9

104

2.5

nother mother mother lst child

compound (Pg/g 2378-T4CDD 23478-P5CDF 12378-P5CDD 123478N6CDF 123678-H6CDF 234678-H6CDF 123478-H6CDD 123678-H6CDD 123789-H6CDD 1234678-H7CDF 1234678-H7CDD OCDD

dat body weigh

origll

matri:

Before 2”dpregnancy

51 69 35

1.1 7.4

40.4 26.3

18.5

3.3 18.5 7.7 3.1 1.5 0.6 3.7 7.5 1.7 1.2 11.6 52

165 237 114

3.6 23.3

106.0 23.6

6.5

1.0 4.8 2.4 1.8 1.3 0.6 2.6 7.9 1.4 1.3 17.6 92 1.7

1.5 1.9

6.3

15.6

9.1 33.5 212 272 1361

66 93 53

153.0 100.0 2.1 11.7

50.0 36.9

5.2 . 17.3 2.7 2.0 25.3 101

3.2

2.6

n.d. 6.5 n.d. n.d. 14.8 108

5.7 4.7

2.3

2.1 13.4

1.4 4.1

I

6195

152 200 95

3.5 23.5

129 93.9

11.3

106 136 63

14.1 42.1

54.9 41.6

6.0

1.4 1.2 10.0 3.7 3.8 1.9 3.3 2.0 2.2 1.5 1.1 1.2 3.7 1.7 14.5 6.1 1.9 1.4 1.3 2.9m 18.6 18.0 72 144

6195 68 kg

notber mother

milk blood

5 mo. after 2”dbirth

1.1

66 87 56

1.5 9.4

42.6 33.3

5.6

n.d. 7.5 n.d. 3.4 m 22.1 139

1.3

1.7

2.6

1.9

3.5

891

167 210

8.1 39.3

114.2 88.1

16.0

100

17.9

5.2 (4.6

22.4

n.d.

3.7 9.8 5.9 7.8 4.1 c2.0

n.a. = not analysed, nd. = not detected (no signal in the relevant time window)

38.6 49.5 25.4

2.1 8.3

46.5 25.1

8.4

1.5 4.8 2.5 2.5 2.3 3.2 2.9 14.2 4.0 6.3 22.4m n.a.

at or shortly after 2”d birth

Concentrations of PCDDs. PCDFs and PCBs in samples of mother II and her first (a) and second (b) child, based on lipids extracted. Bold face: cbildrens’ samples.

samples take1

Table 2

1736 Table 3

Concentrations of PCDDs, PCDFs and PCBs in samples of mother/child pair III, based on lipids extracted. Bold face: childrens’ samples. Empty rows: sample not available.

samples take; matri

at or shortly after birth blood

placenta

cord blood

meconium

5 mo. after birth

transit. stool

milk

milk

bloom

13 mo. after birth blood

blood

nother

child 1196 9.2 kg

origi da! body weigl

mother 12194 70 kg

child

child

12194

12194

12194 3.3 kp:

l/95

compound (Pg/g: 2378-T4CDD 23478-PXDF 12378-PSCDD 123478-H6CDF 123678-H6CDF 234678N6CDF 123478N6CDD 123678-H6CDD 123789-H6CDD 1234678N7CDF 1234678-H7CDD OCDD

2.2 8.5 4.8 5.2 3.7 1.4 4.3 16.5 3.7 6.7 42.6 452

3.0 6.6 3.0 2.3 1.6 Cl.0 1.7 7.0 1.3 2.0 16.9 110


< 2.2 4.5 2.4 3.3 2.6 < 1.7 < 1.9 8.2 < 2.3 5.3 m 26.6 221.8

2.1 8.6 4.3 3.5 2.8 1.3 2.6 14.5 2.6 3.1 24.3 110.1

14.8 4.2 9.1 47.2 379

n.d. 6.8 n.d. 16.8 m 17.0 105

1-W

13.4

9.7

4.1

6.9

11.8

11.5

4.2

114 44

61 14

23.4 8.5

23.4 10.1

112 43.3

81.5 32.4

43.5 23

PCB 105 PCB 118

5.8 23.2

3.6 11.3

3.8 13.8

3.0 8.7

5.4 21.8

3.1 15.6

1.7 8.7

PCB 138 PCB 153 PCB 180

82.9 113 62.3

41.3 55.4 22.7

35.5 47.8 15.2

23.1 26.3 12.6

77.7 94.9 44.31

52.4 67.5 37.9

23.7 28.7 10.9

(&g

PCB 126 PCB 169

child mother

nother mothe

1196 6Okg 1.9 6.3 3.9 5.4 3.9 1.6 4.5

n.d. 2.6 2.2 3.1 2.0 d2.0

m = maximum value, due to possible contribution of a contaminant n.d. = not detected (no signal in the relevant time window)

Changes duringpregnany During second pregnancy,

no important changes of PCDD/PCDF

concentrations

were observed in maternal

blood fat (mother I: 12.3 and 10.3 pg I-TEq/g, mother II: 10.5 and 11.9 pg I-TEq/g fat). In mother II, almost unchanged values were measured for the diierent increased

during

Theoretically,

pregnancy,

a slight decrease

gain during pregnancy.

measured

PCBs. This is in contrast to an early report that PCB levels

gas chromatographically

of PCDD/PCDF/PCB

concentrations

with

a Kaneclor

might be expected

500 standard

[6].

from body weight

1737 Table 4

Concentrations of PCDDs, PCDFs and PCBs in samples of mother/child pair IV, based on lipids extracted. Bold face: childrens’ samples. Empty rows: sample not available

samples taker

at or shortly after birth blood

matliJ

placenta

origin nother 3195 90 kg

date body weigh

3195

6 mo. after birth

cord meco- transit. blood mum stool child child child 3195 3195 3.2 kg

milk

milk blooc

mother 4f95

nother mother 9195 75 kg

12 mo. after birth blood

17 mo. fter birth

blood

blood

nother child 3196 3196 72 kg 9.7 kg

mother 8196 68 kg

2.1 3.0 17.0 9.6 6.1 7.6 4.4 9.6 4.0 9.0 1.7 2.0 6.3 8.8 24.1 33.7 4.1 10.4 14.6 21.0 m 43.1 34.6 730.0 432.3

1.3 7.7 4.2 5.7 5.0 2.0 4.1 19.3 4.3 19.1 48.2 694.0

compound @g/g)

2378-T4CDD 23478-P5CDF 12378-P5CDD 123478-H6CDF 123678N6CDF 234678-H6CDF 123478-H6CDD 123678-H6CDD 123789N6CDD 1234678-H7CDF 1234678-H7CDD OCDD

1.9 9.5 4.5 5.5 4.4 2.3 4.6 20.6 3.7 17.7 46.4 645

2.3 -z 2.7 22.0 4.8 14.4 4.0 7.3 2.5 2.5 2.3 1.0 ~3.6 8.1 < 2.5 11.1 11.1 2.6 e3.5 4.9 12.3 m 23.5 9.2 161 132

I-TEq

14.5

24.4

PCB 126 PCB 169

78.6 55.7

PCB 105 PCB 118 PCB 138 PCB 153 PCB 180

kg/g

0.7 2.4 1.4 2.2 1.5 1.1 1.4 7.7 1.5 6.5 23.1 379.2

1.3 8.5 4.0 3.4 2.5 1.1 3.6 15.2 2.7 5.8 21.7 160.4

1.3 8.7 4.3 3.8 2.9 1.2 3.5 14.6 2.8 5.5 17.9 135.4

9.1

5.1

10.9

11.1

15.8

23.7

12.8

28.4 17.9

10.9 15.3

28.7 21.8

115 72

94.9 61.5

103.0 79.4

143.0 76.0

80.0 52.7

7.2 32

cl.0 5.3

2.2 8.2

2.3 8.8

2.8 18.9

2.8 13

2.3 m 2.9 m 3.5 15.3 m

n.a. n.a.

136 177 127

31.9 45.0 23.8

26.9 35.1 22.0

17.6 26.0 20.3

93 125 56

61 83 43

43.0 60.0 42.0

43.0 57.0 33.0

n.a. n.a. n.a.

m = maximum value, due to possible contribution of a contaminant n.a. = not analysed

Prenatal transjer Lipid based concentrations lower chlorinated

in the newborns were lower than in their mothers, with highest transfer rates for

PCDDrJPCDFs.

were

generally

[1,7], placental

found

Concentrations

of PCDDs and PCDFs were in the same range in fat of cord blood, meconium and transitional

PCDD/PCDF/PCB

body burden

discussed elsewhere

[ 11.

than those

of 2378-T4CDD,

and

of their origin, all samples therefore

to be higher

concentrations

23478-P5CDF

stool. Irrespective

12378-P5CDD

As in other mothers

in maternal

seem to be suitable for a representative

at birth. Details of the prenatal

PCDD/PCDF/PCB

transfer

blood.

analysis of have been

1738 Comparison of concentrations in maternal milk and bloodfat The comparison

of PCDDLPCDF concentrations

in maternal milk and blood fat obtained on the same day or

within 4 weeks (after delivery) shows differences concentrations

would be expected

these compounds.

which are not easy to explain. Based on extracted

to be in the same range, as a consequence

lipids,

of the lipophilic character of

This was actually observed in blood and milk fat of mother Ib (10.3 and 11.9 pg I-TEq/g at

second delivery, 11.2 and 11.0 pg I-TEq/g five months later) and mother III (13.4 and 11.8 pg I-TEq/g at delivery). However, blood

in mother II higher PCDDRCDF

fat (for I-TEq:

PCDD/PCDF

+22%

concentrations

different PCBs corresponded

in 4194, +31%

concentrations

at second

delivery,

were found in milk fat compared +88%

in 6/95).

In contrast,

to

lower

were found in milk fat of mother IV (-25%) compared to blood fat. Levels of more or less to these variations.

Compared to her blood fat data, I-TEq concentration

in milk fat of a mother after delivery of twins has been

reported to have been slightly higher, but clearly lower after more than two years of nursing [8]. Reasons

for the observed

PCDD/PCDF xenobiotics

analyses,

differences systematic

in milk and blood fat remain unclear. investigations

of factors

influencing

Due to the high costs of

the

concentrations

in milk or blood fat are not available, e.g. day-to-day variations, dependency

fat composition, were reported

of these

of the deposition on

or analytical intra- and inter-assay variations. Human milk samples collected in the evening to contain

significantly

higher PCDD/PCDF

concentrations

than in the morning

(average

increase on fat basis + 8 “/) [9]. As observed by others, concentrations

of the less toxic hepta- and octa-chlorinated

PCDD/PCDF

congeners

were distinctly lower in milk fat than in blood fat, obviously due to lower blood-milk transfer rates.

Postnatal transfer via mother’s milk: increasing concentrations in the infant As the result of postnatal xenobiotics

PCDD/PCDF/PCB

was observed in the infants breast-fed

transfer

via mother’s

milk, a distinct accumulation

of the

for six to seven months (duration of equivalent full breast-

feeding). At the end of the first year of life, I-TEq concentrations

in blood fat of the infants were found to be

clearly higher than those measured in maternal blood fat at the same time: 2.4 times in first-born infant I, 3.6 times in first-born

infant II, 2.9 times in second-born

infant II, and 1.5 times in infant IV (1.9 times if the

additional analysis of the maternal blood 5 months later is taken). This accumulation the basis of intake data and assuming complete absorption,

a passive distribution

is as high as expected on following

mainly that of

fat in the body, and a negligible elimination during the first year of life [3]. Lower accumulation

rates were found for higher chlorinated PCDDs/pCDFs,

lower concentrations

in mother’s milk fat (compared to blood fat) and lower intestinal absorption rates [2,3].

For the PCBs measured, accumulation

obviously due to their relatively

rates comparable to those for PCDDs/PCDFs

mentioned above except infant IV (most PCB concentrations

were found in all infants

in the same range as measured in the mother).

1739 Although the second-born TEq concentrations

infant of mother I was breast-fed

for the same duration as the first-born brother, I-

at the end of the first year of life were not different from those in the mother measured at

the same time. Body weight loss during first and second lactation period in this mother was not different. Possible reasons for varying PCDD/PCDF/PCB been discussed. concentrations

A lower

accumulation

concentrations

in mother’s blood and milk fat have already

of these xenobiotics

in this infant may play a role, the PCB

in blood fat in particular were relatively low. Fecal PCDDLPCDF excretion in this infant abler

weaning (age 11 months) [IO] corresponded conditions

well to that in the first-born brother measured under the same

[3].

In infant III, the “accumulation”

rate was only 0.37 for I-TEq, resulting from the shorter duration of nursing

(less than IWOmonths of equivalent full breast-feeding). to the concentrations

I-TEq concentration

in blood fat (4.2 pg/g) was near

measured in two formula-fed infants at the end of the first year of life (2.4 and 3.2 pg/g)

[31. Compared to cord blood fat, I-TEq concentrations 1.9 times higher in second-born

infant II (2.5 times higher compared to meconium and transitional

2.6 times higher in infant IV, both breast-fed period, I-TEq concentration

infants’ blood fat at the end of the first year of life were

for about 30 weeks. In infant III, breast-fed

for a much shorter

in cord blood fat was not different from that measured in blood fat at 13 months.

Comparison of concentrations

in bloodfat offirst- and second-born infants

As a result of the decreasing

maternal PCDD/PCDF

concentrations

stool) and

body burden during the first lactation period, I-TEq

in the second-born infants at the end of the first year of life were less than half those of the

first-born infants at the same age. Similar ratios were calculated for the different PCBs measured in first- and second-born

infant of mother II.

Postnatal transfer via mother ‘s milk: decreasing concentrations in the mother Calculated accumulations

rates (Concentration

ratios: infant’s/matemal

blood fat at the end of the fust year

of life, see above) are not only intluenced by the increasing body burden in breast-fed concomitant

decrease of the maternal body burden. This can be expected from calculations

milk fat transferred However,

infants, but also by a

[3], and was observed

in three of five lactation

periods

of the amount of

lasting at least 17 weeks.

in second lactation period of mother I and in mother IV no decrease in maternal concentrations

was measured. In mother IV, an unexpectedly delivery. Therefore,

high I-TEq concentration

( 15.8 pg/g blood fat) was measured

12 months after

an additional blood sample was collected five months later (Table 4). The I-TEq value

(12.8 pg/g blood fat) was lower (despite a body weight loss of 4 kg during this period), and also slightly lower than at delivery (14.5 pg/g blood fat).

1740 Considerably

decreased

PCDD/PCDF

concentrations

were measured in blood and milk samples of a mother

who nursed twins for 2 years [8], and in milk samples of another mother who nursed her baby for one year [ 111. Statistically, PCDDiPCDF

concentrations

in human milk fat were reported to decrease with the number

of nursed children and with the number of nursing weeks [ 1 l- 141. In 15 human milk samples (from the first, 6” and 12* week after delivery)

analysed for PCDDsiPCDFs,

an average

compared to the first week was observed [ 14, 151, but with considerable

decrease

of 25 % in the 121h

inter-individual

variation [ 151.

CONCLUSION

Accumulation

of PCDDs, PCDFs and PCBs in breast-fed

several months of breast-feeding,

concentrations

infants is as high as expected

of these xenobiotics

theoretically.

Atter

in blood fat of the infant usually clearly

exceed those in blood fat of the mother measured at the same time.

ACKNOWLEDGEMENTS

Thanks to Bruno, Daniel, Johanna, Mira, Sina, Tim and their mothers for outstanding to express our gratitude

for performing

Schilling, Holger Jorgensen,

the sophisticated

cooperation.

clean-up and measurements

and Peter Ebsen at the ERGO Forschungsgesellschaft

We wish

to Anton Lis, Bemd

The study was supported

by the research budget of the pediatric department.

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