Results of Phase I TIE Tests

The results of the Phase I TIE tests performed on the

four target compounds using ET50 values for NPE-9 and 1-MN

and LC50 values for Phenol and Cu are shown in Tables 4-1

and 4-2. From these tables, a summary table of toxicity

reduction for each treatment on all four target compounds

was made. (See Table 4-3). The three categories of toxicity

reduction selected were based on arbitrary judgements using,

as the only standard, the definitions of "significant

reduction" for the LC50 and ET50 (See section 4.1.1.).

No mortality was observed in any of the controls of

Botany Pond water used to measure survival of the test

species in non-toxic control water. Blanks for artifactual

toxicity and controls for reagent dosages added to non-toxic

background wastewater produced zero mortality of C. dubia

unless otherwise stated. Aeration Test controls used to

measure the effect of acid and base addition under quiescent

conditions had no effect on the toxicity of the target

compund spiked stock solution unless noted otherwise.

Nonylphenol Ethoxylate with Nine Moles Ethylene Oxide

per Mole Hydrophobe

The Time-Degradation Test showed a persistence in

toxicity over a 23-day period. This was expected for a

nonionic surfactant. Filtration was not expected to affect

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Table 4-1. ET50 Values (in hours) for Target Compound Solutions of NPE-9 and 1-MN in Modified TIE Phase I Tests

Phase I Characterization Test

Target Compound NPE-9 1-MN Degradation Test Day 0 (Baseline) 4 Day 9 3 Day 14 Day 23 2 FiItration Coarse (1.2uni) 4 Fine (0.2um) 6 Aeration pH3 5 pH Sample 11 pHII 5 C18 Column pH Sample >48

GAC (followed by fine >48

filtration [0.2 um]) 11 3 48 >48 >48 >48 >48 >48 Oxidant Reduction 50 mg/L 450 mg/L

EDTA (After fine filtration

[0.2 um]) 4 24 11.1 mg/L 37 mg/L 370 mg/L 7 6 3 >48 38 7

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Table 4-2. Results of Phase I Testing with Target Compound Solutions of Phenol and Cu; entire TIE protocol

was applied, in which both the 48-h LC50 (.%) and the ET50 (h) are used.

Target Compound

Phase I Characterization Test Phenol Cu

Day 1 (Initial) Day 2 (BASELINE) pH Adjustment pH3 pHII Filtration (I.Oum) 27% 8%, 20h; for C18: 13h <13% <13% pH3 pH Sample pHII Aeration pH3 pH Sample pHII C18 SPE Column pH3 25 mL,150 mL pH Sample 25 mL,150 mL pH9 25 mLJSO mL

GAC (followed by filtration [0.7um])

Oxidant Reduction* .05 mg/L .15 mg/L .25 mg/L .50 mg/L 1.5 mg/L 2.5 mg/L EDTA* 7.5 mg/L 22 mg/L 37 mg/L 75 mg/L 220 mg/L 370 mg/L <13% <13% >100% <13% <13% <13X lOh, 18h 16h, <24h 15h, 12h 74X <24h** <24h** <24h** <24h** <24h** <24h** <24h** <24h** <24h** <24h** <24h** <24h** 12X 22%. <2.5h 45X >50X 31X 45X >50X 23X 31X >50X NA, NA NA, NA NA, NA >50X 2.6h 1.4h 2.2h 1.5h 1.5h 1.4h >48h >48h >48h 24h 3.6h 4.Oh

*Only six of the ten reagent concentrations reconnended were tested in the Oxidant reduction and EDTA tests.

**ET50 cannot be determined accurately since fewer than the standard number of readings were taken; SOX mortal¬

ity could have occurred anytime between the 2h and 24h readings.

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Table 4-3. Qualitative Assessment of Toxicity Reduction for Target Compounds in Phase I TIE Tests

Target Compound

Phase I Characterization Test NPE-9 1-WI Phenol Cu

Degradation Test Day 14 pH Adjustment pH3 pHII Filtration *4r* Coarse (1.2 um filter) Fine (0.2 um membrane) * pH3 (1.0 um) pH Sample (1.0 um) pHII (1.0 um) Aeration pH3 pH Sample pHII

CIS SPE Column

^ or * or ** *** or ** or ** or ** pH3 pH Sample pH9

GAC (followed by filtration)

** *** *** * ** NA NA HA (0.2 um membrane) (0.7 um filter) Oxidant Reduction .05 mg/L .15 mg/L .25 mg/L .50 mg/L 1.5 mg/L 2.5 mg/L 50 mg/L 450 mg/L EDTA (no filtration)

* 7.5 mg/L 22 mg/L 37 mg/L 75 mg/L 220 mg/L 370 mg/L

EDTA (after fine filtration [0.2 um])

* * *** *** *** *** ** 11 mg/L 37 mg/L 370 mg/L

*No or very little toxicity reduction •Moderate toxicity reduction

***Significant toxicity reduction

85

obseirved with fine filtration may be due to adsorption of

the compound into the membrane filter or onto solids which

are removed through filtration. Results of the air

stripping test at pH 3 and pH 11 show virtually no change in

toxicity, (as expected), while the result at initial pH is

anomalous and probably due to a greater loss of NPE-9 in the

form of foam at this pH: while identical beakers were used

for all three aliquots, more (5/3 times as much) volume of

solution was aerated at initial pH, producing enough foam to

escape the beaker. Both the C18 SPE column and GAC

adsorption removed the non-polar NPE-9 as expected. The

additions of Na2S203 in the Oxidant Reduction Test produced

no change in toxicity as expected. The moderate reductions

in toxicity seen at the lower two dosages of EDTA are

probably due to the effect of fine filtration. (Chelation

without filtration was not performed.) The ET50 value (3 h)

observed at the highest EDTA dosage (370 mg/L) is almost

identical to that of the Baseline and is probably the net

result of the decrease in toxicity caused by fine filtration

and an increase in toxicity caused by the toxicity of EDTA

itself. The result of the control of non-toxic wastewater

plus high EDTA concentration (6 h) indicates that EDTA is

highly toxic at this dosage (See Appendix B).

1-Methylnaphtha1ene

As shown in Table 4-1, the toxicity of the 1-MN

solution was greatly reduced over a 14-day period

86

(Degradation test). A breakdown of the compound is

indicated rather than loss of toxicity through

volatilization or adsorption: all aliquots were stored in

head-space free, teflon-capped glass vials. Filtration was

expected to have no effect on 1-MN toxicity. The anomalous

result (48 h) with fine filtration is most probably due to

volatilization produced by vacuum filtration. (Coarse

filtration was performed without vacuum.) Aeration resulted

in "acutely non-toxic" readings (ET50>48h) at all three pH's

as expected. The control designed to measure the effect of

holding the uncovered sample at pH 3 under quiescent

conditions for the duration of the air stripping process (1

hour) was non-toxic (See Appendix B). Likewise, the result

of the parallel control for aeration at pH 11 (31 h)

indicates a great reduction in toxicity. Either toxicity

was lost at extreme pH or else volatilization of 1-MN from

these aliquots was significant. It is noted that stirring

performed during the addition of acid and base would have

accelerated volatilization. Both the C18 SPE column and GAC

adsorption also removed toxicity (ET50>48h); as expected,

1-MN was readily adsorbed in both tests. Oxidant reduction

at low dosage produced no change in toxicity, as expected.

At high dosage, the result of ET50=24h is most probably due

to the dilution effect. (An oversight was made in not using

a lOx higher normality of reagent for the addition.) The 11

mg/L EDTA addition (after fine filtration) produced no

87

expected. The EDTA Chelation Test results for the 37 and

370 mg/L additions reflect a progression of EDTA toxicity.

The result of the control for the high EDTA dosage in non¬

toxic wastewater (6 h) confirms that EDTA is highly toxic at

this concentration (See Appendix B).

Phenol

The Phase I TIE tests with phenol show a large increase

in toxicity from "Day 1" to "Day 2". This suggests the

formation of complex organics from the background wastewater

constituents. The pH adjustment test shows no conclusive

change in toxicity for both aliquots. Filtration produced

an interesting result at high pH (LC50>100%). Apparently

some precipitate is formed with the phenolate ion in a

reversible reaction. Aeration at all three pH's produced

the expected results, i.e., there was no significant change

in toxicity. The C18 SPE column results are compared to the

Baseline toxicity of ET50=13h. As expected for compounds

with low Kow, phenol was not retained by the column at any

pH. In contrast, GAC adsorbs organic compounds that may

have relatively low Kow values. Although GAC was expected

to increase the LC50 to 100%, the data in Table 4-2

indicates an increase in LC50 to only 74%. One possible

explanation is that the GAC dosage (2000mg/L) was not large

enough to reduce the initial phenol concentration (129 mg/L)

sufficiently low to eliminate all toxicity. Finally,

88

oxidant reduction and chelation manipulations produced no

conclusive changes in toxicity, as expected.

Copper

The results of the Phase I TIE tests using copper as

the target compound are shown in Table 4-2. A significant

but unexplainable loss in toxicity was observed from "Day 1"

to "Day 2".

In the pH Adjustment Test, both aliquots displayed a

significant loss in toxicity. In order to interpret these

results it is necessary to examine the Phase I tests that

involve a pH change. The result at pH 11 (LC50>50%) is seen

again in both filtration and aeration at pH 11 but not at pH

3 or initial pH. This suggests a reaction occurring at high

pH that reduces toxicity but that is kinetically slow to

reverse when returned to lowered pH. The result of the pH

Adjustment Test at pH 3 is difficult to explain since other

tests conducted at low pH showed little to no reduction in

toxicity.

Filtration at pH 3 produced a slight reduction in

toxicity; the results at pH 11 have been discussed above.

An unexplainable result indicating a significant reduction

in toxicity is seen in the Filtration Test at initial pH.

Air stripping at pH 3 produced the expected results of

no effect on toxicity; an inexplicable slight reduction in

toxicity is seen at initial pH; the toxicity loss at pH 11

is due solely to the pH change as discussed above.

89

GAC treatment (followed by filtration) resulted in an

unexpected loss of toxicity. Activated carbon can adsorb

metals to a small extent (Faust & Aly, 1987). Another

explanation may be adsorption of a copper-organic compound

onto the filter.

The additions of Na2S203 were not expected to remove Cu

from solution. Four of the six Na2S203 dosages produced no

change in toxicity as measured by the ET50 test. While two

other dosages showed a slight decrease in toxicity, these

results were dismissed as being due to errors in

interpolation of plots to calculate the ET50.

The EDTA Chelation Test was expected to show complete

removal of toxicity in the Cu solution. The lowest three

dosages of EDTA removed toxicity. However, increasing the

EDTA dosage further caused the ET50 value to decrease again.

This toxicity effect is due to unchelated EDTA. An estimate

of free EDTA expected after complexing all the Cu was made.

A Cu concentration of 20ug/L corresponds to 3. Ixl0~'7moles

Cu/L. This concentration of Cu should be complexed by

exactly 3.1xlO~'7 moles EDTA/L or 0.12mg/L EDTA.

Therefore, excess EDTA is available at all dosages

used. Some further amount of EDTA will be complexing with

other cations, e.g., Ca and Mg. However, the hardness of

the background wastewater was not excessive. Accordingly,

EDTA toxicity should be expected as EDTA dosage increases.

These results point to the need to cover a wide range of

EDTA dosage so as to detect a decrease in toxicity if metals

90

are present and then an increase due to EDTA exceeding the

stoichimetric amount.

The results of TIE Phase I testing with target

compounds were predictable for most of the treatments and validate the success of these procedures to characterize toxic compounds as to broad generic groups. However, anomalous results produced by unintentional mechanisms

involved in many of the tests point to uncertainty involved in assessing the nature of toxicants in samples of unknown compounds by means of the TIE.

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