Teratogenicity of bifenox and nitrofen in rodents

The teratogenicity of the diphenyl ether herbicide bifenox [2,4-dichlorophenyl 3'-carboxymethyl-4'-nitrophenyl ether] was compared to that of nitrofen [2,4-dichlorophenyl 4'-nitrophenyl ether] in rats and in mice. Neither compound increased prenatal mortality in mice. Because nitrofen causes both malformations that are compatible with survival to weaning and a high incidence of perinatal (but not of fetal) mortality, emphasis was placed on postnatal parameters of bifenox toxicity. In rats, bifenox caused a low incidence of "bloody tears", but it did not decrease survival to term or to weaning in rats or mice, and did not reduce Harderian gland weight in mice. Because the weight of the Harderian glands is a more objective measure of their status than is the presence of an eye discharge, it is concluded that bifenox is not teratogenic at the levels administered. Nitrofen decreased litter size, pup weight, and Harderian gland weight in mice.     

Persistence of hexaconazole,a triazole fungicide in soils

Abstract

Persistence of hexaconazole (2‐(2,4‐dichlorophenyl)‐l‐(lH‐l,2,5‐triazol‐l‐yl) hexan‐2‐ol) was studied in alluvial, red and black soils under flooded and nonflooded conditions. This fungicide was more persistent in all soils under flooded conditions than under nonflooded conditions and at 27°C than at 35°C. Degradation of hexaconazole in sterilized and nonsterilized soils proceeded at identical rates indicating a minor role of micro‐organisms in its degradation. The soil persistence of hexaconazole was not affected by the addition of wheat straw both under flooded and nonflooded conditions.     

Toxicological assessment of chlorinated diphenyl ethers in the rat

Abstract

Chlorinated diphenyl ethers are environmental contaminants that have been found in Great Lakes fish and birds. Because of their presence in the food chain, and potential for human exposure, the present short‐term study was conducted to assess their toxicity. Groups of 10 male and 10 female rats were each given by gavage 2,2’,4,4'6‐pentachlorodiphenyl ether (CDE1), 2,2’,4,4’,5,6‐hexachlorodiphenyl ether (CDE2) or 2,2’,3,3’,4,6'‐hexachlorodiphenyl ether (CDE3) at dose levels of 0.04, 0.4, 4.0 or 40 mg/kg b.w./day for a period of 28 days. The control group received an equivalent volume of corn oil only (0.5 ml/100 g b.w.). Treatment with the three CDE congeners did not result in suppression of growth rate or food consumption. Increased liver weights were seen in the animals of both sexes fed 40 mg/kg CDE2, in males treated with 40 mg/kg CDE1, and in females with 40 mg/kg CDE3. Hepatic microsomal aminopyrine demethylase activity was significantly higher in the male rats administered 40 mg/kg CDE2, and aniline hydroxylase activity was elevated in the females following the same treatment. Serum glucose, calcium, protein and urea nitrogen of CDE1‐treated males were higher than the control. Levels of uric acid, potassium and LDH of CDE3‐treated females were also elevated. No hematological changes were observed. Histological examination revealed that the liver and thyroid were the target organs affected by CDE treatment but the morphological changes were mild even at the highest dose level. Changes in the liver consisted of nuclear vesiculation and increased cytoplasmic volume. Alterations in the thyroid were characterized by increased epithelial height and follicular collapse. Based on the data presented above, the 3 CDE congeners can only be considered moderately toxic in the rat.     

Effect of maternal dietary hexachlorocyclohexane exposure on pup survival and growth in albino rats

Abstract

In adult albino rats, maternal dietary. ß‐ and ?‐hexachlorocyclohexane (HCH) intake during gestation upto 400 ppm level did not affect the number of litters produced. But about 50 and 100% pup mortality was found in 200 and 400 ppm ß ‐HCH group within 5 days of birth. Maternal mortality was observed in 800 ppm ß ‐HCH group during third week of gestation. The effect of maternal dietary intake of HCH isomers at 50 and 250 ppm level during gestation and/or lactation on perinatal development was also studied. The body weights and sizes of the newborn litters of mother rats exposed to dietary HCH isomers did not. differ from controls. Similarly, the growth and development of the litters of HCH exposed mother rats that survived 28 day lactation period were found to be comparable to controls as evidenced by the body weight and weight of vital organs. However, liver weight increases were found in the 28 day weaned litters wherever the mothers had been exposed to HCH isomers during lactation. Lowered kidney weight was seen in litters of mother rats fed 250 ppm ?‐HCH during gestation and lactation. The brain and testis weights were not affected in the litters of any experimental groups.     

Dioxin and dioxin-like PCB impurities in some Japanese agrochemical formulations

The profile and amount of dioxin impurity in agrochemicals were studied through detailed analysis of historic Japanese formulations. The chemicals analyzed include pentachlorophenol (PCP), 2,4,6-trichlorophenyl-4'-nitrophenyl ether (chloronitrofen, CNP), 2,4-dichlorophenyl-4'-nitrophenyl ether (nitrofen, NIP), tetrachloro-iso-phthalonitrile (chlorothalonil, TPN), 2-methyl-4-chloro-phenoxyacetic acid (MCP) and 2,4-dichlorophenoxyacetic acid (2,4-D). Among the six, two herbicides, PCP and CNP, produced during the 1960s and 1970s, contained very high concentrations of PCDD/DFs and TEQ. Others contained relatively low concentrations of PCDD/DFs. Dioxin-like PCB concentrations in all chemicals studied were low and their contributions to TEQ were negligible. The total dioxin emissions from the use of agrochemicals in Japan during the past 40 years (1955-1995) were estimated to be about a few hundred thousand kg of PCDD/DFs and 250 kg of WHO-TEQ from PCP and 190 x 10(3) kg of PCDD/DFs and 440 kg of WHO-TEQ from CNP. The major dioxin congeners present in PCP formulations were highly chlorinated PCDD/DFs that can be formed by the coupling of PCP and/or 2,3,4,6-tetrachlorophenol, and those in the CNP formulations were tetra- to hexa-chlorinated PCDD/DFs that can be formed from 2,4,6-trichlorophenol and/or 2,3,4,6-tetrachlorophenol.     

Aerobic degradation of diuron by aquatic microorganisms

Abstract

Degradation of diuron [3‐(3,4‐dichlorophenyl)‐l,1‐dimethyl‐urea] by microorganisms obtained from pond water and sediment was determined under aerobic conditions. Enrichment procedures were used to isolate cultures capable of degrading the herbicide. Several mixed fungal/bacterial and mixed bacterial cultures were isolated that could degrade diuron. The mixed cultures degraded 67–99% of the added diuron forming from six to seven products which were separated via TLC. The major degradation product detected in most culture extracts was 3,4‐dichloroaniline. Other identified products formed were 3‐(3,4‐dichlorophenyl)‐1‐methylurea and 3‐(3,4‐dichlorophenyl)urea.     

Decreasing ice coverage will reduce the breeding success of Baltic grey seal (Halichoerus grypus) females

Baltic grey seals (Halichoerus grypus) alternate between land and ice breeding, depending on ice conditions. We show that the fitness of grey seal females in terms of pup mortality and quality is reduced when breeding on land as compared with ice. The mean preweaning mortality rate on land was 21.1% (range 0% to 31.6%), and correlated with birth density (range 0.5-5.2 pups 100 m(-2)). The mean mortality rate on ice was 1.5%, where the highest density was 0.2 pups 100 m(-2) in particularly dense breeding groups. Mean weights of pups born on ice were significantly greater (48.3 +/- 8.1 kg) at the onset of moult as compared with pups born on land (37.4 +/- 7.8 kg). Because indices of life-time net reproductive rate (pup survival) and pup quality (weaning weight and health) were more auspicious on ice as compared with land, diminishing ice fields will lower the fitness of Baltic grey seal females and substantially increase the risk for quasi-extinction.     

Latent effects of early life stage exposure to triclosan on survival in fathead minnows,Pimephales promelas

The objective of this study was to evaluate the effects of early life stage triclosan (5-chloro-2-(2,4, dichlorophenoxy)phenol, TCS) exposure on hatching, development, and survival in the fathead minnow, Pimephales promelas. Embryonic minnows were exposed to TCS (50 and 100 µg L^?1) for 10 days followed by 6 weeks depuration. Mortality and morphological deformities were recorded and quantified during exposure and at the end of depuration. No significant effects on embryonic survival, time to reach the eyed stage, or hatching were found. However, at the conclusion of the depuration period, survival was significantly reduced in TCS exposed fish depending on the concentration. Visual inspection of the exposed fish suggests that mortality is related to spinal deformities, emaciation, and reduced foraging ability. Triclosan exhibits deleterious effects in fish at lower concentrations over longer durations than previously reported. Further, mortality in exposed fish 6 weeks after exposure demonstrates the need for various exposure assays to evaluate effects of TCS.     

Evaluation of HODE-15, FDE-15, CDE-15, and BDE-15 toxicity on adult and embryonic zebrafish (Danio rerio)

Diphenyl ether and its derivatives are widely used in the industry of spices, dyes, agrochemicals, and pharmaceuticals. Following the previous study, we selected 4,4′-dihydroxydiphenyl ether, 4,4′-difluorodiphenyl ether, 4,4′-dichlorodiphenyl ether, and 4,4′-dibromodiphenyl ether as research objects. The LC₅₀ (96 h) values for these compounds in adult zebrafish were determined with the acute test. Also, developmental toxicities of the four substances to zebrafish embryos were observed at 24, 48, 72, and 96 hpf. All the LC₅₀ (96 h) values of these compounds were between 1 and 10 mg/L, suggesting that they all had moderate toxicity to adult zebrafish. The embryonic test demonstrated that with increasing doses, 4,4′-dihydroxydiphenyl ether decreased the hatching rate, while 4,4′-difluorodiphenyl ether, 4,4′-dichlorodiphenyl ether, and 4,4′-dibromodiphenyl ether delayed the hatching time but had little effect on final hatchability at 96 hpf. All of these compounds inhibited larval growth, especially 4,4′-dihydroxydiphenyl ether. Exposure to these chemicals induced embryo yolk sac and pericardial edema. Spine deformation was visible in hatched larvae after 96 hpf 4,4′-dihydroxydiphenyl ether exposure, while tail curvature was observed for the halogenated compounds. The overall results indicated that 4,4′-dihydroxydiphenyl ether, 4,4′-difluorodiphenyl ether, 4,4′-dichlorodiphenyl ether, and 4,4′-dibromodiphenyl ether all had significant toxicity on adult and embryonic zebrafish.     

Excretion balance,metabolic fate and tissue residues following treatment of rats with amitraz and N‘‐ (2,4‐dimethylphenyl)‐N‐methylformamidine

Abstract

Amitraz and its metabolite N‘‐ (2,4‐dimethylphenyl)‐N‐methyl‐formamidine (BTS‐27271) were administered orally to white rats. Both compounds were rapidly metabolized and eliminated primarily via the urine. The cumulative percentage of the dose eliminated in the urine was 77.6 for amitraz and 88.7 for BTS‐27271 by 96 hr posttreatment. Amitraz degradation products present in urine included BTS‐27271, 2,4‐dimethylformanilide, 2,4‐dimethylaniline, 4‐formamido‐3‐methylbenzoic acid, 4‐amino‐3‐methylbenzoic acid, and several unknowns. BTS‐27271 degradation products in rat urine were similar to those found with amitraz. Tissue residues generally were low (<25 ppb) with the exception of those in liver.     

Subacute oral toxicity of BDE-15, CDE-15, and HODE-15 in ICR male mice: assessing effects on hepatic oxidative stress and metals status and ascertaining the protective role of vitamin E

The present study examined the effects of oral exposure of 4,4′-dibromodiphenyl ether (BDE-15), 4,4′-dichlorodiphenyl ether (CDE-15), and 4,4′-dihydroxydiphenyl ether (HODE-15) on hepatic oxidative stress (OS) and metal status in Institute of Cancer Research (ICR) male mice. Furthermore, the role of vitamin E in ameliorating potential OS caused by BDE-15, CDE-15, and HODE-15 was investigated. Three groups of mice were exposed to 1.20 mg/kg(body weight)/day of each of the three toxicants for 28 days. Results showed that none of the three toxicants altered growth rates of mice, but significantly increased (P?<?0.05) relative liver weights and decreased relative kidney weights. Pathological changes including cell swelling, inflammation and vacuolization, and hepatocellular hypertrophy in livers were observed. Significant decreases (P?<?0.05 and P?<?0.01) in superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) activity, and glutathione (GSH) levels, together with increases in malondialdehyde (MDA) content were recorded in all toxicant-treated groups. Hepatic copper levels increased in all toxicant-treated groups. Hepatic zinc levels decreased in the liver of BDE-15-treated mice, whereas they increased in the livers of CDE-15-treated and HODE-15-treated mice. In conclusion, daily exposure to the three toxicants perturbed metal homeostasis and increased OS in mouse liver. Experimental data indicated the hepatic oxidative toxicity of the three toxicants followed the order BDE-15?<?HODE-15?<?CDE-15. Moreover, the study proved that daily supplementation of 50 mg/kg vitamin E is effective to ameliorate the hepatic OS status and metal disturbance in mice.     

The effects of triclopyr on 2,4‐D mineralization in two soils

Abstract

The effects of the herbicide triclopyr (3,5,6‐trichloro‐2‐pyridinyloxyacetic acid) on the mineralization of 2,4‐D (2,4‐dichlorophenoyxacetic acid) in two soils which differed in their histories of prior exposure to the two herbicides were investigated. The relative effects of triclopyr on 2,4‐D mineralization and most probable numbers of 2,4‐D degraders were dependent upon the soil. Triclopyr was shown to increase 2,4‐D mineralization rates in a soil which had been exposed to both 2,4‐D and triclopyr, but decreased the mineralization rate of 2,4‐D and inhibited the increase of most probable numbers of 2,4‐D degraders in a soil that had not been directly exposed to either herbicide.     

Effects of spraying the herbicides 2,4-D and 2,4,5-T on a population of the tortoise Testudo hermanni in southern Greece

A population of the tortoise Testudo hermanni near Olympia in southern Greece was studied by mark-recapture from 1975 to 1984. Part of the site was sprayed with the herbicides 2,4-dichlorophenoxyacetic acid (2,4-D) and 2,4,5-trichlorophenoxyacetic acid (2,4,5-T) each year from 1980, producing symptoms of poisoning (swollen eyes, fluid discharge from the nose and immobility) in tortoises. Survival rates of tortoises 10 cm or larger were significantly lower in the affected areas, with extra mortality of about 34% year-1, against an annual survival rate of 0.85-0.90 in unaffected areas. Changing population structures showed that juveniles were even more strongly affected, with the proportion of juveniles in samples decreased by half. The population in the sprayed area declined to near zero by 1984, due to mortality rather than to emigration, since more movements were recorded into than out of the affected area. There was no difference in body mass condition between sprayed and unsprayed areas, showing that effects were acute; mortality was not due to starvation from loss of food plants. The scale and pattern of mortality was similar to that from a severe scrub fire; spraying is potentially more catastrophic since often repeated at shorter intervals than burning. Possible physiological mechanisms of death are discussed. The susceptibility of tortoises to 2,4-D and 2,4,5-T (or to associated dioxin impurities) presents a warning for conservation of these late-maturing animals.     

Toxicological assessment of chlorinated diphenyl ethers in the rat, Part II

Chlorinated diphenyl ethers (CDE's) are environmental contaminants that have been found in Great Lakes fish. Because of the paucity of toxicity data and potential for human exposure, the present short-term study was conducted to assess their potential toxic effects. Groups of 10 male and 10 female rats were administered the three CDE congeners (2,2',4,4',5-pentachlorodiphenyl ether (PCDE), 2,2',4,4',5,5'-hexachlorodiphenyl ether (HCDE), 2,2',3,4,4',6,6'-heptachlorodiphenyl ether (HPCDE] in diets at levels of 0.5, 5.0, 50 or 500 ppm for a period of 4 weeks. Decreased food consumption was observed with male and female rats fed the diet containing 500 ppm HPCDE. Treatment with the three isomers at the highest dose level produced an increase in liver weight in both sexes. While administration of PCDE produced an increase in hepatic aminopyrine demethylase activity, HCDE caused a significant increase in aminopyrine demethylase, aniline hydroxylase and ethoxyresorufin de-ethylase activities. HPCDE caused a significant increase in ethoxyresorufin de-ethylase activity. HPCDE at the highest dose level also caused a significant reduction in circulating lymphocytes in male rats. The 3 CDE's produced mild and adaptative histological changes in the liver and thyroid, but only HPCDE elicited mild changes in the thymus, bone marrow, and spleen. The above data indicate that HPCDE is immunosuppressive and that all three CDE isomers are considered to be moderately toxic in rats. The no-observable effects levels appear to be between 5-50 ppm in diet (0.36-3.0 mg/kg b.w.) for the three CDE's.     

Reproduction in mice treated with crufomate: effects of dermal treatments on female mice and on their progeny.

Dermal treatments with crufomate 100 or 50 mg/kg or crufomate vehicle 100 mg/kg were applied to mice either on days 35 and 21 before mating or on days 70, 56, 35, and 21 before mating. Two, but not four dermal treatments, with both doses of crufomate reduced the mating reponse and conception rate in mice. The mice either did not produce a litter or the litter died before the age of 7 days. Four treatments with crufomate 100 mg/kg, but not with 50 mg/kg, reduced the weaning weight of progeny weaned at the age of 21 days. The vehicle had no effects on reproduction and increased the weights at maturity of female and male progeny of mice given two and four treatments, respectively.     

2,4-Dichlorophenoxy Acetic Acid Mineralization in Amended Soil

The application of municipal biosolid or liquid hog manure to agricultural soils under laboratory conditions at 20°C influenced the fate of the herbicide 2,4-D [2,4-(dichlorophenoxy)acetic acid] in soil. When 2,4-D was added to soil at agronomic rates immediately after the addition of manure or biosolids to a coarse-textured soil, the percentage of 2,4-D mineralized at 100 days was about 47% for both treatments, compared to only 31% for control soils without amendments. The enhanced 2,4-D mineralization as a result of amendment addition was due to an increased heterotrophic microbial activity, with the greatest increases in soil respiration occurring for soils amended with biosolids. When additions of 2,4-D were delayed for one, two, or four weeks after the amendments were applied, the additions of amendments generally reduced 2,4-D mineralization in soil, particularly for manure, indicating that the effect of amendments on enhancing soil microbial activities diminished over time. In contrast, the mineralization of 2,4-D in control soils was less dependent on when 2,4-D was applied in relation to pre-incubations of soil for zero, one, two, or four weeks. The effect of manure on decreasing 2,4-D mineralization in specific soils was as large as the effect of soil texture on differences in 2,4-D mineralization across soils. Because manure was not found to impact 2,4-D sorption by soil, it is possible that 2,4-D mineralization decreased because 2,4-D transformation products were strongly sorbed onto organic carbon constituents in manure-amended soils and were therefore less accessible to microorganisms. Alternatively, microorganisms were less likely to metabolize the herbicide because they preferentially consumed the type of organic carbon in manure that is a weak sorbent for 2,4-D.     

Neurotoxic effects of leptophos (PhosvelR) in chickens and rats following chronic low-level feeding.

Leptophos (O-[4-bromo-2,5 dichlorophenyl] O-methyl phenylphosphonothioate) (PhosvelR) was administered orally to chickens and rats in doses of 0.5 and 5.0 mg/kg/day for 26 weeks. Hens fed 5.0 mg/kg, except one, showed ataxia and became paralysed in the legs at varying times from 8 to 19 weeks. A fifth hen showed ataxia early in the experiment but recovered fully for the remainder of the experiment. Rats fed both doses and chickens fed 0.5 mg/kg showed no signs of delayed neurotoxicity. All hens fed 5.0 mg/kg stopped laying by about the third week. Animals of both species fed 5.0 mg/kg either lost weight (chickens) or gained less weight (rats) than the others. Erythrocyte acetylcholinesterase (AChE) of the chickens given both doses was significantly depressed at first, then increased, and later dropped to control levels. AChE of rats fed 0.5 mg/kg was significantly inhibited but soon recovered to within control levels. On the other hand, the AChE of rats fed 5.0 mg/kg was inhibited throughout the experiment. Plasma cholinesterase (ChE) of both species was first inhibited and then recovered erratically for both insecticide concentrations. Histological alterations in the spinal cord of paralysed hens included axon and myelin degeneration in the ventral, lateral and posterior columns. In the paralysed hens, 79% of the neurotoxic esterase in the brain were inhibited, whereas in the non-paralysed hens (including the one non-paralysed hen receiving 5.0 mg/kg/day) and all rats only about half as much was inhibited.     

Effect of maternal dietary hexachlorocyclohexane exposure on pup survival and growth in albino rats.

In adult albino rats, maternal dietary beta- and gamma-hexachlorocyclohexane (HCH) intake during gestation upto 400 ppm level did not affect the number of litters produced. But about 50 and 100% pup mortality was found in 200 and 400 ppm beta-HCH group within 5 days of birth. Maternal mortality was observed in 800 ppm beta-HCH group during third week of gestation. The effect of maternal dietary intake of HCH isomers at 50 and 250 ppm level during gestation and/or lactation on perinatal development was also studied. The body weights and sizes of the newborn litters of mother rats exposed to dietary HCH isomers did not differ from controls. Similarly, the growth and development of the litters of HCH exposed mother rats that survived 28 day lactation period were found to be comparable to controls as evidenced by the body weight and weight of vital organs. However, liver weight increases were found in the 28 days weaned litters wherever the mothers had been exposed to HCH isomers during lactation. Lowered kidney weight was seen in litters of mother rats fed 250 ppm gamma-HCH during gestation and lactation. The brain and testis weights were not affected in the litters of any experimental groups.     

A two-generational reproductive toxicity study of zinc in rats

A two-generation reproductive toxicity study of zinc chloride (ZnCl₂) was conducted in rats. F_o male and female rats were administered 0.00 (control), 7.50 (low), 15.00 (mid) and 30.00 (high) mg/kg/day of ZnCl₂. Selected F₁ male and female rats were exposed to the same doses received by their parents (F_o). Exposure of F₀ parental rats to ZnCl₂ showed significant reduction in fertility, viability (days 0 and 4), and the body weight of F₁ pups from the high-dose group but caused no effects on litter size, weaning index, and sex ratio. Similarly, the continued exposure of F₁ parental rats to ZnCl₂ also reduced fertility, liter size, viability (day 0), and the body weight of F₂ pups within the high-dose group but caused no effects on weaning index and sex ratio. Exposure of ZnCl₂ to F₀ and F₁ parental males resulted in a significant reduction in their body weights, and the F₀ and F₁ parental females did not show any significant difference in their body weights compared to their control groups. However, the postpartum dam weights of both F₀ and F₁ female rats were significantly reduced compared to their controls. Exposure of ZnCl₂ to F_o and F₁ generation parental rats did not produce any significant change of their clinical signs as well as their clinical pathology parameters, except the alkaline phosphotase (ALK) level, which showed an upward trend in both sexes of both generations. Exposure of ZnCl₂ to F₀ rats resulted in a reduction of brain, liver, kidney, spleen and seminal vesicles weights of males and in the spleen and uterus of females. Similarly, exposure of F₁ rats to ZnCl₂ also resulted in reduction of brain, liver, kidney, adrenal, spleen, prostate and seminal vesicles weights of males and in spleen and uterus of females. ZnCl₂ exposure resulted in grossly observed gastro-intestianla (GI) tract, lymphoreticular/hematopoietic, and reproductive tract lesions in parental rats in both generations. Reduced body fat was also recorded in F₁ parental rats.     

Residues of 2,4‐D in air samples from Saskatchewan: 1966–1975

Abstract

Residues of 2,4‐D (2,4‐dichlorophenoxyacetic acid) in air samples from several sampling sites in central and southern Saskatchewan during the spraying seasons in the 1966–68 and 1970–75 periods were determined by gas‐liquid Chromatographic techniques. Initially, individual esters of 2,4‐D were characterized by retention times and confirmed further by co‐injection and dual column procedures. Since 1973, however, only total 2,4‐D acid levels in air samples have been determined after esterification to the methyl ester and confirmed by gc/ms techniques whenever possible.

Up to 50% of the daily samples collected during the spraying season at any of the locations and during any given year contained 2,4‐D, with butyl esters being found most frequently. The daily 24‐hr mean atmospheric concentrations of 2,4‐D ranged from 0.01 to 1.22 μg/m³, 0.01 to 13.50 μg/m³, and 0.05 to 0.59 μg/m for the iso‐propyl, mixed butyl and iso‐octyl esters, respectively. Even when the samples were analysed for the total 2,4‐D content, i.e. from 1973 onwards, the maximum level of the total acid reached only 23.14 μg/m. In any given year and at any of the sampling sites, about 30% of the samples contained less than 0.01 μg/m³ of 2,4‐D. In another 40% of the samples, the levels of 2,4‐D ranged from 0.01 to 0.099 yg/m. Only about 30% of the samples contained 2,4‐D concentrations higher than 0.1 μg/m³, with only 10% or less exceeding 1 μg/m³.

None of the samples, obtained with the high volume particu‐late sampler, showed any detectable levels of 2,4‐D, indicating little or no transport of 2,4‐D adsorbed on dust particles or as crystals of amine salts.