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Tap Water Results

09:57 PM CDT on Wednesday, August 6, 2008

Report on Pharmaceuticals and Personal Care Products

in Illinois Drinking Water

Bureau of Water, Illinois EPA

June 2008

 

 

Introduction

 

While the presence of pharmaceuticals and personal care products (PPCPs) in raw (untreated) and finished (potable) drinking water has become an issue of concern recently, the original reports of pharmaceutical chemicals’ presence in water go back three decades.  Garrison et al. (1976) and Hignite and Azaznoff (1977) both reported the presence of clofibric acid, a breakdown product of several blood lipid regulators, in wastewater, and Hignite and Azaznoff also found salicylic acid, an aspirin breakdown product, in their study.  As analytical techniques became increasingly sensitive and detection limits approached and sometimes surpassed the low nanograms per liter (ng/L) or parts-per-trillion (ppt) level, many more PPCPs have been reported in waste water, ambient water, and drinking water.  In one recent survey of 139 U.S. streams, Kolpin et al. (2002) found PPCPs in 80% of the streams, while in another report Heberer (2002) reviewed research on pharmaceuticals in water and listed 80 drugs and breakdown products that had been detected.

 

The issue of PPCPs in drinking water was brought to the forefront earlier this year when the Associated Press released a three-part series of reports that found PPCPs in the drinking water of 24 U.S. metropolitan areas serving approximately 41 million residents.  Acting on these reports, Governor Blagojevich requested that the Illinois Environmental Protection Agency (Agency) monitor water samples for the presence of PPCPs, and that the Agency and the Illinois Department of Public Health (IDPH) assess the effects on public health of any chemicals that might be found.

 

Purpose

 

Illinois EPA Bureau of Water (Division of Public Water Supplies) staff collected samples of raw and finished drinking water that were analyzed for the presence of pharmaceuticals, in order to evaluate whether detectable amounts are present in sufficient concentration to cause adverse human health effects. 

 

Methodology

 

Sample Selection – Chicago and four other communities were selected for sampling.  Chicago was chosen because of the large population served, considering the city itself and the numerous neighboring communities that purchase water from Chicago.  Four communities (Elgin, Aurora, Rock Island and East St. Louis) were chosen because they use surface water (Fox River and Mississippi River) as a drinking water source and are located downstream near a wastewater treatment plant discharge.  Since the major route for pharmaceuticals’ entry to surface water is primarily through discharge of treated municipal wastewater, the selected water supplies are more likely than others to show detectable levels of these substances.

 

Sample Collection – Samples were collected starting Monday, March 24 and continued through Thursday, March 27, 2008.  The samples were collected following standard procedures by Agency staff, using bottles provided by the laboratory.  Samples were express shipped to the South Bend, IN office of Underwriters Laboratories on the day of collection.  Once the laboratory received the samples, results of analyses were to be available within 21 to 28 days.  For the initial set of analyses, untreated and potable water samples were collected from Chicago, Elgin, Aurora, Rock Island, and Illinois American Water Company – East St. Louis Division.

 

Chemical Analyses – Underwriters Laboratories was selected to perform the analyses of the water samples, using their certified methods L220 and L221 for Pharmaceutically Active Compounds.  These methods are capable of detecting 56 compounds that are found in many types of PPCPs, such as pain relievers, antibiotics, anticonvulsants, antidepressants, replacement hormones, an insect repellant, and chemicals related to coffee and tobacco.  Chemicals reported by these methods, their detection limits, and a brief description of the chemicals are listed in Table 1.

 

Screening Levels – Upon receipt of the analyses after final quality assurance from the laboratory, the results were provided to Agency and IDPH toxicologists for review and interpretation of whether there are possible adverse human health effects that may be associated with consumption of the potable water.  Since there are no established standards or guidelines for the chemicals analyzed for this project, it was necessary to develop Screening Levels for these chemicals.  In consultation with IDPH toxicologists and other health professionals, the Agency chose to develop the Screening Levels for the PPCPs using a conservative risk assessment approach.  This approach drew heavily on the procedures used in the recently finalized Australian Guidelines for Water Recycling (2008) to develop Drinking Water Guidelines (DWGs) to be applied to recycled wastewaters in Australia.

 

The Australian procedures rely on two large sources of toxicological data as the starting point for deriving the DWGs for pharmaceuticals.  The first source is the Acceptable Daily Intakes (ADIs) developed for human exposures to pharmaceuticals with agricultural and veterinary applications. The ADIs have been developed by the European Medicines Association Committee for Veterinary Medical Products, the Joint FAO/WHO Expert Committee on Food Additives, or the Australian Therapeutic Goods Administration, and are used unaltered in the development of the DWGs.  The Agency and IDPH toxicologists have also chosen to use the unaltered ADIs in deriving the Screening Levels for this project.

 

The second source is the Lowest Daily Therapeutic Doses (LDTDs), in milligrams per day (mg/d), developed for human pharmaceuticals.  The LDTD represents a balance between the beneficial effect of the drug and its known or potential adverse side effects.  While human drugs receive extensive safety evaluations before release, much of the testing data remain confidential and thus unavailable for use in deriving drinking water criteria.  In developing the DWGs, therefore, the Australians assumed that the LDTD represents the lowest observable effect level (LOEL) for side effects, and then applied safety factors appropriate to the drug to extrapolate from the LDTD to a dose that would be without effect even for sensitive subgroups of the


population.  For most drugs the safety factor is 1,000, and an additional safety factor of 10 is applied to highly cytotoxic (ex., chemotherapy) or hormonal (ex., birth control) drugs.

 

The Agency and IDPH toxicologists also chose to use this approach, but decided that for developing our ADIs a safety factor of 10,000 is appropriate initially, rather than using a safety factor of 1,000 and additional factors added for specific types of drugs.  Thus, the LDTD was divided by a series of four safety factors, each a value of 10, that took into account extrapolation from a LOEL to a no observable effect level (NOEL), intrahuman variability (adults vs. children), short-term vs. long-term effects, and therapeutic use vs. no therapeutic need, to arrive at the ADIs to be used in developing the Screening Levels.  Since the LDTDs are expressed in mg/d, it was also necessary to convert this into a dose based on body weight, in milligrams per kilogram of body weight per day (mg/kg/d).  We chose to use the average body weight for a young child of 10 kg, as discussed below, in making this conversion.  As an example of the development of an ADI for this project, the LDTD for carbamazepine is 200 mg/d, which was divided by the safety factor of 10,000 to obtain a safe level of 0.02 mg/d.  This was then divided by the assumed 10 kg body weight to derive the ADI for this project of 0.002 mg/kg/day.  Since the units used for the analytical results in this report are nanograms per liter (ng/L), all other units in this report will be converted to nanograms; thus for carbamazepine the ADI of 0.002 mg/kg/d is equivalent to 2,000 nanograms per kilogram per day (ng/kg/d). 

 

There also were four chemicals detected that are not human or animal drugs and thus do not have ADIs or LDTDs: caffeine, nicotine, paraxanthine, and DEET.  The Agency and IDPH toxicologists determined that there are no appropriate toxicological data available at this time to allow development of an ADI for the first three chemicals.  Regarding DEET, the California Environmental Protection Agency has developed a Risk Characterization Document for this chemical, which identified a two-year study with rats that found a NOEL of 100 mg/kg/d for reduced body weight and food consumption and increased cholesterol (Goldenthal, 1995).  The Agency and IDPH toxicologists used this study as the basis for developing an ADI, by dividing this NOEL by three safety factors of 10, or a total safety factor of 1,000, to account for extrapolation from animals to humans, for intrahuman variability, and for protection against seizures that have been reported in a small number of children who used large amounts of DEET.  Thus, the ADI for this project is 0.1 mg/kg/d, or 100,000 ng/kg/d.  It should be noted that California EPA also calculated Annual Average Daily Dosages (AADDs) in various age groups from dermal exposures based on the results of a survey of DEET use, and the ADI falls within the reported AADD range of 37,000-130,000 ng/kg/d.

 

The final step in the process of deriving the Screening Levels was to determine the maximum concentrations of the PPCPs in drinking water that would not result in people consuming amounts of the PPCPs in excess of the ADIs.  This was done by using the procedures used by many regulatory agencies to derive drinking water criteria:

 

            Criterion (ng/L) = [(ADI x BW)/IR] x RSC, where

                        ADI = Acceptable Daily Intake (ng/kg/d)

                        BW = body weight (kg)

                        IR = drinking water ingestion rate (L/d)

                        RSC = relative source contribution (% of daily intake attributable to

                                    drinking water)

 

The Australians used standard risk assessment assumptions for lifetime exposures for the BW and IR inputs to the equation, assuming an adult body weight (BW) of 70 kg and an adult water ingestion rate (IR) of 2 liters per day (L/d), but decided that the default RSC of 20% of the daily exposure derives from drinking water was unreasonable.  Instead, they reasoned that the daily exposure from sources other than water will be zero unless the drug has been prescribed for the person, so the RSC should be 100%.  The Agency and IDPH toxicologists agreed with the RSC selection, but decided that the BW and IR terms should reflect a young child’s exposure rather than an adult’s.  Therefore, values of 10 kg for BW and 1 L/d for IR were chosen.  These changes resulted in Screening Levels that are 3.5 times more restrictive than the Australian DWGs for most PPCPs.  The Agency and IDPH toxicologists believe that this conservative approach is very protective of public health.  The Screening Levels derived from these procedures are listed in Table 2.

 

Results and Discussion

 

In order to evaluate the PPCP concentrations detected in the samples from the five public water supplies, the Agency compared the reported concentrations to the Screening Levels to calculate a Hazard Index (HI) for each chemical.  The HI is a ratio of the actual exposure to the acceptable exposure, and if the HI does not exceed 1.0 the exposure is at an acceptable level.  Concentrations detected in the raw and finished water samples, the Screening Levels, and the corresponding HIs for the finished water samples are listed in Table 2.

 

As can be seen from this Table, all HIs are much lower than the critical value of 1.0, ranging from 0.003-<0.00000001.  This indicates that the concentrations of the PPCPs in the samples do not pose a public health hazard at this time.  The largest HI of 0.003, for cotinine (a breakdown product of nicotine) in the Elgin sample, suggests that there is a margin of safety of at least 333 (1.0/0.003), and likely considerably higher because of the conservative nature of the Screening Levels, for exposure to this chemical in the drinking water.

 

There are some interesting features that are apparent from the results.  The Chicago sample of raw water suggests that Lake Michigan is a relatively clean source of drinking water, with less total numbers of PPCPs detected (4 chemicals) in comparison with the supplies drawing from river sources (9-14 chemicals).  This result may be representative of lakes in general, since results reported to the Agency for raw water from Lake Springfield, analyzed using the same two analytical methods as in this project, also are lower (7 chemicals) than the range for the river samples (chemicals and levels not presented).  The Lake Michigan sample also had generally lower concentrations of the PPCPs that were detected than the corresponding results from the river sources; concentrations of cotinine, nicotine, and gemfibrozil were higher in the river samples, while the levels of monensin were comparable.

 

The results from the untreated water samples from the rivers suggest that agricultural sources may be important contributors to the load of pharmaceuticals in the source water of these supplies.  Several drugs that are primarily or exclusively used in agricultural or veterinary treatments (lincomycin, monensin, sulfadimethoxine, and sulfamethazine) were detected in the river samples, although the HIs were very low.  These results suggest a potential control point if these chemicals become a concern in the future.

 

The results for the untreated versus finished samples from all facilities except Aurora indicate that routine water treatments are capable of reducing or eliminating the levels of some of the PPCPs found in the raw water while other chemicals are only minimally reduced.  (The Aurora results are not comparable to the results from the other facilities since the finished water at the time the sample was collected was a blend of approximately equal amounts of water from the river and the facility’s well field).  The results listed in Table 2 show that diltiazem, lincomycin, sulfadimethoxine, sulfamethoxazole, and trimethoprim are mostly or fully removed from the raw water by the facilities’ treatments, while the results for caffeine, fluoxetine, paraxanthine, and sulfamethazine are inconclusive because of insufficient or conflicting data.  On the other hand, the results show that carbamazepine, cotinine, DEET, gemfibrozil, monensin, naproxen, and nicotine are minimally removed by treatment.  These last results are not surprising, as most of these chemicals have been reported to persist in drinking water following treatment in studies of the effectiveness of treatment processes in removing PPCPs (Stackelberg et al., 2007; Westerhoff et al., 2005).

 

While the concentrations detected and HIs calculated for this project were very low, it is likely premature to suggest that the issue of PPCPs in drinking water is resolved at this time, as some uncertainties remain.  Obviously, the database developed in this project is small, leaving considerable uncertainty about the potential range of chemicals and concentrations that may be present in untreated and potable drinking waters across the state.  The timing of the sample collection (late-March), when the rivers involved in this project were at high flow levels, likely contributed to an underestimate of the levels of the PPCPs that might be present in the water, due to dilution.  Indeed, a study by Loraine and Pettigrove (2006) reports a significant difference in the concentrations of some PPCPs between low-flow and high-flow stream conditions, with some chemicals measured at low-flow conditions approaching levels found in wastewater discharges.

 

Another potentially significant uncertainty for this project is that the analytical methods used in this project are not capable of detecting some chemicals/chemical families that have been identified as potential problems because of high use, high levels found in some studies, and/or high toxicity reported in studies of PPCPs in water.  Examples include:

 

  • codeine – high use (maximum detected in raw water = 1,000 ng/L, Kolpin et al., 2002)
  • diazepam (Valium) – high use, high toxicity (Screening Level = 500 ng/L)
  • the anti-acid drug ranitidine (Zantac) – very high use
  • the beta-blockers bisoprolol and propanolol – high toxicity (bisoprolol Screening Level = 125 ng/L), some high levels found (bisoprolol maximum concentration in raw water = 2,900 ng/L, Daughton and Ternes, 1999)
  • the chemotherapy drugs cyclophosphamide and isophosphamide – high toxicity, and
  • the estrogenic hormones 17 beta-estradiol and 17 alpha-ethinyl estradiol – very high estrogenic activity (Screening Levels = 500 and 30 ng/L, respectively).

 

If funding were to become available, it would be informative to follow up this project with additional samples to expand the coverage of drinking water sources across space and time, and to include other PPCPs if appropriate analytical procedures can be identified.

 

 

Conclusions

 

This project has identified 16 PPCPs in the untreated or potable water of five public water supplies in Illinois.  The results for the potable water samples were compared against conservative Screening Levels developed by Agency and IDPH toxicologists, and were found to not present a public health hazard at this time.  These comparisons suggest that even the chemical with the highest Hazard Index has a margin of safety of at least 333, and likely much larger.  However, there are also considerable uncertainties that suggest that further sampling is appropriate if funding can be made available.

 

REFERENCES

 

Australian Guidelines for Water Recycling: Augmentation of Drinking Water Supplies.  May 2008.  A publication of the Environmental Protection and Heritage Council, the National Health and Medical Research Council, and the National Resource Management Ministerial Council.

 

California Environmental Protection Agency, Department of Pesticide Regulation.  September 2000.  N,N-Diethyl-meta-Toluamide (DEET) Risk Characterization Document.  Document # RCD 00-01.

 

Daughton CG and Ternes TA.  1999.  Pharmaceuticals and personal care products in the environment: agents of subtle change?  Environ. Health Perspect. 107 (Suppl. 6): 907-937.

 

Garrison AW, Pope JD, and Allen FR.  1976.  Analysis of organic compounds in domestic wastewaters.  In: Identification and Analysis of Organic Pollutants in Water (Keith CH, ed.).  Ann Arbor, MI: Ann Arbor Science Publishers.  pp 517-556.

 

Goldenthal EI. (International Research and Development Corp.).  1995.  Evaluation of DEET in a two-year dietary toxicity and oncogenicity study in rats.  DEET Joint Venture/Chemical Specialties Manufacturers Assoc.  DPR Vol. 50191-176, Rec. No. 133986.

 

Heberer T.  2002.  Occurrence, fate, and removal of pharmaceutical residues in the aquatic environment: a review of recent research data.  Toxicol. Lett. 131: 5-17.

 

Hignite C and Azaznoff DL.  1977.  Drugs and drug metabolites as environmental contaminants: chlorophenoxyisobutyrate and salicylic acid in sewage water effluent.  Life Sci. 20: 337-342.

 

Kolpin DW, Furlong ET, Meyer MT, et al.  2002.  Pharmaceuticals, hormones, and other organic wastewater contaminants in U.S. streams, 1999-2000: a national reconnaissance.  Environ. Sci. Technol. 36: 1202-1211.

 

Loraine GA and Pettigrove ME.  2006.  Seasonal variations in concentrations of pharmaceuticals and personal care products in drinking water and reclaimed wastewater in southern California.  Environ. Sci. Technol. 40: 687-695.

 

Stackelberg PE, Gibs J, Furlong ET, et al.  2007.  Efficiency of conventional drinking-water-treatment processes in removal of pharmaceuticals and other organic compounds.  Sci. Total Environ. 377: 255-272.

 

Westerhoff P, Yoon Y, Snyder S, et al.  2005.  Fate of endocrine-disruptor, pharmaceutical, and personal care product chemicals during simulated drinking water treatment processes.  Environ. Sci. Technol. 39: 6649-6663.

 


TABLE 1. CHEMICALS REPORTED BY UNDERWRITERS LABORATORIES METHODS

L220 AND L221

 

CHEMICAL

DETECTION LIMIT (ng/L, ppt)

DESCRIPTION

Method L220

 

 

Acetominophen

5.0

Pain Reliever

Antipyrine

1.0

Antibiotic

Azithromycin

1.0

Antibiotic

Bacitracin

500

Antibiotic

Caffeine

50

Found in coffee, Pain relievers

Carbadox

50

Antibiotic

Carbamazepine

1.0

Anti-epileptic

Ciprofloxacin

50

Antibiotic

Cotinine

1.0

Nicotine metabolite

DEET

5.0

Insect repellant

Dilantin

50

Anticonvulsant

Diltiazem

1.0

Blood pressure medicine

Enrofloxacin

500

Antibiotic

Erythromycin

1.0

Antibiotic

Fluoxetine (Prozac)

1.0

Antidepressant

Lasalocid

1.0

Veterinary growth hormone

Levothyroxine (Synthroid)

50

Thyroid hormone replacement

Lincomycin

0.1

Veterinary antibiotic

Monensin

0.1

Veterinary antibiotic

Narasin

0.1

Veterinary antibiotic

Nicotine

5.0

Tobacco product

Norfloxacin

500

Antibiotic

Oleandomycin

1.0

Antibiotic

Paraxanthine

5.0

Coffee metabolite

Prednisone

5.0

Synthetic steroid

Roxithromycin

1.0

Antibiotic

Salinomycin

0.1

Livestock growth promoter

Simvastatin

1.0

Cholesterol regulator

Sulfachloropyridazine

5.0

Veterinary antibiotic

Sulfadiazine

5.0

Antibiotic

Sulfadimethoxine

0.1

Veterinary antibiotic

Sulfamerazine

5.0

Veterinary antibiotic

Sulfamethazine

1.0

Veterinary antibiotic

Sulfamethizole

5.0

Antibiotic

Sulfamethoxazole

5.0

Antibiotic

Sulfathiazole

5.0

Aquatic antibiotic

Theobromine

50

Coffee metabolite, heart medicine

Trimethoprim

1.0

Antibiotic

Trimethoprim

1.0

Antibiotic

Tylosin

1.0

Veterinary antibiotic

Virginiamycin M1

1.0

Veterinary antibiotic

TABLE 1, continued.

 

CHEMICAL

DETECTION LIMIT

(ng/L, ppt)

DESCRIPTION

Method L221

 

 

Aspirin

50

Pain reliever

Bezafibrate

0.5

Blood lipid regulator

Chloramphenicol

5.0

Antibiotic

Chlortetracycline

50

Antibiotic

Clofibric Acid

0.5

Active metabolite of several lipid regulators

Diclofenac

0.5

Anti-inflammatory drug

Dilantin

2.0

Anticonvulsant

Doxycycline

50

Antibiotic

Gemfibrozil

0.5

Blood lipid regulator

Ibuprofen

50

Pain reliever

Levothyroxine (synthroid)

2.0

Thyroid hormone replacement

Naproxen

2.0

Pain reliever

Oxytetracycline

500

Antibiotic

Penicillin G

2.0

Antibiotic

Penicillin V

2.0

Antibiotic

Prednisone

2.0

Synthetic steroid

Salinomycin

2.0

Livestock growth promoter

Sulfachloropyridazine

50

Veterinary antibiotic

Sulfadiazine

50

Antibiotic

Sulfadimethoxine

5.0

Veterinary antibiotic

Sulfamerazine

500

Veterinary antibiotic

Sulfamethazine

500

Veterinary antibiotic

Sulfamethizole

5.0

Antibiotic

Sulfamethoxazole

2.0

Antibiotic

Sulfathiazole

50

Aquatic antibiotic

Theophylline

5.0

Coffee metabolite, asthma medicine

Triclosan

5.0

Antibacterial, disinfectant

Tylosin

50

Veterinary antibiotic

Virginiamycin M1

0.5

Veterinary antibiotic

 


TABLE 2. CHEMICALS DETECTED IN RAW AND FINISHED DRINKING WATER, SCREENING LEVELS, AND HAZARD INDICES

 

CHEMICAL

DETECTED AMOUNT

(ng/L, ppt)

SCREENING LEVEL

(ng/L, ppt)

HAZARD INDEX, FINISHED

 

RAW

FINISHED

 

 

Chicago

 

 

 

 

Cotinine

1.0

2.0

2,000

0.001

Monensin

0.6

<0.1

100,000

<0.000001

Nicotine

6.0

<5.0

NA

----

Gemfibrozil

0.9

0.6

120,000

0.000005

 

 

 

 

 

Elgin

 

 

 

 

Carbamazepine

8.0

2.0

20,000

0.0001

Cotinine

5.0

6.0

2,000

0.003

DEET

16

12

1,000,000

0.000012

Diltiazem

2.0

<1.0

12,000

<0.000083

Lincomycin

0.5

<0.1

10,000,000

<0.0000001

Nicotine

11

5.0

NA

----

Paraxanthine

10

<5.0

NA

----

Total Sulfa

10.2

<5.1

100,000, Total Sulfa(1)

<0.000051

 

Sulfadimethoxine

0.2

<0.1

 

 

 

Sulfamethoxazole

10

<5.0

 

 

Trimethoprim

2.0

<1.0

200,000

<0.000005

Gemfibrozil

12.1

3.0

120,000

0.000025

Monensin

<0.1

0.1

100,000

0.000001

 

 

 

 

 

Aurora (NOTE: Finished water approximately 50:50 surface & well water

Caffeine

50

<50

NA

----

Carbamazepine

9.0

<1.0

20,000

<0.00005

Cotinine

12

<1.0

2,000

<0.0005

DEET

15

<5.0

1,000,000

<0.000005

Diltiazem

3.0

<1.0

12,000

<0.000083

Lincomycin

0.4

<0.1

10,000,000

<0.00000001

Monensin

0.8

<0.1

100,000

<0.000001

Nicotine

59

<5.0

NA

----

Paraxanthine

10

<5.0

NA

----

Total Sulfa

12.1

<5.1

100,000, Total Sulfa(1)

<0.000051

 

Sulfadimethoxine

0.1

<0.1

 

 

 

Sulfamethoxazole

 

 

 

 

 

Method L220

12

<5.0

 

 

 

Method L221

2.0

<2.0

 

 

Trimethoprim

4.0

<1.0

200,000

<0.000005

Gemfibrozil

10.5

0.8

120,000

0.0000067

Naproxen

2.0

<2.0

44,000

<0.000045

TABLE 2, continued

 

CHEMICAL

DETECTED AMOUNT

(ng/L, ppt)

SCREENING LEVEL

(ng/L, ppt)

HAZARD INDEX, FINISHED

E St Louis

 

 

 

 

Carbamazepine

8.0

7.0

20,000

0.00035

Cotinine

4.0

4.0

2,000

0.002

DEET

12

8.0

1,000,000

0.000008

Fluoxetine

2.0

1.0

2,000

0.0005

Lincomycin

8.5

<0.1

10,000,000

<0.00000001

Monensin

1.4

2.8

100,000

0.000028

Nicotine

11

11

NA

----

Paraxanthine

6.0

14

NA

----

Total Sulfa

20

<13

100,000, Total Sulfa(1)

<0.000013

 

Sulfadimethoxine

 

 

 

 

 

 

Method L220

0.5

<0.1

 

 

 

 

Method L221

11

7.0

 

 

 

Sulfamethazine

1.0

<1.0

 

 

 

Sulfamethoxazole

 

 

 

 

 

Method L220

8.0

5.0

 

 

 

Method L221

2.0

2.0

 

 

Gemfibrozil

13.5

10.6

120,000

0.000088

Naproxen

4.0

3.0

44,000

0.000068

Caffeine

<0.05

0.05

NA

----

Rock Island

 

 

 

 

Carbamazepine

6.0

4.0

20,000

0.0002

Cotinine

2.0

3.0

2,000

0.0015

Lincomycin

5.2

<0.1

10,000,000

<0.00000001

Monensin

1.3

2.6

100,000

0.000026

Nicotine

7.0

5.0

100,000

 

Total Sulfa

9.4

<5.1

100,000, Total Sulfa(1)

<0.0000051

 

Sulfadimethoxine

0.4

<0.1

 

 

 

Sulfamethoxazole

 

 

 

 

 

Method L220

9.0

<5.0

 

 

 

Method L221

2.0

<2.0

 

 

Trimethoprim

1.0

<1.0

20,000

<0.00005

Gemfibrozil

17.4

7.5

120,000

0.0000625

 

 

(1) The screening level pertains to the sum of all sulfa drugs.