1

Internal Report 

Title: The distribution of atrazine in the Wistar rat following gestational/lactational 

exposures. 

By: Tammy E. Stoker, Leah Zorrilla, Lilian Strader, Emily Gibson, Alaa Kamel, Yaorong 

Qian, and Lynda Podhorniak. 

Endocrine Toxicology Branch, Toxicity Assessment Division (TAD), 

NHEERL, ORD, RTP, NC 

Analytical Chemistry Branch (ACB), Biological and Economic Analysis Division (BEAD), 

Office of Pesticide Programs, USEPA, Ft. Meade, MD.

Please address all correspondence to Tammy E. Stoker, ETB, TAD, NHEERL, ORD, USEPA< 

RTP< NC 27711. Phone: 919-541-2783, Fax: 919-541-5138, E-mail: stoker.tammy@epa.gov

This Internal Report was prepared for the use by the Office of Pesticide Programs, Office of 

Chemical Safety and Pollution Prevention. July 14, 2010 

Disclaimer: This manuscript has been reviewed in accordance with the policy of the National 

Health and Environmental Effects Research Laboratory, Office of Research and Development, 

U.S. EPA, and approved for publication. Approval does not signify that the contents necessarily 

reflect the views or policy of the Agency, nor does mention of trade names or commercial 

products constitute endorsement or recommendation for use. 
2

Abstract 

Several studies have examined the potential health effects of a gestational or lactational 

exposure to the chlorotriazine herbicide, atrazine. Such exposure to atrazine and/or its 

metabolites have been linked to a number of effects on reproductive function and development, 

including delays in puberty onset, altered testosterone secretion, altered mammary and prostate 

gland development. To our knowledge, the transfer of atrazine and/or metabolites into the fetus 

during gestation has not been examined. In a previous study in our laboratory, lactational 

transfer of C14-labeled atrazine was evaluated. However, that study examined only total 

chlorotriazines following the administration of radiolabeled atrazine, so it could not identify the 

transfer of the specific atrazine metabolites. For this reason, TAD, NHEERL in collaboration 

with the BEAD lab, conducted a study to examine the gestational and postnatal lactational 

transfer of maternally administered atrazine and its metabolites into plasma, milk and tissues 

(brain, adrenal, mammary glands and gonads). Three exposure paradigms were used, including 

(1) gestation day (GD) 18 to 20, (2) GD 14 to 20 and (3) GD 14 to postnatal day (PND) 10. At 

the end of the designated treatment period (two hours after last dose), blood was drawn by 

cardiac puncture and the dam was perfused with saline to clear the blood from the tissues. When 

the pregnant dams were killed, two males and two female fetuses were collected from the uterus 

on GD 20. For those rats killed on PND 10, the pups were removed from the dam three hours 

prior to kill. One hour after separation, the dams were dosed. The pups were then returned to 

the dam and allowed to nurse for 30 minutes before collection of samples. This fresh milk was 

in the pup stomach for collection at the time of the kill. Plasma, brain, adrenal and gonads were 

also collected from the neonates at kill. The results show that DACT accounted for the highest 

concentration in the plasma and tissues, followed by DIA and DEA. Interestingly, the parent 
3

compound, atrazine, was present in only very low amounts. The OH- metabolites of DEA and 

DIA were not quantifiable and the OH- metabolite of atrazine was not detected in the majority of 

the samples. It appeared that the amount of DACT present in the neonates on PND 10 following 

18 days exposure to the dam (8 gestational and 10 postnatal) was due to the amount in the milk, 

which was much higher than the amount present in the plasma in the neonate. None of the other 

metabolites were present in the neonate. There did appear to be a transfer of atrazine from the 

dam to the fetus on GD 20 following either 3 or 7 days of exposure. 
4

Introduction 

 During the last decade, a number of studies have examined the potential adverse health 

effects of atrazine and related chlorotriazines on human health and wildlife. One of the more 

consistent observations has been that these compounds do influence reproductive development in 

laboratory rodents. For example, atrazine treatment to the dam during the perinatal period has 

been reported to result in prostatitis in the male offspring (Stoker et al., 1999; Raynor et al., 

2007). Others have reported that prenatal (Rosenberg et al. 2009) and peripubertal (Stoker et al., 

2000 Trentacosta et al., 2000, Friedman et al., 2002; Pogrmic et al., 2009) exposure to atrazine 

can lead to altered male reproductive development, decreased testosterone secretion and a 

decrease in testosterone dependent target tissues. 

These studies and studies in the adult female indicate that the brain may be an important 

target organ for atrazines effects on the neuroendocrine control of reproduction. For example, 

atrazine has been shown to impair the hypothalamic control of luteinizing hormone (LH) 

(Cooper et al., 2000; McMullin et al, 2003 ; Foradori et al., 2009) and stimulate the release of 

adrenocorticotropic hormone (ACTH) (Fraites et al., 2009; Laws et al., 2009). As a 

consequence, these neuroendocrine alterations lead to altered gonadal and adrenal hormonal 

regulation. 

 In contrast to these well-documented changes in the neuroendocrine control of 

reproductive and adrenal function, there is relatively little information available describing the 

blood levels of atrazine and its metabolites following exposure to this herbicide. In vitro studies 

indicate that ATR is metabolized primarily by cytochromes P450 (P450s). The major P450-

derived metabolites of ATR detected in these in vitro studies are the N-dealkylated products 

desethyl atrazine (DEA) and desisopropyl atrazine (DIA). However, didealkyl atrazine (DACT) 
5

is the major in vivo metabolite of ATR detected in rat plasma (Brzezicki et al., 2003; McMullin 

et al., 2003) and in mouse plasma and urine (Ross and Filipov, 2006). In humans, major ATR 

metabolites detected in urine of occupationally exposed subjects are DE, DIP, and DACT 

(Catenacci et al., 1993, Ross et al, 2009). 

While the above research on serum and tissue concentrations of atrazine and its 

metabolites have focused on exposure to the adult animal, very little is known about the effects 

of gestational and lactational exposures to the offspring. Stoker and Cooper (2007) examined 

lactational transfer of C14-labelled atrazine from dams to pups. Although lactational transfer 

was confirmed, it was not possible to discern how much of the parent compound or its 

metabolites were actually transferred. We are unaware of any studies in which the transplacental 

transfer of atrazine and/or metabolites into the fetus has been evaluated. 

The present study is the result of a cooperative effort between TAD, ORD and BEAD, 

OPPTS. The purpose was to examine the gestational and lactational transfer of atrazine and its 

metabolites into the fetus and neonate. As atrazine has been reported to target the brain, another 

objective of this study was to examine the ability of atrazine and its metabolites to cross the 

blood-brain barrier. Finally, we examined the concentration of this herbicide and its metabolites 

in the adrenal and the mammary glands, two other tissues of concern for atrazine toxicity. The 

target analytes of interest were the parent compound ATR, along with metabolites desethyl 

atrazine (DEA) and OH-DEA, desisopropyl atrazine (DIA) and OH-DIA, desethyl-desisopropyl 

atrazine (DACT), and hydroxyl atrazine (OH-ATR). 

 

Methods 
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This work was performed by both NHEERL, ORD in RTP, NC and Analytical Chemistry 

Branch, BEAD, OPP in the Environmental Science Center in Ft. Meade, MD. 

Dosing Solutions

Atrazine (97% purity, Novartis, Greensboro, NC) was administered as a suspension in 1.0% 

methyl cellulose (M-7140, Sigma Chemical Co., St. Louis, MO) in distilled water. The doses 

included 0 (vehicle), 5 and 25 mg/kg body weight, delivered by oral gavage in 5.0 ml dosing 

solution per kg body weight. 

Animals

Timed pregnant Wistar rats were obtained from Charles Rivers Laboratories (Raleigh, NC) on 

GD 6 and maintained under controlled temperature (20-24o C), humidity (40-50%), light (14 h 

light/10 h dark; on at 6 am off at 8 pm EST) conditions with Purina Laboratory Rat Chow 5001 

and water available ad libitum in an AAALAC accredited facility. Polycarbonate cages with 

heat-treated pine shavings were used for housing the dams. 
7

Three different dosing paradigms were employed, including dosing from (1) GD 14 to 20, 2) 

dosing from GD 18 to 20, and 3) GD 14 to PND 10. Three dams from each treatment period 

were dosed with 0 (vehicle), 5 or 25 mg/kg. Two hours following the last dose on GD 20, 

blood was collected from dams (from the GD 14 to 20 and GD 18 to 20 exposure periods) 

under halothane anesthesia, followed by perfusion of the tissues with saline. Two males and 

two female fetuses per dose group were then collected from the dams and weighed. In 

addition, the brain, adrenal and mammary glands from each dam were collected and 

weighed. In the GD 14 to PND 10 group, the neonates were removed from the dam for 3 

hours before kill and then allowed to nurse for thirty minutes just prior to kill. Following this 

nursing period, one male and one female PND 10 pup were perfused and plasma, milk from 

the stomachs, adrenal gland and the gonads (ovaries and testes) from each was collected and 

weighed. All milk, plasma and tissues collected were frozen prior to and during shipment for 

analysis by the BEAD lab. 

Sample Analysis

Chlorotriazine concentrations in the milk, plasma and tissue samples were determined 

using a modified protocol from Ross et al. (2006, 2009) using the Waters Acuity/Xevo 

LC/MS/MS for concentrations of atrazine, DEA and OH-DEA, DIA and OH-DIA, DACT, and 

OH-ATR. The plasma concentrations were determined on a per volume basis, and the tissue, 

whole fetus and milk samples were determined on a per gram basis. Sample sets included a 

method blank (procedural blank), matrix blank (control), and a matrix spike at 2x LOQ with all 

target analytes. All sample sets were calibrated with standard reference compounds. Standards 

were obtained the standards from the US EPA National Pesticide Standard Repository in Ft. 

Meade, MD. An instrument calibration curve, with a minimum of four concentration levels, 
8

(typically between estimated limit of detection (LOD) to 10x limit of quantitation (LOQ) was 

established for each analyte prior to the analysis of actual samples. The LOQ was estimated as 3 

X LOD, so that any value between the LOD and LOQ is considered an estimation. The proper 

controls and spiked samples were used to determine recovery, bias and precision. The 

correlation coefficient (R2) of the calibration curve, for each quantitated analyte, was > 0.990. 

Confirmation of the presence of each analyte was achieved by monitoring a second 

precursor/product ion transition. The ratio of both ion transitions was within 20% of the ratio of 

the same ion transitions found in standards. 

Results 

 The results presented in this section are limited to those metabolites which demonstrated 

reliable measures in this study. The hydroxymetabolites of DIA and DEA were only semiquantifiable as they were present in low concentrations and the extraction efficiencies in plasma 

and tissues were low. For this reason, they will not be included in the results and tables. The 

hydroxyatrazine metabolite had extraction efficiencies of acceptable limits, but the majority of 

the samples analyzed revealed undetectable hydroxylatrazine values. These values were 

included in the results and tables to compare the levels of OH-ATR to the concentrations of the 

other non-hydroxylated metabolites. To summarize and compare the data, the LOQ (level of 

quantitation) was inserted as the default concentration when the concentrations were either nondetectable or lower than the LOQ. 

Gestational Exposure

Dam 
9

 In the dam, the most prominent chlorotriazine metabolite detected in all tissues examined 

was DACT, (Table 1 and 2). DACT accounted for the largest percent of chlorotriazines detected 

in dams treated for 3- and 7-days prior to kill. For example, in the GD 20 plasma from both 

dosing periods , DACT accounted for 74% and 82% of the total chlorotriazines (atrazine plus all 

metabolites) detected. Atrazine itself represented only 0.8 % or less of the total chlorotriazines 

in both treatment periods. It is also of note that the concentration of this metabolite was 

relatively similar in all tissues examined. For example, examination of the brains of the treated 

dams revealed that DACT accounted for approximately 85% of the total chlorotriazines and 

atrazine less than 1.0 % of the total. The two intermediate metabolites, DIA and DEA, were 

detected in concentrations that were higher than that of atrazine itself, but they were still present 

at concentrations lower than that observed for DACT. 

A dose-dependent increase for atrazine and its three metabolites was consistent in the 

dams under both dosing regimens and in all tissues examined. For example, there was 

approximately 700 and 2500 ng/g of DACT in the brain following the exposure to 5 and 25 

mg/kg atrazine, respectively, in both the GD 18 to 20 and GD 14 to 20 dosing periods. In the 

mammary gland, there was approximately 500 ng/g and 1650 ng/g following the 5 and 25 mg/kg 

in the two dosing periods. In contrast, in the adrenal, there was less DACT found following the 

7-day exposure period (90 and 260 ng/g) as compared to the 3-day exposure in the dam (200 and 

750 ng/g). 

 To summarize both dosing paradigms, DACT, DIA and DEA accounted for 85%, 10% 

and 2% of the total in brain tissue, respectively. Atrazine accounted for less than 1% of the total 

chlorotriazines in the brain of the GD 20 dam. However, in the adrenal and mammary tissue of 

the dam, atrazine was present in higher amounts, accounting for approximately 13% of the total 
10

in the adrenal and 5% of the total in the mammary gland. DACT, DIA and DEA accounted for 

65%, 19% and 7% in the adrenal and 65%, 22%, and 6% in the mammary gland. The amounts of 

the hydroxy-chlorotriazines in the tissues and plasma were negligible (<0.1% or undetectable). 

Fetus 

 The amount of chlorotriazines found in the whole fetus was similar whether the dams 

were treated for 3 or 7 days (Table 1 and 2). Again, DACT accounted for approximately 78% of 

the total chlorotriazines in the fetus, with atrazine, DIA and DEA accounting for less than 1%, 

17%, and 3% of the total, respectively. Again, the hydroxyl-chlorotriazines in the tissues and 

plasma were negligible (<0.1% or undetectable). 

Gestational/Lactational exposure

Dam 

 The concentrations and distribution of the chlortriazine metabolites in the plasma, brain, 

adrenal and mammary gland of dams exposed from GD 14 to PND 10 and killed on PND 10 

(Table 3) were similar to those observed in the dams killed on GD20 (Table 1 and 2) in the 

plasma, brain adrenal and mammary gland (Table 3). There did appear to be less chlorotriazines 

detected in the adrenal gland as compared to the amount detected after just 3 days of exposure, 

similar to the decreased amount in the 7 day exposure, as mentioned earlier. 

 DACT accounted for the majority of the chlorotriazines in the tissues and plasma 

collected. For example, in the plasma, DACT represented 90% of the chlorotriazine metabolites 

detected. In contrast, atrazine accounted for only 0.3 % of the total at both doses. DIA and DEA 

represented 6 and 2% of the total, respectively. A similar amount was observed in the brain of 

the dam, with DACT accounting for 95% of the total and atrazine only 0.5% of the total. DIA 

and DEA accounted for 3 % and 1% of the total in brain tissue, respectively. However, in the 
11

adrenal atrazine was present in higher amounts, accounting for 10% of the total. DACT 

accounted for 75% of the total chlorotriazines detected in the adrenal, with DIA and DEA 

accounting for 8 and 5%, respectively. Unlike the previous exposures, atrazine only accounted 

for 0.7% of the total in the mammary gland, with DACT at 90%, DIA at 6% and DEA at 2%. 

The amount of OH-ATR was increased in this exposure as compared to the previous exposures, 

accounting for 0.7% in the adrenal gland and 0.5% in the mammary tissue. However, the 

amounts of the other two hydroxy-chlorotriazines (OH-DIA and OH-DEA) were still negligible 

(<0.1% or undetectable) following this exposure. 

Neonate 

The neonatal plasma, milk and tissues contained primarily DACT (Table 4). For 

example, in the plasma, DACT accounted for 99% of the total chlorotriazines detected with no 

atrazine and 0.6 and 0.2% of DIA and DEA, respectively. The milk obtained from the neonatal 

stomachs following the 30 minute nursing period contained primarily DACT (91% of total), but 

also contained DIA, DEA, Atrazine and OH-atrazine at 6, 2, 0.4 and 0.3%, respectively. The 

adrenal gland contained only DACT. DACT accounted for 96% of the brain chlorotriazine 

levels, with relatively small amounts of atrazine (2.5%), DIA (0.4%), DEA (0.1%) and OHatrazine (1%) present. Again, the hydroxyl-chlorotriazines in the tissues and plasma were 

negligible (<0.1% or undetectable). 

 The gonads of the neonates were analyzed for all metabolites, but only DACT was 

detected (Table 5). The testes showed a dose response increase of the concentration of DACT, 

with 77 and 278 ng/g in the 5 and 25 mg/kg dose group. However, in the ovary DACT was only 

detected at the 25 mg/kg dose. 
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Summary 

This study demonstrates that the primary metabolite found in the dam and fetus/neonate 

following a gestational or gestational/lactational exposure to atrazine in the dam is 

diaminochlorotriazine (DACT). However, atrazine and the metabolites DIA and DEA were also 

detected. The hydroxyl metabolites were not detected in most cases, and when they were, the 

contribution to the total chlorotriazines observed was negligible. DIA was present to a greater 

extent in the tissues and plasma, as compared to DEA or atrazine. It appeared that atrazine was 

able to cross the placenta to get into the fetal circulation, as the whole fetus had appreciable 

levels of most of the metabolites, including DACT, DIA, DEA and atrazine. In the neonate, the 

plasma only contained significant concentrations of DACT, reflecting the presence of significant 

concentrations of DACT in the dam’s milk . It was also interesting that the neonatal brains 

contained both DACT and atrazine, demonstrating the ability of these compounds to cross the 

blood-brain barrier in the neonates. 
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studies with [14C]atrazine. J. Toxicol. Environ. Health A 66, 941–964, (2003). 

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and Applied Pharmacology 218(3):238-48. 
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Table 1. Chlorotriazine concentrations in the dam following oral exposure of the dam to Atrazine from GD 18 to 20 (3 day exposure).  Atr 

dose 

ATR OH-ATR DACT DIA DEA 

Plasma ng/ml 0 0.2 ^ 1.0 ^ 3.0 ^ 1.0 ^ 0.5^  5 2.9 ± 0.8 1.4 ± 0.2 980.0 ± 88.6 108.3 ± 27.0 24.7 ± 6.2  25 37.3 ± 9.5 7.3 ± 1.5 3333.3 ± 540.1 953.3 ± 155.2 190.0 ± 25.5 Adrenal ng/g 0 0.2 ^ 1.0 ^ 3.0 ^ 1.0 ^ 0.5^  5 18.6 ± 6.1 4.0 ± 3.7 192.6 ± 61.7 23.7 ± 1.5 13.3 ± 1.8  25 194.9 ± 3.7 5.7 ± 5.7 746.7 ± 328.8 286.8 ± 91.0 106.3 ± 29.8 Brain ng/g 0 0.2 ^ 1.0 ^ 3.0 ^ 1.0 ^ 0.5^  5 2.8 ± 0.9 1.0 ^ 776.7 ± 96.5 31.0 ± 5.1 10.6 ± 2.4  25 31.0 ± 4.3 1.4 ± 0.3 2700.0 ± 561.3 373.3 ± 137.9 93.0 ± 25.5 Mammaryng/g 0 0.2 ^ 1.0 ^ 6.0 ± 3.7 1.8 ± 1.0 0.5^ 

 5 15.2 ± 5.1 1.0 ^ 466.7 ± 71.5 66.0 ± 14.2 24.0 ± 6.5  25 210.0 ± 44.2 4.6 ± 1.0 1763.3 ± 660.0 720.0 ± 237.9 206.7 ± 64.2 

GD 20 

Fetuses

 0 0.2 ^ 1.0 ^ 3.0 ^ 1.0 ^ 0.5^  5 4.3 ± 0.9 1.0 ^ 1094.2 ± 70.5 102.7 ± 25.6 21.0 ± 4.2  25 77.9 ± 14.5 1.3 ± 0.1 4070.0 ± 582.5 1075.0 ±195.5 220.0 ± 43.6 

Mean ± SEM (standard error of the mean). One mammary gland, 5th

^ LOQ or limit of quantitation was used if the sample concentration was undetected or below the LOQ 
16

Table 2. Chlorotriazine concentrations in the dam following oral exposure of the dam to Atrazine from

GD 14 to 20 (7 day exposure).  Atr 

dose 

ATR OH-ATR DACT DIA DEA 

Plasma ng/ml 0 0.2 ^ 1.0 ^ 19.1 ± 17.1 2.2 ± 1.1 0.6 ± 0.2  5 1.5 ± 0.6 1.4 ± 0.2 883.4 ± 108.0 108.3 ± 27.0 21.0 ± 5.0  25 8.0 ± 3.5 4.3 ± 0.9 3100.0 ± 717.7 573.3 ± 290.2 88.7 ± 40.9 Adrenal ng/g 0 0.2 ^ 1. 0 ^ 9.3 ± 7.8 1.0^ 0.5 ^  5 17.4 ± 6.6 3.5 ± 3.1 93.3 ± 19.5 19.0 ± 3.2 10.9 ± 1.9  25 55.3 ± 16.3 4.7 ± 4.5 260.1 ± 37.4 71.7 ± 27.5 27.7 ± 10.8 Brain ng/g 0 0.2 ^ 1.0^ 13.2 ± 10.9 1.5 ± 0.6 0.5 ^  5 2.3 ± 0.9 1.0 ^ 630.0 ± 129.6 34.7 ± 14.9 10.0 ± 3.9  25 11.1 ± 4.1 1.0 ^ 2366.7 ± 549.3 218.3 ± 118.7 43.3 ± 20.9 Mammaryng/g 0 0.2 ^ 1.0 ^ 9.6 ± 7.0 1.5 ± 0.6 0.6 ± 0.61  5 16.1 ± 5.5 1.0^ 416.5 ± 82.7 73.0 ± 23.1 27.7 ± 7.4 25 79.0 ± 27.1 3.9 ± 0.5 1600.0 ± 255.0 406.7 ± 180.9 108.0 ± 41.7 GD 20 fetuses 0 0.2 ^ 1.0 ^ 17.8 ± 9.9 1.8 ± 0.7 0.6 ± 0.1  5 3.7 ± 0.9 1.0 ^ 875.0 ± 69.5 100.8 ± 22.9 21.8 ± 4.1  25 18.5 ± 5.6 1.2 ± 0.1 3466.7 ± 563.2 639.2 ± 225.8 108.0 ± 36.4 Mean ± SEM. One mammary gland, 5th . 

^ LOQ or limit of quantitation was used if the sample concentration was undetected or below the LOQ 
17

Table 3. Chlorotriazine concentrations in the dam following oral exposure of the dam to Atrazine from GD 14 to PND10.  ATR 

dose 

mg/kg 

ATR OH-ATR DACT DIA DEA 

Plasma ng/ml 0 0.2 ^ 1.0 ^ 3.0 ^ 1.0 ^ 0.5 ^  5 0.9 ± 0.4 1.1 ± 0.1 953.3 ± 29.4 38.0 ± 6.7 11.2 ± 1.9  25 9.8 ± 8.3 3.3 ± 1.7 2500.0 ± 860.4 174.0 ± 112.8 64.4 ± 43.2 Adrenal ng/g 0 0.2 ^ 1.0 ^ 3.0 ^ 1.0 ^ 0.5 ^  5 10.2 ± 4.2 2.0 ± 1.3 333.3 ± 152.7 11.0 ± 6.5 6.2 ± 3.6  25 58.6 ± 45.6 4.3 ± 4.1 426.7 ± 172.4 44.5 ± 28.5 27.0 ± 15.3 Brain ng/g 0 0.2 ^ 1.0 ^ 3.0 ^ 1.0 ^ 0.5 ^  5 1.2 ± 0.2 1.0 ^ 713.3 ± 40.7 10.9 ± 1.9 4.5 ± 0.7  25 10.6 ± 8.9 1.0 ^ 1953.3 ± 673.4 55.6 ± 37.3 27.7 ± 20.0 Mammary ng/g 0 0.2 ^ 1.0 ^ 3.0 ^ 1.0 ^ 0.5 ^  5 3.1 ± 0.5 1.8 ± 0.3 736.7 ± 68.0 27.0 ± 2.4 11.5 ± 1.2 

 25 15.5 ± 8.1 11.8 ± 7.0 2180.0 ± 821.5 140.3 ± 78.4 54.0 ± 31.5 

Mean ± SEM. One mammary gland, 5th . 

^ LOQ or limit of quantitation was used if the sample concentration was undetected or below the LOQ 
18

Table 4. Postnatal Day 10 neonatal chlorotriazine concentrations following exposure of the dam to Atrazine from GD 14 to PND 10.  Atr 

dose 

ATR OH-ATR DACT DIA DEA 

Plasma ng/ml 0 0.2 ^ 1.0 ^ 3.0 ^ 1.0 ^ 0.5 ^  5 0.2 ^ 1.0 ^ 95.8 ± 5.6 1.0 ^ 0.5 ^  25 0.2 ^ 1.0 ^ 330.0 ± 126.5 1.8 ± 0.5 0.8 ± 0.3 Milk ng/g 0 0.2 ^ 1.0 ^ 3.0 ^ 1.0 ^ 0.5 ^  5 1.0 ± 0.7 1.9 ± 0.5 383.5 ± 179.1 18.5 ± 12.3 5.2 ± 3.5  25 5.9 ± 2.8 4.6 ± 1.1 1365.0 ± 438.6 91.6 ± 24.0 30.0 ± 13.6 Adrenalng/g 0 0.2 ^ 1.0 ^ 3.0 ^ 1.0 ^ 0.5 ^  5 3.0 ± 3.1 1.0 ^ 3.0 ^ 1.0 ^ 0.5 ^  25 0.2 ^ 1.0 ^ 86.9 ± 79.1 1.0 ^ 0.5 ^ Brain ng/g 0 0.2 ^ 1.0 ^ 3.0 ^ 1.0 ^ 0.5 ^  5 5.7 ± 8.5 1.4 ± 0.5 100.4 ± 16.0 1.1 ± 0.2 0.5 ^  25 9.7 ± 16.0 4.5 ± 6.1 382.1 ± 162.5 1.6 ± 0.5 0.7 ± 0.3 Mean ± SEM. ^ LOQ or limit of quantitation was used if the sample concentration was undetected or below the LOQ 
19

Table 5. Concentration of DACT in PND pup gonads from dams dosed GD 14 to PND 10. 

ATR dose Ovary (ng/g) Testes (ng/g) 

0 3.0 ^ 3.0 ^ 5 3.0 ^ 77.3 ± 5.3 

25 58.8 ± 41.3 277.7 ± 120.6 

Mean ± SEM. ^ LOQ or limit of quantitation was used if the sample concentration was undetected or below the LOQ