Lecture 10 Pesticides: Trends in Environmental and …Lecture 10 Pesticides: Trends in Environmental and Tissue Residues I. Overview A. Monitoring for pesticide residues pre-dates

ES/RP 532 Applied Environmental Toxicology Page 1 of 26

ESRP532 Lecture 10.doc Fall 2004

October 4, 2004

Lecture 10 Pesticides: Trends in Environmental and Tissue Residues

I. OverviewA. Monitoring for pesticide residues pre-dates WWII.

1. In the 1920’s and 1930’s, researchers were pre-occupied with lead arsenate residueson food (owing to possible subchronic toxicity) both domestically as well as forexport.a. Lead arsenate had it greatest use on pome fruits.

2. Assessment of lead arsenate residues was also important because a change incropping systems could mean the subsequent crop might suffer phytotoxicity, one ofthe consequences of a buildup of lead arsenate with repeated use in orchard soils.

3. Lead arsenate residues cause problems today as orchards are being converted toresidential uses. If residues exceed MTCA (Washington’s Model Toxic Control Act)standards (250 ppm lead; 1 ppm DDT) than theoretically a clean up could be orderedprior to land conversion. However, the WA DOE, the agency with jurisdiction overthis issue, often makes a decision on a case by case basis. Nevertheless, WA DOEbegan a program during 2002 to focus on remediation of soils containing leadarsenate.

B. Ever since Rachel Carson published Silent Spring as a book in 1962, pesticide residuesbecame, and continue to remain, the most heavily scrutinized chemical technology.Residue analysis would naturally be expected to be an important part of this scrutiny.1. Although Rachel Carson is popularly credited with bringing to our attention the

problem of pesticide residues in the environment, especially DDT residues, she citedas references papers dating to the late 1940’s.a. Indeed, the discovery that DDT could be transferred to milk was made by a

USDA scientist in the 1940’s. Subsequently, DDT residues were shown to occurin milk when barns were treated for fly control. Perhaps these early experienceskicked off the popular notion of pesticide residues everywhere.

b. It is true however, that by the 1950’s, DDT residues (i.e., DDT plus metabolites,especially DDE) were detected in human blood, as well as in milk.

C. Because chlorinated hydrocarbon and cyclodiene insecticides were heavily used just afterWWII, and because they were known to be quite persistent, residues could be looked forin literally any matrix, including animal tissues.1. Ironically, environmental persistence was originally considered beneficial to insect

control and therefore desired.D. Today, monitoring of food residues still continues under the auspices of the FDA and the

USDA (although the FDA has regulatory enforcement authority for nearly all foods, butthe USDA has authority over eggs and meat).

E. The USGS has a research program for monitoring pesticide residues in water (surface andground water in a program known as the National Water Quality Assessment Program orNAWQA), but states have responsibilities under the Safe Drinking Water Act to monitorpublic water supplies.

F. Soils are not routinely being monitored by any agency. Obviously, wherever pesticideswere used, residues would likely be found. However, all registered pesticides are



biodegradable, so their residues would be less frequently found than the older, suspendedcompounds if a survey were conducted.

G. This lecture will focus on pesticide residues in tissues (including food and wildlife),water, and air.1. Of course, knowing the environmental concentrations is the first step to exposure

assessment. However, the mere detection or presence of a detectable residues is notthe same thing as an exposure dose. How much the organism absorbs will depend onbioavailability (i.e., the phase transfer from the environment to the organisms “skin”and movement across membrane barriers).

2. However, residues in tissues are used to diagnose pesticide related disease in wildlife(usually death is the endpoint); residues in food are one variable used to calculatehuman (i.e., consumers) exposure; and residues in water are used to assess thelikelihood of population level effects.

II. Pesticide Residues in Water: Historical PerspectiveA. The former peer reviewed EPA journal, Pesticides Monitoring Journal (PMJ), published a

wealth of contaminant data for all media starting in 1967.1. A review of the data from the late 1960’s and early 1970’s showed widespread

detection of organochlorine hydrocarbon and cyclodiene pesticides in surface watersamples.a. Many studies published by USGS scientists were able to achieve detection limits

of 10 ppt!!2. Pesticide residues were found in agricultural and urban drainage systems and in

National Parks (see figure, top of next page)a. Truhlar and Reed, 1976, PMJ 10:101-110, [Occurrence of pesticide residues in

four streams draining different land-use areas in Pennsylvania, 1969-1971]1. They reported that maximum concentrations of DDT plus metabolites (DDTr)

were highest from urban drainage;2. Note that DDTr was found in base flow at low levels from agricultural and

forested areas, but not from the urban areas;3. Also note how DDTr spiked during runoff events

B. Pesticides in Drinking Water Supplies, Surface and Well Sources1. The earliest major study that I could find reporting well water contamination by

pesticides was in published 1975 (Richard et al. 1975, PMJ 9:117-123, [Analysis ofvarious Iowa waters for selected pesticides: atrazine, DDE, and dieldrin--1974]a. This paper was also perhaps the first to report atrazine in drinking waterb. All three pesticides (atrazine, DDE, and dieldrin) were detected in shallow wells

as well as finished water supplies using wells as a raw water source (see tables onthe next page)

c. The authors noted that treatment, even with activated carbon, did not reduce theconcentrations of pesticides



Pesticide concentrations in finished water of Iowa cities using surface water as raw water source:Location Sampling Date Atrazine (ng/L) DDE (ng/L) Dieldrin (ng/L)Davenport 7/30/74 405 5 2Iowa City 7/30/74 200 3 5Des Moines 7/29/74 29 2 0.4

Pesticide concentrations in finished water of Iowa cities using wells as raw water source:Location Sampling Date Atrazine (ng/L) DDE (ng/L) Dieldrin (ng/L)Cedar Rapids 7/30/74 483 28 0Marshalltown 6/24/74 60 0 0Oskaloosa 7/29/74 14 <0.5 <0.5Waterloo 8/10/74 4 <0.5 <0.5

Pesticide Concentrations--Des Moines, IA water supply, raw and finishedSource Date Atrazine (ng/L) DDE (ng/L) Dieldrin (ng/L)Racoon River 7/29/74 25 6 2InfiltrationGallery

7/29/74 82 5 0.5

Prefilter 7/29/74 47 4 0.5Finished Water 7/29/74 29 2 0.4Finished Water 8/1/74 60 2 1

2. Atrazine was also reported from the Mississippi River by New Orleans, LA, whichillustrated the potential for long distance movement of contaminants by transport inrivers (the source was not necessarily Iowa, but further down river). Less atrazinewould be used because of less intensity of corn production as one goes downriver;



corn production in LA is very low compared to the Midwestern Corn Belt states alongthe Mississippi River.

C. Pesticide detections in well water were not discussed much prior to 1980; aldicarbdetections in Long Island starting in 1979 changed the picture (reference on aldicarb inGW: Moye and Miles, 1988, Rev. Environ. Contam. Toxicol. 105:99-146, [Aldicarbcontamination of groundwater]1. Prompted by a 1977 Coop. Extension report about the extensive use of aldicarb in

potato fields on Long Island (very sandy soil, very shallow wells), a 1979 survey ofwells by Union Carbide Corporation at the request of the Cornell University LongIsland Horticultural Research Lab showed traces of aldicarb. Of the 330 wellsinitially tested, 23% were contaminated at levels ≥ 7 ppb, the NAS (NationalAcademy of Sciences) guideline for safe levels at the time. As a result of the survey,Union Carbide requested from EPA and was granted an amendment to the aldicarblabel which banned its use in Suffolk County, NY.a. About 3-4 years after the ban, several wells were re-sampled; residues in water

from areas with shallow water tables were found to have decreased residues whilethose in water from areas with deeper water tables increased, indicating an overalldownward movement of residues with time.

b. Also, aldicarb residue concentrations peaked earlier and higher in areas closer tosites of aldicarb application and later and lower in down gradient areas.

c. The factors contributing to the pervasive contamination of wells on Long Islandby aldicarb residues included:1. Pervasive and high rates of aldicarb use;2. High water solubility of aldicarb and its environmental metabolites, aldicarb

sulfoxide and aldicarb sulfone (>0.4%);3. Heavy spring rains following application;4. Very permeable soils in glacial outwash deposits;5. Cold soil temperatures in spring;6. Acid soil conditions;7. Low soil OM (organic matter);8. Shallow water table;9. Presence of many shallow wells immediately down gradient of treated fields.

2. After the discovery of aldicarb in Long Island, a Union Carbide sampling programdiscovered aldicarb residues in the shallow GW of the Central Sands areas ofWisconsin (circa 1980-81);a. The WI Central Sands area was similar in hydrogeology to Long Island and also

had extensive potato production; however, soil pH tended to be higher. Thecontamination was concentrated in a 1.5 m thick zone near the water table.

3. Thus, it was the detections of aldicarb in GW that moved agencies and researchers tospend much of their time in the 1980’s and early 1990’s on studying pesticides inGW;a. Just from first principles of environmental chemistry and reports from Richard et

al. in Iowa (1975) coupled with the more easily attainable detection limits atlevels of 10 ppt, one could have predicted that pesticide residues would be foundeverywhere one looked, especially in regions of heavy agricultural use.



b. Yet, what prompted everyone to look so hard was the finding of an insecticidewith a very high acute toxicity; but an examination of the state data, collected asof 1991, showed very limited contamination by most pesticides at levels thatwould be considered unsafe (i.e., concentrations violating the MCL [maximumcontaminant limit] which has a large safety factor built in).

4. The widespread detection of atrazine and alachlor in GW from the Corn Belt States,especially the reports from IA in the mid-1980’s, raised new concerns about pesticidecontamination because these compounds were labeled as class B2 carcinogens by theUSEPA.

D. The Shifting Focus--Surface Water1. While everyone was reorienting from surface water (and contamination by

chlorinated hydrocarbons and cyclodienes) to ground water by the early 1980’s, someresearchers were still collecting a lot of surface water data, especially flow weighteddata. With flow-weighted data, loads of pesticides could be calculated andconcentrations could be adjusted so that they represented an average during a giventime frame (as opposed to just representing concentration at one point in time).

2. One research group at Heidelberg College, led by David Baker, showed seasonallybut transient peaks of various corn and soybean herbicides draining the Lake ErieBasin in the Ohio area (Baker, D. B. 1985, J. Soil Water conservation 40:125-132,[Regional water quality impacts of intensive row-crop agriculture: A Lake Erie Basincase study]a. The seasonal peaks occurred around the time of pesticide application, which is in

mid-April to very early June in the Midwest.b. Studies showed that tile drains, pervasive in the Midwest, had water contaminated

at greater levels than in the streams and rivers, leading to the hypothesis that tileswere conducting pesticides into streams and runoff/erosion was not the onlymechanism of transport to surface water.

3. Drinking water supplies drawn from surface water were much more frequentlycontaminated, with ≥70% of samples having detectable amounts (this compares tosignificantly less than 15% of rural wells contaminated and an even less percentagefor public supply wells)

III. Current Status of Pesticide Residues in WaterA. The most comprehensive nationally focused sampling program of ground and surface

water quality has been carried out by the U.S. Geological Survey in its National WaterQuality Assessment Program (http://water.wr.usgs.gov/pnsp/).

B. The NAWQA Program focuses on selected major watershed basins around the U.S.1. For ex., in WA State, reports are available for--

a. The Puget Sound Basin (http://wwwdwatcm.wr.usgs.gov/ps.pub.html)b. The Columbia Basin (http://wwwdwatcm.wr.usgs.gov/ccpt/pubs/)c. The Yakima River (http://or.water.usgs.gov/yakima/pubs.html)

2. Reports are also available for the Willamette Basin in western OR and the UpperSnake River Basin in Idaho. (Use GOOGLE and plug in the key words ‘USGS andWillamette River’ or ‘USGS and Snake River’

C. A summary of results from around the U.S. can be downloaded athttp://water.wr.usgs.gov/pnsp/allsum/



1. Examples of the types of data available:a. USGS will produce glossy sheet reports listing the pesticides detected and their

concentrations distribution on a log scale along with WQ criteria; for surfacewater, they list the suggested criterion for protection of aquatic biota (note in thePuget Sound data below [ released in 1999] the circles representing individualsamples, and the red and blue lines representing WQ criteria.

b. USGS also displays its data in a semi-probabilistic format showing the percentileconcentrations detected and the maximum concentration.1. The following table is from Martin et al., Table 1, Pesticides in streams at

agricultural sites, 1991-2001 (http://ca.water.usgs.gov/pnsp/pestsw/Pest-SW_2001_table1_ag.html). A similar table is available for urban influenced



streams and sites where large streams and rivers converge (known asintegrator sites) and may include both urban and agricultural influencedlandscapes.

Pesticide FrequencyofDetection(%)

50th

Percentile(µg/L)

75th

Percentile(µg/L)

95th

Percentile(µg/L)

Maximum(µg/L)

HerbicidesAtrazine 90.4 0.071 0.220 2.86 201Deethyl atrazine 82.1 0.018 0.051 0.186 3.032,4-D 15.4 <0.150 * <0.150 0.350 15.0Diuron 13.0 <0.050 <0.050 0.260 14.0Metolachlor 68.0 0.029 0.120 1.38 77.6Metribuzin 18.4 <0.006 <0.006 0.053 6.61

InsecticidesAzinphos-methyl 1.31 <0.050 <0.050 <0.050 0.500Carbaryl 9.2 <0.041 <0.041 <0.041 5.20Chlorpyrifos 11.4 <0.005 <0.005 0.009 0.260Diazinon 13.2 <0.005 <0.005 0.015 2.50Malathion 5.0 <0.027 <0.027 <0.027 0.523* Note that if the residue value is stated as <0.XXX, than that value is the maximum

reporting limit for the USGS laboratory that conducted the analysis.

D. In a comprehensive report released during 1999, USGS summarized its findings from allof its NAWQA watersheds around the U.S. [Larson, S. J., R. J. Gilliom, and P. D. Capel.1999. Pesticides in streams of the United States--initial results from the National WaterQuality Assessment Program. U.S. Geological Survey Water-Resources InvestigationReport 98-4222, Sacramento, CA :99 pp (can be downloaded as PDF fromhttp://water.wr.usgs.gov/pnsp/)].1. USGS found that urban watersheds were just as likely to contain pesticide residues as

agricultural watersheds.2. However, urban watersheds more frequently had insecticide detections, and the

detections tended to be at higher levels than in agricultural watersheds.E. Potential for Human Exposure to Water Residues and Health Risk Assessment

1. The widespread detection of pesticide residues raises the issue of biological effects,both from the human perspective and from an ecological perspective.

2. Perhaps the best study to date on this issue (i.e., human perspective) comes from astudy by Richards et al. 1995 (Environ. Sci. Technol. 29:406)a. They have shown that only a small proportion of the exposed population would be

drinking water above the MCL for atrazine; remember that the MCL is consideredthe safe level, and it is still over 1000 fold lower than the no-observable-adverse-effect level.

b. The MCL is the legal maximum contaminant level that should not be exceededunder regulation of the Safe Drinking Water Act; if no legally enforceable



standard is promulgated, then a Health Advisory Level or HAL is used until anMCL is officially approved).1. The MCL is calculated from the reference dose (RfD), the transformation of

the RfD to the DWEL (drinking water equivalent level) multiplied by therelative source contribution (RSC; assumed to be 20% for water), and adjustedby an additional safety factor (or UF).a. The RfD is calculated from the NOAEL divided by an uncertainty factor,

UF, which is usually 100c. At the time that the MCL was developed, the NOAEL for atrazine was 0.48

mg/kg bw/day based on a one-year dog oral feeding study with the most sensitiveendpoint as mild cardiac pathology that intensified at higher doses.1. Thus, the RfD was estimated as 0.005 mg/kg bw/day using an uncertainty

factor of 100.2. The DWEL was estimated as (0.0048 mg/kg/day) x (70 kg body weight)

divided by (2 L water/day) or 0.168 mg/L3. The MCL was estimated from the DWEL by multiplying by 0.168 mg/L (the

water concentration) by 0.20 (i.e., 20% for the RSC) and dividing by an extraUF of 10 owing to the possible carcinogenic potential of atrazine. The finalMCL was proposed as 0.003 mg/L (or 3 ppb).

F. An alternative perspective is provided by the environmental advocacy group known asthe Environmental Working Group (http://www.ewg.org/



1. For example, in “Tap Water Blues”, EWG concluded that millions of people in theCorn Belt are at risk from consuming water contaminated with herbicides designatedas carcinogens by EPA.

G. Under the mandates of the Food Quality Protection Act (FQPA), EPA does aggregateexposure to pesticide residues in food and in drinking water.1. EPA models the concentrations of pesticides in drinking water using a combination of

two models: PRZM (Pesticide Root Zone Model) and EXAMS (ExposureAssessment Modeling System)a. PRZM models movement of pesticides either through overland flow or through

leaching to a water body.1. The water body is assumed to be a 1-ha pond, 2 m deep. In other words it is a

static enclosed water body.b. EXAMS models the dissipation of the pesticide within the water body. The

model is not used in a manner that can account for volatilization.1. Furthermore, the body of water is considered static. In other words, it is not

considered to be flowing, as streams and rivers are. Even large reservoirshave volume changes!

2. The results of the modeling produce pesticide residue concentrations that are muchhigher than what is observed in the USGS NAWQA program, even when aprobabilistic analysis is used and the 95th percentile of contamination is examined.a. For example, in EPA’s risk assessment for the organophosphate insecticide

diazinon, modeling of surface water concentrations (the output concentration iscalled an EEC, or expected environmental concentration) yielded 70 ppb.However, the USGS monitoring data showed a maximum concentration of 3 ppb.1. The modeled ground water EEC was 0.8 ppb, but monitoring data showed

0.02 ppb.

IV. Pesticide Residues in Air: Historical PerspectiveA. In 1965, Wheatley and Hardman (Nature 207:486) reported finding ppt levels of lindane,

dieldrin, and DDT residues in rainfall collected in Wellesbourne, Warwick, England. Asfar as I can tell, this was the second report indicating atmospheric transport anddeposition of pesticide residues and is cited by later studies (within a few years ofWheatley and Hardman’s report) showing long-range transport of chlorinatedhydrocarbon pesticides.1. Interestingly, Wheatley and Hardman cite two earlier studies (1950 and 1961)

indicating significant atmospheric loss during spraying (1950) and volatilization as amajor loss pathway (1961)

2. A study by Adams et al. in Weeds 12:280 (1964) may have been the first report ofairborne residues; they reported low volatile, isooctyl 2,4-D residues in air samples.

B. A 1965 paper in Science (vol. 150:1476) reported by Antommaria et al. showed DDT insuspended particulate matter in Pittsburgh air.

C. A 1968 paper by Risebrough et al. (Science 159: 1233) were probably the first to showmovement of chlorinated pesticides in airborne dust from European-African land areas toBarbados (tropical Atlantic).

D. George Ware in 1968 was studying DDT residues in alfalfa in Arizona (the milk fromcows produced on this forage crop was contaminated with DDT; yet DDT had not been



recommended for use on forage during the 10 year period prior to the study). Warestated “Since recent work indicates that DDT is not translocated to any significant degreethrough the roots to the above-ground portions of alfalfa, the residues must originate fromother sources. Quite logically, indirect sources of contamination would be windblowncontaminated dust or rain-splashed soil [my note: cotton, a heavy user of DDT at thetime, was grown in fields intermixed with alfalfa fields, i.e., in close proximity]; a directsource would be the drift from agricultural application of insecticides during the growingseason”.

V. Pesticide Residues in Air: Sources to the Atmosphere & Role of Drift and VolatilizationA. Pesticides transport to air via drift of aerosols during spraying, or secondarily as a result

of volatilization after spray deposition; there are hypotheses of wind-blown dusttransport, but samplings of particulates (either airborne or as dry deposition) cannot bedistinguished from phase transfers after volatilization or actual blowing dust from the soilsurface.

B. The nature of drift (i.e., point sources during spraying)1. During spraying particles or aerosols of various sizes are produced; some are

deposited under the influence of gravity a short distance from the spray swath; thesmaller particles (<50 µm) become airborne and disperse rapidly into the atmosphereand can thus be carried much longer distances (deposition over miles!!)

2. Particle sizes; these are usually reported as volume median diameter (vmd), which isdefined as the one-half of the volume of spray containing droplets whose diameter issmaller than the vmd, and one-half of the volume whose diameter is larger than thevmd. The number median diameter (nmd) would just refer to the diameter withoutreference to the volume. (Matthews, “Pesticide Application Methods”, 1992, p. 72)

a. What sizes of particle are expected:1. Varies according to application method--ground sprayer or aircraft) (p. 91,

Grover, CRC Press, Environmental Chemistry of Herbicides, vol. II)a. Because of the higher velocities associated with spray release from aircraft

and the height of release of spray, expect smaller particles and greater drift



than from ground tractors, where velocity of sprayer is slower, and heightof release is lower.1. For ex., a study by Yoshida and Grover, 1978 (Air Pollut. Control.

Assoc. J., vol. 28) showed droplets of 220-280 VMD emitted fromaircraft sprayers and 440-860 VMD emitted from ground sprayer inseveral field trials with the herbicide 2,4-D

2. In another experiment, Grover (p. 621, Grover et al., Can. J. Plant Sci58:611-622) reported that in a spray swath (the stuff coming out of thenozzles, which are attached to a boom) had 14% of the droplets <100µm; but in a drift cloud, ~50% of droplets were less than 13 µm indiameter.a. Furthermore, the vmd of spray droplets in the swath are much

larger than in the “drift cloud” (p. 621, Grover et al., Can. J. PlantSci 58:611-622); ~185 - 190 vmd vs. ~18 - 21 vmd, respectively

b. Thus, there is a substantial number (but smaller volume relative tothe total droplets) available for longer-range transport.

2. Pressure and type of nozzle are large determinants of particle size ranges andcharacteristics. Note below how VMD is larger from a ground sprayeroperating under comparatively low pressure. Also notice that the volume (orproportion) of spray in the drift cloud is small compared to the volumeemitted; however, it can be fairly large from some aerial spray operations.

Sprayer,Nozzle

Size

Pressure(psi)

Windspeed(mph)

% of SprayVolume in

Swath (areaunder nozzles)

VMD inSwath(µm)

% of SprayVolume in

Drift Cloud

VMD inDrift

Cloud(µm)

Ground,8002

30.5 9 104 590 1.2 15

Ground,8002

14.5 10 106 860 0.6 17

Air -- 9 54 220 31.3 100Data are from Maybank, J. K. Yoshida and R. Grover. 1978. Spray drift from agriculturalpesticide applications. J. Air Pollution Control Association 28:1009-1014.

C. How far can we expect a field spray application to travel1. Based on known physical relationships between the settling rate of a particle in a

viscous meeting, engineers can predict how far a particle (aerosol) will travel before itfalls a distance of 10 feet; this gives us some idea of the potential of different sizeaerosols to travel after emission from the sprayer;a. Note that the smallest aerosols can travel for distances of ~2 miles before

depositing; however, the density of particles at that distance may be so small as tobe biologically irrelevant although perhaps still measurable (depending on thespecific chemical and its detection limit capability)



2. Aerial spraysa. Research with aerial sprays of 2,4-D show that the maximum detectable distance

was 500 m; note this research was based on a single swath (a swath is the areacovered by the spray boom when it makes one pass across a sprayed field,orchard, forest, or right-of-way).

b. A comprehensive synthesis of many studies (~45) by Bird (1995, Chapt. 18,Agrochemical Environmental Fate, CRC Press) shows in some cases 1% of sprayscould be detected at distances of about 500 m when experimental single swathsprays are adjusted for 20 swaths.

D. Note that deposition distances beyond the edge of a field or orchard (i.e., downwinddeposition) varies depending on weather conditions.1. Aerosols can become trapped in atmospheric inversions (distinct temperature

stratifications in the atmosphere under very calm or non-turbulent conditions) and becarried longer distances before the aerosols deposit on the ground or on a plant as aresult of gravity or impaction.a. The following graphs show the difference in downwind deposition of two

pesticides, carbaryl (a methyl carbamate insecticide) and captan (a dicarboximidefungicide) applied by an airblast sprayer.1. An airblast sprayer forces spray in a ~90° arc from each side of the sprayer as

it is being pulled behind a tractor.



2. Note that the distance of measurable deposition actually increases during aninversion.

3. When the airborne residues of captan were measured following aerialapplication (turbulent conditions), airblast sprayer application (turbulentconditions), and airblast sprayer application in an inversion, residues arerecovered for a longer period of time after spray application under conditionsof an inversion than under a turbulent atmosphere (see third graph on nextpage).a. An inversion does not allow mixing of air masses. Contaminants in an

inversion can travel great distances along the laminar flow of an invertedair mass.

b. Such contaminants remain in the air longer as a concentrated mass.1. Thus, when they impact a target, the relative concentration is much

higher than if the contaminant had dispersed in a turbulent atmosphere.2. Thus, you can think of turbulence that causes air mixing as a type of

dilution (fixed mass of contaminants in a rapidly changing airvolume).

Graphs redrawn from MacCollom, G.B.; Currier, W.W.; Baumann, G.L. 1985. Pesticide drift and quantificationfrom air and ground applications to a single orchard site. American Chemical Society Symposium Series no. 273,pp. 189-199.

2. Naturally, the detection of residues leads to the question of “what’s the hazard”. Onesimple way is to examine the magnitude of the residues against some health criteria orbenchmark.a. In the case of air residues, we could be conservative and examine the recovered

amounts relative to the TLV.1. The TLV is the air concentration of a contaminant that should not be exceeded

in any 8-hour work period. It is a criterion developed by the OccupationalSafety and Health Administration (OSHA).



a. For captan, it is equivalent to 5000 µg/cm3.2. Under worst case conditions--aerially applied spray, immediately after

application--the potential exposure is ~100 fold less than the TLV (see nextgraph, which was redrawn from MacCollum et al. (1985).

E. Modeling Spray Drift1. About a decade ago, a consortium of agrochemical manufacturers (called the Spray

Drift Task Force) proposed to empirically study drift and develop a model fordownwind deposition. The objective was to develop a model that could be used topredict off-target residues for risk assessment, and therefore obviate the need for anactual drift study.

2. The culmination of the Spray Drift Task Force was the development of the modelAgDrift, now sanctioned and used by the EPA, that predicted drift from groundsprayers, orchard sprayers (airblast sprayers), and fixed-wing and rotary aircraft. Themodel has been described in the peer-reviewed literature and the aerial applicationmodule validated.a. Teske, M. E., S. L. Bird, D. M. Esterly, T. B. Curbishley, S. L. Ray, and S. G.

Perry. 2002. AgDRIFT¨: a model for estimating near-field spray drift fromaerial applications. Environ. Toxicol. Chem. 21(3):659-671.

F. The nature of secondary drift (i.e., volatilization after deposition) belies modeling byAgDrift at this point in time.1. This problem was perceived during the 1950’s in WA and CA when grapes, which

are very sensitive to 2,4-D, were observed to be injured during the wheat sprayseason; of course, this injury could have also resulted from direct sprayinga. Butyl esters of 2,4-D were know to be highly volatile

1. Use of certain high volatile ester formulations was eventually banned by theWSDA (Washington State Department of Agriculture).

b. Secondary drift can result in contamination of nontarget crops, possibly creating aviolation of residue tolerances.

VI. Pesticide Residues in Air: Atmospheric Residues and DepositionA. A plethora of pesticide residues have been measured in precipitation, giving evidence to

their presence in the atmosphere.



1. Presumably, the pesticide residues are entrapped either from vapor phase by acombination of condensing water vapor or alternatively by sorption to air-borneparticulates.

2. Deposition (and thus transfer of contamination from air to terrestrial/aquaticenvironments) occurs as a result of--a. Wet/dry deposition (rainfall, particulate fall-out)b. Air-water partitioningc. Fog impactiond. Snowfall

B. Wet deposition is a significant source of pesticide residues in the Mississippi River Basinas the graph below shows (stream transport would be residues that arise as a result ofrunoff and subsurface flow. (Goolsby et al., 1997, ES&T 31:1325)

C. Net loading of DDT to Great Lakes, considered a sink for deposition of many persistentenvironmental contaminants, seems to be decreasing in Lake Huron and is low relativelyto other chlorinated insecticides (Hillery et al. 1998, ES&T 32:2216). However, HCHs(hexachlorocyclohexanes, derived from the technical pesticide lindane) seem to still beincreasing.1. Note that lindane can still be used a crop seed treatment whereas DDT had not been

used (legally) for over 40 years.



D. Giving further evidence of the importance of volatilization as a source of atmosphericresidues that are then eventually redeposited, many studies have measured concentrationsof herbicides and insecticides in rainfall. The next two graphs are a compilation of manystudies (Felsot, A. S. 1999. Estimated contributions of atmospheric deposition of pesticide residues toenvironmental loading. Abstract & presentation, 217th American Chemical Society National Mtg.,Anaheim, CA. 21-25 March). The data are presented as box plots to show the 10th 25th, 50th,75th, and 90th percentile of residue concentrations. The average (mean) is indicated by thered solid square).



E. What goes up must come down!! Illustrating the old cliché are the next two graphs thathave complied several studies where herbicide and insecticide deposition on an area basishave been measured (mg/ha).



F. So what does it all mean?1. Assume the herbicides and/or insecticides are falling on a 1-hecatare pond, 2 meters

deep (these are the dimensions that EPA uses for ecological risk assessment);2. Assume there was a 2.5 cm rainfall resulting in uniform and instantaneous mixing

with the pond water;3. Calculate the maximum water concentrations based on concentrations in rainfall, and

then compare to aquatic criteria for the protection of aquatic biota.

G. A similar exercise can be conducted for deposition of herbicides in terrestrial habitats,especially where there are sensitive plants. All one needs is an estimate of the depositionrate (mg/ha) and the toxicity of the targets. (See graph titled “Deposition of Herbicides”below)1. This exercise can be made somewhat probabilistic by looking at the estimated

deposition relative to the percentile distribution of NOELs.



2. Note for 2,4-D, one study has estimated deposition of 2,4-D in the wheat growingregion of Canada as 1.4 g/ha. This deposition rate is near the NOELs for certainsensitive crops like grapes. (See graph below titled Estimate of Risk fromAtmospheric Deposition of 2,4-D).a. The graph shows the distribution of NOELs (circles) taken from studies of

phytotoxicity of 2,4-D to various plant species and the estimated deposition of2,4-D (1.4 g/ha; heavy line).

VII. Pesticide Residues in FoodA. Recall from the lecture that discussed pesticide regulations, that the main objective under

FFDCA is to obtain a residue tolerance, or a legal maximum residue concentration.1. The FQPA mandates all tolerances be safe, but a tolerance itself is not a safety

standard in the strictest sense of the word.2. Tolerances range from hundredths of ppm to 10’s of ppm depending on the

commodity, its use, and of course, specific pesticide toxicological characteristics.



3. Tolerances are proposed by a potential pesticide registrant, but EPA validates themdepending on their risk assessment results.

4. The basis for the magnitude of the tolerance is practical;a. Field trials are done in major regions of the U.S. that will grow the commodity;b. Pesticides are applied at the proposed pre-harvest interval (i.e., the time between

the last application of a pesticide and the harvest of the commodity);c. Residues are determined; the maximum residue is picked out;d. The potential registrant proposes the tolerance above this level;

1. By proposing the tolerance based on field studies, the registrant hedges hisbets against the tolerance being exceeded and lessens the risk of commoditiesbeing embargoed should the FDA (remember, that agency has jurisdiction forenforcing tolerances) detect a violation.

B. The fact that the law allows the establishment of pesticide residue tolerances on cropssuggests that food has detectable residues. Indeed it does, but the mere detection ofresidues is not the same as concluding a hazard exists or that risk of effects is likely.1. To characterize risk, one must estimate (as realistically as possible exposure)

exposure;2. The next lecture will focus on how EPA estimates human exposure to pesticide

residues and uses the information to characterize risk.3. The following section of this lecture gives an overview of residues in food.

C. Realistic exposure assessment for residues in food depends on systematic monitoring ofresidues (especially for compounds commercialized for a long time) and updated foodconsumption statistics. Currently, there are three main ways to obtain realistic residuedata: the FDA Compliance/Surveillance and Total Diet Study; the USDA Pesticide DataProgram; and industry sponsored Market Basket Surveys.

D. The Food and Drug Administration Programs is the agency nationally responsible (bystatute) for monitoring the food supply and enforcing the tolerances. This responsibilityis carried out in three separate programs: (Note that reports and data can be accessed athttp://www.cfsan.fda.gov/~lrd/pestadd.html)1. Regulatory monitoring (surveillance and compliance monitoring)

a. Surveillance monitoring1. Inspectors randomly collect commodities from wholesalers or distributors or

storage sites and bring them to one of the 18 FDA regionally located labs foranalysis

2. FDA monitors both domestic and imported foodsb. Compliance monitoring

1. These include follow-up sampling to the finding of an illegal residue or whenevidence indicates a residue problem may exist

c. FDA summarizes its data by calculating the percentage detections of residuesabove the tolerance, below the tolerance, and below the analytical detection limit.1. The percentages for each commodity group are remarkably stable from year to

year, whether the food is domestic or imported.2. Historically, roughly 60-65% of the food (all categories) have no detectable

levels of pesticides;3. About 30-35% have residues but below the tolerances;4. About 1-3% have residues that violate the tolerances



a. Violations may be due either to too much residue or no U.S registration.

Frequency of Pesticide Detections in the Year 2002 Regulatory Compliance MonitoringSamples: Domestic Food Supply (n = 2,122 samples)

Frequency of Pesticide Detections in the Year 2000 Regulatory Compliance MonitoringSamples: Imported Food (n = 3,998 samples)



2. Incidence/Level monitoringa. A select group of pesticides are analyzed in a specifically collected subset of

foods1. For ex., ALAR, EBDCs (i.e., “hot” compounds--those deemed especially

hazardous)2. For ex., food prevalently consumed by children3. In 2002, FDA completed a study of OP insecticide residues in fruit and

vegetables.3. Total Diet Study (TDS)

a. Food is purchased from grocery stores in four regions of the U.S. and returned tothe labs for preparation to simulate what the typical consumer would do.

b. Far fewer samples are actually analyzed then in the regulatory monitoringprogram (1030 food items analyzed in the TDS during 2002).

c. Surprisingly, DDT shows up as the most frequently detected residue. (Thefollowing table is from the FDA 2002 report.)

Pesticide Total No. ofFindings

% Occurrence Range, ppm (mg/kg)

DDT 212 21 0.0001 – 0.025Chlorpyrifos-methyl 175 17 0.0002 – 0.059Malathion 156 15 0.0007 – 0.071Endosulfan 142 14 0.0001 – 0.166Dieldrin 115 11 0.0001 – 0.010Chlorpropham 62 6 0.0007 – 1.278Chlorpyrifos 49 5 0.0001 – 0.105Permethrin 43 4 0.0004 – 1.680Carbaryl 42 4 0.001 – 2.040Dicloran 33 3 0.0002 – 0.263Thiabendazole 31 3 0.013 – 0.991Lindane 20 2 0.0001 – 0.002Methamidophos 19 2 0.001 – 0.345Hexachlorobenzene 19 2 0.0001 – 0.002Dicofol 19 2 0.002 – 0.538Pirimiphos-methyl 17 2 0.001 – 0.024Quintozene 17 2 0.0001 – 0.0424Toxaphene 17 2 0.002 – 0.028Acephate 16 2 0.002 – 0.350Ethion 16 2 0.0003 – 0.007

E. Starting in ~1991, Congress charged the USDA Marketing Service with systematic (butnon-regulatory) monitoring of the food supply. The program is called the USDA PDP(Pesticide Data Program).1. The program was intended to be representative of the whole food supply.

a. Thus, USDA chooses wholesale distribution centers that are representative of x%of the area where each commodity in the program is grown.



2. Annual results of the USDA PDP since its first report in 1993 can be accessed athttp://www.ams.usda.gov/science/pdp/index.htm

3. In its current risk assessment procedures, the EPA relies most heavily on the USDAPDP data.

VIII. Pesticide Residues in TissuesA. Humans have been studied for DDT/DDE levels since the early 1950’s

1. Levels of DDT/DDE have been monitored in adipose tissue (deceased subjects!),breast milk, and blood.

2. Correlations between levels in tissues and various diseases have been attempted.a. The most controversial of the last decade has been attempts to relate DDE levels

in sera with incidence of breast cancer1. For example, Wolff et al. found 11.0 +/- 9.1 ppb in patients with breast cancer

(case patients) and 7.7 +/- 6.8 ppb in controls; regression coefficient forquintile of DDE serum level and odds ratio was 0.0823, but slope wassignificant (p = 0.0037) (Wolff, M. S., P. G. Toniolo, E. W> Lee, M. Rivera,and N. Dubin. 1993. Blood levels of organochlorine residues and risk ofbreast cancer. J. National Cancer Institute 85(8):648-650.)

2. Since the publication of Wolff et al. (1993), numerous other studies have beenpublished concluding that DDE in sera is not a good predictor of breastcancer; essentially the correlations were not significant.a. The health effects of DDT were reviewed from the perspective of public

health in 1997, and the authors downplayed the link to cancer.1. Longnecker, M. P., W. J. Rogan, and G. L. Lucier. 1997. the human

health effects of DDT (dichlorodiphenyl trichloroethane) and PCBs(polychlorinated biphenyls) and an overview of organochlorines inpublic health. Annu. Rev. Public Health 18:211-244.

3. Levels of DDT/DDE in breast milk, and by implication adipose tissue, have beendecreasing since the worldwide ban of the pesticide (note that some countries still useDDT for control of malaria carrying mosquitoes, but crop use is nil).a. Noren and Meironyte (2000) analyzed breast milk from women residing in

Sweden over the last thirty years and reported an exponential decrease inDDT/DDE levels and the methyl sulfonated metabolite of DDE. They also founda decrease in dieldrin levels. (See next two graphs; note that the DDT/DDE levelsare expressed as ng per lipid; in other words the concentrations are normalized tothe lipid content in the breast milk).1. Noren, K. and D. Meironyte. 2000. Certain organochlorine and

organobromine contaminants in Swedish human milk in perspective of past20-30 years. Chemosphere 40:111-1123.



B. DDT and chlorinated cyclodiene insecticide residues in tissues had historically received alot of attention.1. They were the most intensely used insecticides on the market since the early 1950’s2. They were fairly easy to analyze at low levels once the electron capture detector for

the gas chromatograph was developed in the late 1950’s3. They accumulated in lipid rich tissues (for example, the brain, the liver, the adipose

tissue)C. DDT and chlorinated cyclodiene residues were often used as diagnostics to determine

reasons for observation of dead birds in a locale.1. For example, analysis of DDT levels in brains of dead birds showed levels of 10’s of

ppm (mg/kg).a. Thus, while DDT itself was not too toxic to birds based on acute oral LD50s, it

could accumulate in nervous tissue to lethal levels after chronic feeding oncontaminated organisms (Blus, L. J. 1996. DDT, DDD, and DDE in birds.Environmental Contaminants in Wildlife. Interpreting Tissue concentrations. W.



N. Beyer, G. H. Heinz, A. W. Redmon-Norwood (ed). CRC Press, Boca Raton,FL. pp. 49-71.)1. Levels of 15 µg/g in the brain of robins exhibiting tremors have been found in

the field;2. Under experimental feeding conditions, levels of 25 µg/g have been proven

lethal.D. DDE tissue analyses were also use to hypothesize the reasons for decline of bird

populations during the period of heavy DDT use.1. Lethality alone (i.e., dead birds) was not viewed as sufficient explanation for why

certain bird populations (especially predatory birds, whether fish eating or rodenteating) seemed to be declining.

2. However, in the 1960’s, associations began to be made with comparatively thineggshells in certain bird populations and declining populations.a. Ratcliffe, D. A. 1967. Decrease in eggshell weight in certain birds of prey.

Nature 215:208-210.3. DDE levels in eggs seemed to correlate inversely with egg thickness.

a. Hickey, J. J. and D. W. Anderson. 1968. Chlorinated hydrocarbons and eggshellchanges in raptorial and fish-eating birds. Science 162:271-273.

4. Not everyone agreed that DDE correlations with egg shell thinning was a plausiblehypothesis to explain reductions in populationsa. Hazeltine, W. 1972. Disagreements on why brown pelican eggs are thin. Nature

239:410-411.b. Switzer, B. C., F. H. Wolfe, and V. Lewin. 1972. Eggshell thinning and DDE.

Nature 240:162-163.5. Personally, I’ve always found the hypothesis to be somewhat weak

a. While experimental feeding studies with some birds (and there are exceptions)showed high doses were correlated with thinner eggshells relative to the control,there were definite thresholds; furthermore, hatching success was not too differentthan controls.1. Smith, S. I., C. W. Weber, and B. L. Reid. 1969. The effect of high levels of

dietary DDT on egg production, mortality, fertility, hatchability and pesticidecontent of yolks in Japanese quail. Poultry Science 48:1000-1004. (LOAELwas 200 ppm dietary)

2. Heath , R. G., J. W. Spann, and J. F. Kreitzer. 1969. Marked DDEimpairment of mallard reproduction in controlled studies. Nature224(October 4):47-48. (LOAEL for eggshell thinning was 40 ppm dietary)a. Note that only dietary DDE, not DDT, affected hatching success.

b. In the field, broken eggshells were collected and compared to museum specimenscatalogued prior to 1947. Considering that the measurements are made with amicrometer to a precision of <1 mm, I always thought there could have been a lotof error, not to mention an ignorance of polymorphism in shell thickness amongdifferent populations (especially if the specimens were collected from verydifferent geographical locations).

c. DDT was banned in the U.S. in 1973, although its use had been on a significantdecline since the mid to late 1960’s. Yet, a 1975 paper mentioned recoveringbrown pelican populations as a result of lower DDE levels in the eggs.



1. Because DDE could accumulate in egg lipids, it seemed odd that recoverywould occur so quickly (unless of course there is a definite threshold for heeffect to occur).a. Anderson, D. W., J. R. Jr. Jehl, R W. Risebrough, L. A. Jr. Woods, L. R.

Deweese, and W. G. Edgecomb. 1975. Brown pelicans: improvedreproduction off the southern California coast. Science 190:806-808.

6. Despite my skepticism, the standard hypothesis of DDE “causing” eggshell thinningand thus population declines has not been seriously challenged by anyone who hastaken the time to critically analyze the earlier papers.a. One publication argued (based on an experimental study with white ibis) that egg-

breaking strength was a better indicator of reproductive success than eggshellthickness.1. Henny, C. J. and J. K. Bennett. 1990. Comparison of breaking strength and

shell thickness as evaluators of white-faced ibis eggshell quality. Environ.Toxicol. Chem. 9:797-805.

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Lecture 10 Pesticides: Trends in Environmental and …Lecture 10 Pesticides: Trends in Environmental and Tissue Residues I. Overview A. Monitoring for pesticide residues pre-dates