Dermal Exposure Related to Pesticide Use - American Chemical Society

Downloaded via UNIV OF CALIFORNIA SANTA BARBARA on July 22, 2018 at 11:12:51 (UTC). See https://pubs.acs.org/sharingguidelines for options on how to legitimately share published articles.

17 Dermal and Respiratory Exposure of Applicators and Residents to Dichlorvos-Treated Residences 1

2

ROGER Ε. GOLD and TERRY HOLCSLAW 1

University of Nebraska, Lincoln, NE 68583-0802 University of Nebraska Medical Center, Omaha, NE 68105

2

Applicators and residents of dichlorvos (DDVP) treated structures were monitored for evidence of insecticide exposure using exposure pads, air samplers, serum and red blood cell acetylcholines terase (AChE) tests, and urine analysis. There was no evidence of DDVP or dichloroacetic acid (DCAA) in the urine of applicators or cooperators. There were slight but significant differences (P≤0.05) in serum AChE activity of residents of treated units, but erythrocyte AChE was unchanged. Applicator AChE test results were inconclusive. It was concluded that there was not a significant risk, in terms of acute toxicity, to either the pesticide applicators or the residents of treated structures.

P e s t i c i d e s are t o x i c a n t s t h a t are d e l i b e r a t e l y added to the e n v i ronment i n an e f f o r t t o i n s u r e our food and f i b e r s u p p l y , p r o t e c t our homes and s t r u c t u r e s , and guard our h e a l t h . P e s t i c i d e use i s c o n s i d e r e d e s s e n t i a l by many g r o u p s , but i t i s i m p o s s i b l e t o o v e r l o o k the hidden c o s t s ( e x t e r n a l i t i e s ) a s s o c i a t e d w i t h t h e i r u s e . In 1962, Durham and Wolfe (I) e x p r e s s e d the o p i n i o n t h a t t h e r e was not a s i n g l e p e s t i c i d e f o r which t h e r e i s d e f i n i t i v e i n f o r m a t i o n c o n c e r n i n g the i n t e r r e l a t i o n s h i p s between o c c u p a t i o n a l exposure by d i f f e r e n t r o u t e s , the f a t e o f the compound i n t h e human body, and i t s chemical e f f e c t s . A l t h o u g h t h a t statement can no l o n g e r be made u n c o n d i t i o n a l l y , t h i s premise remains v a l i d f o r d i c h l o r v o s [2,2-dichlorovinyl d i m e t h y l phosphate (DDVP)], a pesticide used both i n a g r i c u l t u r a l and urban s e t t i n g s . DDVP i s an i n s e c t i c i d e t h a t has been s u b j e c t e d t o the " s p e c i a l review" p r o c e s s by the U . S . E n v i r o n m e n t a l P r o t e c t i o n Agency (USEPA) based on r e p o r t e d m u t a g e n i c i t y , r e p r o d u c t i v e and f e t o t o x i c effects,

0097-6156/85/0273-0253$06.00/0 © 1985 A m e r i c a n C h e m i c a l Society

Honeycutt et al.; Dermal Exposure Related to Pesticide Use ACS Symposium Series; American Chemical Society: Washington, DC, 1985.

254

DERMAL EXPOSURE RELATED TO PESTICIDE USE

oncogenicity and neurotoxicity (2-5). Studies have been conducted on the respiratory and dermal exposure of humans to DDVP formulated i n r e s i n s t r i p s (.6-9 ) ; however, l i m i t e d research data are a v a i l able on the exposure of humans to other formulations of DDVP used by commercial pest control applicators and homeowners (10 ) within structures. Materials and Methods The dermal exposure of applicators who applied DDVP i n these r e p l i c a t e d t r i a l s was monitored by using the techniques described by Durham and Wolfe (1), Gold e t a l . (10-12 ), and L e a v i t t et a l . (13). Applicators wore a one-piece polyester jumpsuit with an open c o l l a r and long sleeves, a hard hat, r e s p i r a t o r , and rubber gloves. They were f i t t e d with both inside and outside dermal exposure pads placed on the outer c l o t h i n g and on the skin beneath the c l o t h i n g . Internally located pads (those beneath the clothing) ware p o s i tioned c a r e f u l l y to avoid overlap with the external pads (those attached t o the outer c l o t h i n g ) . Pad locations were: head (both under and on top of the hard h a t ) , forearm (just above the w r i s t ) , leg (just above the ankle), chest, and back. Exposure pads were constructed i n three layers. The bottom layer was a 10.2 by 10.2 cm glassine paper. An equal s i z e d sheet of f i l t e r paper (Whatman Chromatography Paper, 0.16 itm thickness) was used as a second l a y e r . Top layer was an eight-ply gauze pad (Steri-Pad). Layers were fastened together with s t r i p s of masking tape with a 6 . 4 by 6 . 4 cm area l e f t exposed. Preliminary analysis indicated exposure pads contained no materials that would i n t e r f e r e with DDVP detection. Following p e s t i c i d e a p p l i c a t i o n s , the exposure pads were removed from the applicators and were placed i n Ziplock Sandwich Bags and stored on i c e i n an insulated cooler u n t i l frozen i n the laboratory. T o t a l amount of DDVP found on the exposure pads was divided by the exposed area of the pads and elapsed a p p l i c a t i o n time t o give an estimated r a t e of exposure ^g/an2/hr). Dermal exposure was further monitored by washing both of the hands of each applicator i n 200 ml o f a 50:50 mixture of ethanol: water. Each hand was placed i n the s o l u t i o n and shaken vigorously for approximately 30 seconds. Wash solutions were sealed i n a glass j a r and immediately placed on i c e i n an insulated cooler u n t i l they could be stored a t 5°C i n the laboratory. Preliminary experimental r e s u l t s indicated that DDVP was soluble i n the washing solution. The amount of DDVP found on the hands following each a p p l i c a t i o n was divided by the area of both hands to give an estimate of hand exposure ^g/cm2/hr). Applicator respiratory exposure was monitored with a batterypowered personnel a i r pump (Telmatic Model 150A) f i t t e d with a 30 ml glass midget impinger (Houston Glass Fabricating). The impinger was of the s t r a i g h t shank type with the shank end embedded i n a p l a s t i c bubbler (Bendix). The impinger was f i l l e d with 5 ml of water plus 15 ml of ethylene g l y c o l . Preliminary t e s t r e s u l t s showed t h i s mixture was e f f e c t i v e i n scrubbing DDVP from the a i r . The a i r sampler was bolted to a f i b e r b e l t and worn on the lower back. One end of a Tygon tube (15 mm i n t e r n a l diameter) was attached over the shoulder to r e s t on the upper chest. Air samplers pumped a mean of 4 4 . 6 l i t e r s / h r when worn by the


17.

GOLD AND HOLCSLAW

Exposure

to DDVP-Treated

Residences

255

applicators. A t the end o f the exposure period, the impinger was removed and immediately stored i n i c e . In the laboratory, the s o l u t i o n was transferred t o a capped glass v i a l and held a t 5°C u n t i l analysis. Data r e s u l t i n g from respiratory monitoring was expressed as ug DDVP/liter o f a i r , calculated by d i v i d i n g the amount o f DDVP i n the impinger by the length o f a p p l i c a t i o n time and the pumping rate. The respiratory rate o f the applicators was assumed t o be 1,740 l i t e r s / h r (1). Both blood and urine samples were c o l l e c t e d from the a p p l i cators p r i o r t o (time 0) and then a t regular i n t e r v a l s throughout the study period. Each subject had two 5 ml blood samples taken from the antecubital vein v i a Vacutainer. One blood sample was used t o derive serum and the other was used as whole blood. Both the serum f r a c t i o n and erythrocytes derived from the whole blood were assayed f o r acetylcholinesterase (AChE) a c t i v i t y by the srjectrophotometric method o f Ellman e t a l . (14) using a c e t y l t h i o choline as substrate. Urine samples were c o l l e c t e d from each applicator a t the time blood samples were drawn. Each urine sample was frozen f o r l a t e r analysis o f DDVP and d i c h l o r a c e t i c a c i d (DCAA) by a modification o f the gas chromatographic method o f Schultz e t a l . (15). One resident from each o f the 20 DDVP treated units was i n volved i n p e s t i c i d e exposure monitoring. Each oooperator provided both urine and blood samples before (time 0) and 24 hrs a f t e r t h e i r residence had been treated. A t the time the i n i t i a l and posttreatment samples ware c o l l e c t e d , each resident was interviewed t o c o l l e c t data on age, sex, health h i s t o r y , medications taken (including use o f alcohol and tobacco), p e s t i c i d e s used, amounts o f time spent i n the treated units f o r the 24 hrs following EDVP a p p l i c a t i o n , and any adverse health e f f e c t s noted as a r e s u l t o f the treatment. Environmental exposure was monitored by placement o f the same type o f exposure pads as used i n dermal monitoring on top o f the r e f r i g e r a t o r , stove, kitchen table, and kitchen f l o o r (center). Pads were i n place p r i o r t o i n s e c t i c i d e a p p l i c a t i o n and were c o l l e c t e d 2 hrs posttreatment. Pads from a l l locations (within each unit) were combined and analyzed using the procedures f o r dermal pads. Room a i r samplers were used t o monitor DDVP concentrations p r i o r t o , during, and following DDVP a p p l i c a t i o n . The a i r samplers were designed and constructed s p e c i f i c a l l y f o r t h i s work and u t i l i z e d a vacuum pump (Neptune Dyna-Pump Model 4K) connected i n s e r i e s with a Dwyer Model RMA-14-1MV flow meter, and a double impinger assembly with 5 ml ethanol and 15 ml ethylene g l y c o l ( t o t a l volume of each impinger was 20 ml). The a i r pumps were c a l i b r a t e d t o operate a t 66 l i t e r s / h r , and a Cramer Conrac Type 635 G minute meter was used t o record the actual time the pump was i n operation. A i r samplers were operated i n residences scheduled f o r treatment for 24 hrs t o measure background l e v e l s o f DDVP. On the day o f treatment, a i r samplers were operated f o r 24 hrs; however, the impingers were replaced a t 2 hrs, with the l a s t sample a t 24 h r s posttreatment (samples taken a t 2 and 24 h r s ) . I t was therefore possible t o determine the amount o f DDVP i n ambient a i r both during treatment and the 24 hr posttreatment i n t e r v a l . Extraction and analysis o f the room a i r samples were as described f o r personnel a i r samples.


256


A t o t a l o f 20 single-family residences were treated with a 0.5% water emulsion spray o f DDVP prepared from Vaponite 2BC (24.7% Vapona). Application was made with a 3.8 l i t e r Β & G hand sprayer operated a t 137.9 kPa pressure f i t t e d with a m u l t i - t i p nozzle s e t f o r fan spray. Insecticide was applied i n a continuous band along the baseboards; around the doorways, windows and a l l entrances; beneath the sink, stove and r e f r i g e r a t o r ; i n and on a l l shelves and cabinets; and around plumbing and other u t i l i t y i n s t a l l a t i o n s . Gooperators were required t o remove materials from a l l shelves, closets and storage areas p r i o r t o treatment, and were asked t o stay out o f the treated residences during treatment and f o r 2 h r s posttreatment. Records were maintained as t o the amount o f DDVP applied per residence and the time required t o make the treatment. Exposed dermal and environmental monitoring pads were kept a t -10°C u n t i l analysis t o reduce v o l a t i l i z a t i o n and degradation o f EDVP. P r i o r t o extraction, the tape edge o f each pad was cut away leaving the exposed gauze surface. The glassine backing was discarded and pads ( i n t e r n a l and external pads were extracted separately) were folded and pushed into a 33 by 94 mm Whatman s i n g l e thickness c e l l u l o s e thimble. Extraction proceeded f o r 3 hrs i n 150 ml o f g l a s s - d i s t i l l e d acetone i n a soxhlet extractor f i t t e d with a b o i l i n g f l a s k . Following extraction, acetone was concentrated t o 5 ml with a vacuum rotary evaporator (Model R Buchi Rotovapor) i n a 40°C water bath. The extract was transferred t o a 12 ml graduated centrifuge tube t o which 2.5 ml o f toluene was added. A nitrogen stream and 40°C water bath was used t o evaporate the extract t o a volume o f 2.0 ml. A f t e r a l l acetone had evaporated and the sample was i n toluene, analysis was accomplished by gas chromatography (GC). Personnel a i r pump samples (20 ml) were poured into a 60 ml separatory funnel. D i s t i l l e d water (20 ml), part o f which had been used t o r i n s e the sample container, was added. Two grams o f r e agent grade sodium chloride plus 9 ml o f g l a s s - d i s t i l l e d d i c h l o r o methane were added. Contents o f the funnel were shaken vigorously f o r two minutes. A f t e r phase separation, the lower dichloromethane phase was decanted i n t o a 12 ml graduated centrifuge tube. A second extraction was made with 5 ml o f dichloromethane and the extracts combined. A nitrogen stream i n conjunction with a 40°C water bath was used t o reduce the volume o f the extracts t o 5 ml, whereupon 2.5 ml o f reagent toluene was added. Evaporation was continued t o a f i n a l volume o f 2.0 ml. Following evaporation, 0.5 grams o f anhydrous sodium s u l f a t e was added t o the toluene t o absorb mois ture. Analysis proceeded using a GC. Hand wash samples were poured i n t o a 500 ml separatory funnel t o which was added 200 ml o f water. F i f t e e n grams o f reagent grade sodium chloride plus 20 ml o f g l a s s - d i s t i l l e d dichloromethane were added t o the funnel. A f t e r shaking vigorously f o r two minutes, phase separation was achieved. The dichlorcmethane phase was drawn o f f i n t o a 250 ml f l a s k . O r i g i n a l handwash solution was once again extracted with 10 ml o f dichloromethane, the extracts combined, and volume reduced t o 5 ml with a vacuum rotary evaporator. Toluene (2.5 ml) was added and extraction, evaporation and a n a l y t i c a l procedures were as f o r pads and a i r samples. Analysis o f a l l residue samples was performed with a HewlettPackard 5840A gas chromatograph equipped with a nitrogen-


17.

GOLD AND HOLCSLAW

Exposure

to DDVP-

Treated

Residences

257

phosphorous specific thermionic detector. The separation column was a 180 cm by 2 mm I. D. glass column packed with 3% OV-25 on 100-120 mesh Chromosorb W HP. Temperatures were as follows: detector, 300°C; inlet, 165°C; and column oven, 155°C. Gas flows were 1.02 liters/hr for the nitrogen carrier, 0.18 liter/hr for hydrogen, and 0.30 liter/hr for a i r . Quantitation was accomplished with external standardization methodology by frequent recalibration and peak area measurement. Serum pseudo-cholinesterase (referred to hereafter as serum cholinesterase) activities were determined from a five minute reaction period at room temperature with a modification of the method of Ellman et a l . (14). Briefly, a 10 μΐ aliquot of serum was added to both a reference and sample cuvette containing 3.0 ml of 5,5-dithiobis-(2-nitrobenzoate) (DTNB) buffer (0.25 mM in ph 8.0, 0.1 M sodium phosphate buffer) and mixed with a micro-stirring rod. The reaction was started i n the sample cuvette by the addition of 20 μΐ of acetylthiocholine iodide (78 mM) and stirred. The reference cuvette received 20 μΐ of d i s t i l l e d water i n place of substrate. Absorbance was measured at 412 nm over a five minute period and the rate calculated from the slope of the derived curve. Erythrocytes were prepared from whole blood samples to measure acetylcholinesterase activity. A 7.0 ml aliquot of 0.9% saline was added to 1.0 ml of whole blood from each subject in a screw cap culture tube. Tubes were shaken for two minutes at high speed i n a reciprocal shaker after which they were centrifuged for 10 minutes at 2000 RPM. The clear supernatant was discarded and an additional 7.0 ml of saline (0.9%) was added to the tubes and the above procedure repeated. The wash step was repeated a third time prior to analysis of enzyme activity. To the erythrocyte pellet was added 1.0 ml of 0.9% saline which was gently vortex mixed. A 10 μΐ aliquot of the erythrocyte suspension was then added to 6.0 ml of sodium phosphate buffer (0.1 M, pH 8.0). A 3.0 ml aliquot of the erythrocyte suspension was placed i n the sample and reference cuvettes to which 25 μΐ DTNB buffer (10 mM) were added and mixed with a micro-stirring rod. Finally, 20 μΐ of substrate acetylthio choline (78 mM) or water was added to the appropriate cuvettes. Absorbance was measured as for serum assays over a five minute period. Enzyme activity was expressed as change in absorbance per gram of hemoglobin. Urine samples were thawed at room temperature and centrifuged for 30 minutes at 2,000 rpm to separate salts and proteins. The clear urine was collected and divided into fractions for DDVP and DCAA extraction. In order to extract DDVP, 10.0 ml of sample urine was added to a centrifuge tube containing 2.0 ml of ethanol (95%) and mixed. This was followed by the addition of 18.0 ml of hexane. Tubes were shaken for 15 minutes at high speed on an Eberbach reciprocal shaker and then centrifuged for 10 minutes at 2,000 RPM. A 17.0 ml aliquot of the n-hexane phase was removed and added to another tube containing 2.0 grams of anhydrous sodium sulfate and stored overnight at 4°C. A 16.0 ml aliquot was placed i n a tube and evaporated under a nitrogen stream to a final volume of 1.0 ml. A 1.5 ml aliquot of toluene was added to the 1.0 ml hexane. The remaining hexane was evaporated until the sample was i n toluene which was injected directly into the GC. A standard curve for DDVP was prepared using diluted stock solutions ranging from 0.1-100 Honeycutt et al.; Dermal Exposure Related to Pesticide Use ACS Symposium Series; American Chemical Society: Washington, DC, 1985.


258

ug/ml i n e t h y l acetate. Recovery samples were obtained by spiking urine samples with varying amounts (1.35, 2.69, 3.40, 10.80 ug) of EDVP i n ethyl acetate. Recoveries were 85-90% with minimum d e t e c t a b i l i t y f o r DDVP a t 1.0 ppb. Dichloracetic a c i d (DCAA) was quantitated i n urine samples following d e r i v i t i z a t i o n . A 5.0 ml aliquot of urine was added to a 50 ml screw cap centrifuge tube containing 2.0 g of sodium chloride and mixed. To each tube was added 5.0 ml of s u l f u r i c a c i d (16N) while the tubes were held i n an i c e bath. A f t e r removal from the i c e bath, 25.0 ml of e t h y l ether were added t o each tube a f t e r which they were shaken a t high speed f o r 15 minutes. Following extraction of DCAA i n t o ether phase, the ether was removed and d r i e d over 10 grams of anhydrous sodium s u l f a t e i n a 50 ml centrifuge tube. Samples were allowed to stand f o r a t l e a s t 30 minutes. Following extraction, a 9.5 ml a l i q u o t of the ether phase was placed i n a t e s t tube and evaporated under a stream of nitrogen a t 40°C i n a water bath t o a f i n a l volume of 1.0 ml. To each tube was added 3.0 ml of boron t r i f l u o r i d e (BF ) i n methanol (14% V:V) and vortexed f o r 10 seconds. A l l tubes were heated i n a 70°C water bath f o r 15 minutes and then allowed to cool t o room temperature. A f t e r cooling, 5.0 ml of aqueous saturated sodium chloride solution were added t o each tube followed by 10.0 ml of reagent grade benzene. Samples were vortexed f o r one minute. A f t e r phase separation, the organic phase containing the derivatized DCAA was held f o r i n j e c t i o n d i r e c t l y i n t o the GC column. This column was a 1.83 m by 3.18 mm I.D. glass column packed with 10% carbowax TPA on 80-100 mesh Gas Chrom Q. C a r r i e r gas was 5% methane i n argon a t a flow rate of 1.02 l i t e r / h r . Detector temperature was 250°C while i n l e t and column temperatures were 130°C and 124°C, respectively. Controls were urine samples without DCAA c a r r i e d through the e n t i r e extraction and d e r i v a t i z a t i o n procedures. Recovery determinations were made with 1.0 ml of methanol containing various amounts of DCAA (0.1-10 ug) added to urine blanks and c a r r i e d through the procedures. Recovery values routinely averaged 89.4% with a minimum d e t e c t a b i l i t y f o r DCAA of 1.5 ppb. T o t a l dermal exposure was calculated by multiplying the sum o f the unclothed body areas by the appropriate exterior exposure rate and adding to the product the t o t a l clothed areas m u l t i p l i e d by the appropriate i n t e r i o r exposure rate and then adding to t h i s t o t a l the hand exposure value. T o t a l body surface areas were calculated from the applicator height and weight using the formula of Dubois and Dubois (16) with s p e c i f i c body surfaces apportioned by the Berkow method (17). T o t a l respiratory exposure was calculated by multiplying the a i r concentration of DDVP by the mean v e n t i l a t i o n rate of a man doing l i g h t work (1). T o t a l percent of a t o x i c dose per hr was calculated according t o the formula of Durham and Wolfe (1) assuming that the dermal LD50 of DDVP t o humans i s 107 mg/kg body weight (18). 3

Results and Discussion 2

Applicators took a mean o f 25.5 minutes to apply 0.19 gm (A.I. )/m of DDVP (38.7 ml/m of f i n i s h e d spray) to each of the 20 residences included i n t h i s study. Residences s i z e averaged 103.0±33.2 m and received a mean of 19.6 gm (A.I. ) DDVP based on the f l o o r area of 2

2


17.

GOLD AND HOLCSLAW

Exposure

to DDVP-

Treated

Residences

259

each structure. Applications were made at a mean temperature o f 26.1°C and 82% r e l a t i v e humidity. Applicators who applied DDVP i n t h i s study were exposed t o the insecticide. Dermal exposure as determined by measurement of DDVP on gauze pads attached t o the applicators during treatment was 0.499±0.274 μg/cm /hr on e x t e r i o r pads, 0.102±0.062 ug/cm /hr on i n t e r i o r pads (those located beneath the c l o t h i n g ) , and 0.024^0.021 ug/cm /hr on the hands. Recovery o f DDVP on i n t e r i o r pads was interpreted t o indicate movement o f i n s e c t i c i d e through the c l o t h i n g with approximately 20% o f the chemical contacting the outer garments penetrating t o the s k i n beneath ( 1 0 ) . This penetration i s approximately 2-3 times more than noted i n s i m i l a r experiments with carbaryl (Sevin WP) i n s e c t i c i d e ( 1 1 , 1 3 ) . Rubber gloves worn by applicators apparently minimized hand exposure; DDVP a p p l i c a t i o n and handling resulted i n 0.024 pg/cm /hr. Hand contamination accounted f o r 0.9% o f t o t a l dermal exposure (Table 1) as compared with 87% i n carbaryl exposure studies ( 1 1 , 13) where hand protection was not worn. The f a c t that DDVP was recovered from the hands o f the applicators i n a l l 20 treatments demonstrated the need to stress hand protection and decontamination even when rubber gloves are worn. P o t e n t i a l applicator respiratory exposure as measured by the personnel a i r samplers was 0.021±0.019 u g / l i t e r , 2.1% o f the threshold l i m i t value (TLV) set by the American Conference o f Governmental I n d u s t r i a l Hygienists (18 ) a t 1 mg/m . There was c l e a r evidence o f p o t e n t i a l applicator exposure t o DDVP through r e s p i r a t i o n based on the sampler data, but the values ranged from 0.4-6.4% o f the TLV i n d i c a t i n g that minimal negative impact would be expected ( 1 0 ) . T o t a l applicator exposure (Table 1) was estimated based on measurements o f both t o t a l dermal and respiratory exposure. T o t a l dermal exposure was 2.354 mg/hr or 0.028 mg/kg/hr f o r an applicator weighing 84 kg and wearing an open-neck, long-sleeve s h i r t , f u l l length pants, shoes and socks, head gear, and rubber gloves ( 1 0 ) . P o t e n t i a l respiratory exposure f o r the applicators was 0.037 rrigThr or 0.0004 mg/kg/hr assuming a v e n t i l a t i o n rate o f 1740 l i t e r s / h r (1). The percent t o x i c dose o f DDVP t o applicators was 0.028±0.021%/hr as calculated by the formula o f Durham and Wolfe (1) where respiratory exposure i s considered 10 times more t o x i c than dermal exposure. A "worst case" estimate o f percent t o x i c dose f o r a completely unprotected applicator would have been 0.11%/hr. DDVP and i t s hydrolysis products ( dimethylphosphate, desmethyldichlorvos, dichloroethanol, d i c h l o r o a c e t i c acid) are known to appear i n the urine of animals including man following s i g n i f i cant exposure ( 1 9 - 2 2 ) . However, our r e s u l t s on urine samples o f applicators of DDVP f a i l e d t o demonstrate detectable q u a n t i t i e s of i n s e c t i c i d e a t any of the experimental time periods. This occurred i n s p i t e o f known applicator exposure as indicated by dermal and r e s p i r a t o r y r e s u l t s . Assay s e n s i t i v i t y (1 ppb) was well within the range for detecting DDVP i n trace amounts. As a r e s u l t o f not detecting DDVP i n urine and considering i t s known r a p i d metabolism i n mammals, urine samples were examined f o r the metabolite DCAA. No s i g n i f i c a n t amounts of DCAA were i d e n t i f i e d i n urine samples o f any of the subjects (applicators or residents). I t was believed 2

2

2

2

3



260

Table I.

T o t a l Exposure of Applicators of DDVP i n Residences Surface Area (S.A. i n cm ) 2

Exposure Route Dermal

Body Part

Face, front "V" chest Head (minus face) Back neck Back trunk (minus back neck) Front trunk (minus front neck, "V" chest) Upper arms Forearms Thighs Legs and feet Hands

T o t a l Dermal Exposure Respiratory Lungs (Ventilation rate "V.R. " liters/hr)4 TOTAL EXPOSURE

1

2

3

2

3

T o t a l Exposure Exposure % Toxic Calculation mg/kg/hr Dose/hr (mg/hr)

910

0.454

460 120

0.047 0.060

3420

0.349

3790 1340 1390 3660 3760 930

0.387 0.137 0.142 0.373 0.383 0.022

19,708

2.354

0.028

1740

0.037

0.0004

2.391

0.0284

0.028

Applicator wore head gear, an open neck, long sleeve s h i r t , pants and gloves (10). T o t a l body surface was calculated from the height and weight o f the applicators using the formula o f Dubois and Dubois ( 1 6 ) , and then apportioned by the Berkow method (17) f o r s p e c i f i c body areas. T o t a l exposure c a l c u l a t i o n s based on a 84 kg applicator applying EDVP with a dermal LD50 of 107 mg/kg ( 1 8 ) . The percent t o x i c dose per hour was calculated by the formula of Durham and Wolfe (1).

4

1

V e n t i l a t i o n rate of a man doing l i g h t work (jL).


17.

GOLD AND HOLCSLAW

Exposure

to DDVP-Treated

Residences

261

that the assay f o r DCAA was appropriately s e n s i t i v e and s e l e c t i v e for the analysis. I t i s recognized that two other major metabo l i t e s are formed and excreted i n urine, but they were not examined. The e f f e c t s o f DDVP on both serum and erythrocyte a c e t y l cholinesterase (AChE) have been well documented i n the l i t e r a t u r e . In the present study when DDVP applicators were evaluated f o r serum cholinesterase a c t i v i t y a t various time periods following i n i t i a t i o n of applications (Applicator 1 a t 7 and 30 hrs; Applicator 2 a t 8, 24, 30, 48, and 56 h r s ) , s i g n i f i c a n t reductions i n AChE a c t i v i t y were noted (10). Applicator l was forced, due t o i l l n e s s , t o discontinue DDVP applications during the 7th hour o f the experi ments. The exact cause o f the i l l n e s s was not confirmed by the medical s t a f f overseeing the experiments, but p e s t i c i d e poisoning could not be r u l e d out. His serum AChE a c t i v i t y was reduced by 59% by the 7th hours of exposure, but had rebounded s i g n i f i c a n t l y by 30 hrs p o s t - i n i t i a t i o n . Applicator 2 experienced a 21% reduction i n serum AChE a c t i v i t y i n the f i r s t exposure period, but enzyme a c t i v i t y returned t o baseline within 48 hrs. Erythrocyte AChE a c t i v i t y r e s u l t s were d i f f i c u l t t o i n t e r p r e t due t o inconsistent response to DDVP. Applicator 1 had an increase i n AChE a c t i v i t y during a period of decreased serum AChE a c t i v i t y . With the rebound i n h i s serum AChE a c t i v i t y was noted a s i m i l a r but disproportionate increase i n erythrocyte AChE a c t i v i t y . Applicator 2 was noted t o have a general decline i n erythrocyte AChE a c t i v i t y which was correlated with increased exposure to DDVP. Decreases i n erythro cyte AChE a c t i v i t y were considered s l i g h t but consistent with what would have been expected f o r low dermal and respiratory exposure (10). A t o t a l o f 20 residents of DDVP-treated structures were included i n the study population. Fran questionnaires completed by cooperators when blood and urine samples were taken, i t was deter mined that: mean age o f the participants was 40.7±16.2 years (range 19-64 y r s ) ; 70% were female; none had taken cholinesterase i n h i b i t i n g medications during the 24 hrs of the study, but 5% and 10% had used tobacco and a l c o h o l , respectively; 70% had used p e s t i cides i n t h e i r residence within the preceeding 3 months; the mean time spent i n the DDVP-treated structure was 15.8±3.3 hrs p r i o r t o f i n a l blood and urine samples; and 15% indicated that the treatment to t h e i r residence had caused a f e e l i n g o f i l l n e s s (headache was only symptom indicated). Results o f the environmental monitoring indicated that DDVP was present i n the treated residences up to 24 hrs following i n i t i a l treatments. A i r samplers operated i n the structures f o r 24 hrs, including the time of a p p l i c a t i o n , c o l l e c t e d measurable DDVP residues. Greatest concentrations o f DDVP were c o l l e c t e d during the f i r s t 2 hrs p o s t - i n i t i a t i o n with 0.548±0.297 μg/liter recovered. This i s 54.8% of the TLV and represents a 26-fold increase over the concentrations recovered by the personnel a i r sampler worn by the applicator who spent a mean of 25.5 minutes i n the structure. The f a c t that the room a i r sampler c o l l e c t e d s i g n i f i c a n t l y more DDVP than personnel a i r samplers i s explained i n part by the f a c t that the room a i r samplers were positioned i n the k i t c h e n / u t i l i t y areas which received approximately 50-60% of the t o t a l volume of f i n i s h e d spray applied to the residence (23), and that the applicator was constantly moving to areas of the structure that were a t that point



262

untreated. Of the 337.5 ug DDVP collected by the room a i r samp lers , 21.4% was attributed to the time of application and the two hrs following initiation of treatments. Concentration of DDVP in the treated residences was 0.21 ug/liter or 21.3% of the TLV through the 24 hrs of the study. Residents who spent a mean of 15.8 hrs in the treated structures would have been exposed to 0.08 mg/kg, assuming the same ventilation rate as the applicators and a mean body weight of 75 kg. Potential respiratory exposure to residents was 10 times that of the applicators who mixed and applied DDVP to the structures. Even though the potential respiratory exposure was significantly greater to the residents than applicators, the level of exposure was considered to be slight based on either the oral (80 mg/kg) or dermal (107 mg/kg) ID Q of DDVP (18). Dermal exposure to residents to DDVP could not be assessed; however, i t was noted that the environmental exposure pads received 0.319±0.183 μg/cm /hr during the application and the two hrs postinitiation. This represents 63.9% of the total dermal exposure of the applicators. The serum and erythrocyte acetylcholinesterase activity measurement in this work basically confirm the findings of Cavagna et a l . (8) who investigated the effects of DDVP plastic resin strips on human subjects. Data analysis revealed a slight but statistically significant (P£0.05) reduction in serum cholinesterase activity in the overall resident population at 24 hrs posttreatment. Mean enzyme activity prior to spraying was 1.400±0.348 International Units (I.U. ), whereas the mean activity dropped to 1.296±0.316 I.U. by the end of the 24 hr period (10). Mean difference between enzyme activities was slight (0.104 I.U.) representing a 7.9% decrease suggesting only minor exposure of the population to the insecticide. Fluctuations in activity of this magnitude are not unusual even in the absence of pesticide exposure (13). Analysis of erythrocyte acetylcholinesterase activity before (0.36±0.10 absorbance change/minute/gram hemoglobin X 10~ ) and following treatment (0.36±0.10) revealed no significant differences for the test population; however, there were decreases in activity ranging from 5.3 to 37.5%. These decreases could represent normal fluctuations for the study population. 5

2

2

Conclusions There was evidence of pesticide exposure to applicators based on results of dermal and respiratory monitoring, but the percent toxic dose (0.028%/hr) and results of serum and erythrocyte acetylcholin esterase testing were interpreted to indicate low probability of significant acute exposure to DDVP when label directions were followed. It was demonstrated that normal work apparel does pro vide an effective barrier to the penetration of DDVP to the skin of applicators and that hand protection i s strongly recommended. Residents of DDVP-treated structures were noted to have expo sure to DDVP based on results of room a i r sampler data analysis and serum and erythrocyte acetylcholinesterase determinations. Resident exposure was estimated at 0.03% toxic dose/hr had they been present during application of DDVP and remained in the treated structure for the f u l l 24 hrs posttreatment. Based on these results i t is recommended that unprotected residents not be allowed in structures Honeycutt et al.; Dermal Exposure Related to Pesticide Use ACS Symposium Series; American Chemical Society: Washington, DC, 1985.

17.

GOLD AND HOLCSLAW

Exposure

to DDVP-Treated

Residences

263

during application (10) and that exposure be further reduced by thoroughly ventilating treated areas. Nontechnical Summary Twenty residential structures were treated with dichlorvos insecticide (DDVP) for German cockroach control. Dermal exposure pads, air samplers, blood tests for serum and erythrocyte acetyl cholinesterase (enzyme) activity and urine analyses were used to monitor both applicators and residents for evidence of exposure to DDVP. There was evidence of pesticide exposure to applicators based on results of dermal and respiratory monitoring. However, the percent toxic dose (0.03%/hr) and results of serum and erythrocyte acetylcholinesterase testing were interpreted to indicate low probability of significant acute exposure to DDVP when label directions were followed. It was demonstrated that normal work apparel does provide an effective barrier against DDVP penetrating to an applicator's skin; however, hand protection is strongly recommended. Based on analysis of room air samples, and serum and erythro cyte acetylcholinesterase tests, i t was concluded that residents of EDVP-treated structures were exposed to the pesticide. Resident exposure was estimated at 0.03% toxic dose/hr had the person been present during the DDVP application and remained continuously in the treated structure for 24 hours after the pesticide was applied. Based on these results, i t is recommended that unprotected residents not be allowed in structures during application and that exposure be further reduced by thoroughly ventilating treated areas. Acknowledgments This project was supported through the North Central Region Pesticide Impact Assessment Program. The authors wish to express their appreciation to Dr. James Ballard and Duane Tupy of the University of Nebraska for their assistance in the collection and analysis of samples.

Literature Cited 1. Durham, W. F.; Wolf, H. R. Bull. W.H.O. 1962, 26, 75-91. 2. Kimbrough, R. D.; Gaines, T. B. Arch. Environ. Health 1968, 16, 805-8. 3. Krause, W; Homola, S. Bull. Environ. Contam. Toxicol. 1974, 11, 177-81. 4. Voogd, C. E.; Jacobs, J. J. J. Α. Α.; Van Der Stel, J. J. Mutation Res. 1972, 16, 417-9. 5. Ashwood-Smith, M. J.; Trevino, J ; Ring, R. Nature 1972, 20, 418-20. 6. Leary, J. S.; Keane, W. T.; Fontenot, C.; Feichtmeir, E. S.; Shultz, D; Koos, D. Α.; Hirsch, L.; Lavor, Ε. M.; Roan, C. C.; Hine, C. H. Arch. Environ. Health 1974, 29, 308-14. 7. Cavagna, G.; Locati, G.; Vigliani, E. C. Arch. Environ. Health 1969, 19, 112-23. Honeycutt et al.; Dermal Exposure Related to Pesticide Use ACS Symposium Series; American Chemical Society: Washington, DC, 1985.

264

DERMAL

E X P O S U R E RELATED TO P E S T I C I D E U S E

8. Gillet, J . W.; Harr, J . R.; Linstrom, F. T.; Mount, D. A.; St. Clair, A. D.; Weber, L. J . Residue Rev. 1972a, 44, 115-59. 9. Gillet, J . W.; Harr, J. R.; St. Clair, A. D.; Weber, L. J . Residue Rev. 1972b, 44, 161-84. 10. Gold, R. E.; Holcslaw, T.; Tupy, D.; Ballard, J . B. J. Econ. Entomol. 1984, 77, 430-436. 11. Gold, R. E.; Leavitt, J . R. C.; Ballard, J . J . Econ. Entomol. 1981, 74, 552-4. 12. Gold, R. E.; Leavitt, J. R. C.; Holcslaw, T.; Tupy, D. Arch. Environ. Contam. Toxicol. 1982, 11, 63-7. 13. Leavitt, J . R. C.; Gold, R. E.; Holcslaw, T.; Tupy, D. Arch. Environ. Contam. Toxicol. 1982, 11, 57-62. 14. Ellman, G. L.; Courtney, K. D.; Valentino, A.; Featherstone, R. M. Biochem. Pharmacol. 1961, 7, 88-95. 15. Schultz, D. R.; Marxmiller, R. L.; Kcos, B. A. J. Agr. Food Chem. 1971, 19, 1238-43. 16. Dubois, D.; Dubois, E. F. Arch. Intern. Med. 1916, 17, 863-6. 17. Berkow, S. G. Am. J . Surg. 1931, 11, 315. 18. "Doaimentation of the Threshold Limit Values for Substances in Workroom Air," American conference of Governmental Industrial Hygienists, 1971, 3rd ed. 19. Arthur, B. W.; Casida, J . E. J . Agric. Food Chem. 1957, 5, 186-92. 20. Casida, J . E.; McBride, L.; Niedermeier, R. P. J . Agric. Food Chem. 1962, 10, 370-7. 21. Tracy, R. L.; Woodcock, J . G.; Chodroff, S. J . Econ. Entomol. 1960, 53, 593-601. 22. Teicher-Kuliszewska, K.; Szymezyk, T. Bromatol. Chem. Toksykol. 1980, 13, 37-40. RECEIVED

September 6,1984


Dermal Exposure Related to Pesticide Use - American Chemical Society

Recommend Documents