In a two-generation study, groups of 24 male and 24 female Wistar rats were given diets containing imazalil (purity, 98.0%) at a nominal dose of 0, 5, 20, or 80 mg/kg bw per day for 60 days before mating (both sexes), during a 3-week mating period (both sexes), during gestation, and until weaning of the first generation. The F₀ males were killed after mating. The first generation (F₁) received imazalil during growth, mating, gestation, and weaning of the second generation (F₂). The F₁ males were killed after mating. The doses during the premating period were equal to 0, 4.2, 18, and 70 mg/kg bw per day for males and 0, 5.0, 22, and 100 mg/kg bw per day for females. During the F₀ gestation, the intakes were 0, 4.0, 16, and 87 mg/kg bw per day, and those during the F₁ gestation were 0, 4.3, 19, and 88 mg/kg bw per day. Thus, the intakes tended to be slightly lower than the nominal doses. The animals were observed daily for general health, appearance, and behaviour. Body weights were recorded weekly before mating and, for females, on days 1 and 22 after copulation. Body weights were also recorded during the 3-week lactation period. Food consumption was recorded weekly before mating for both sexes and during gestation and lactation for females. The body weights of both F₁ and F₂ pups in each litter were recorded 8–12 h after parturition and on days 4, 14, and 21. The kidneys, liver, and reproductive organs of the parental and F₁ generations were examined histologically.

Two F₁ females at the high dose were killed in extremis, and one F₂ female at the high dose and one control died soon after parturition or during lactation. F₀ males at the highest dose showed decreased weight gain before mating; a similar but less pronounced effect was seen in females before mating, but an effect was also seen in F₁ and F₂ dams during gestation, at parturition, and at days 4, 14, and 21 of lactation. No effects on weight gain were seen in other treated groups, and there was no clear effect on food consumption in any group. Histopathological changes (liver vacuoles) were seen in F₀ males at the highest dose, but no lesions were seen in the male reproductive system at any dose. Decreased numbers of corpora lutea were seen in F₀ females. At the highest dose, both F₁ and F₂ generations had considerably reduced numbers of live pups and larger numbers of stillborn pups, and the F₁ generation had fewer implantations; the duration of gestation was increased in both generations, by approximately 1 day, with an associated increase in the incidence of dystocia. The survival rates of pups during lactation were decreased in all F₁ treated groups on days 4, 14, and 21; in the F₂ generation, survival was decreased at all times at the highest dose and on days 14 and 21 at the lower dose; at the intermediate dose, the survival was comparable to that of controls, so that there was no dose–response relationship. No differences in body weight were seen between F₁ and F₂ pups. No teratogenic effect was observed.

The NOAEL for maternal toxicity was 20 mg/kg bw per day on the basis of reduced maternal weight gain. The NOAEL for fetotoxicity was 20 mg/kg bw per day on the basis of decreased numbers of live pups and increased numbers of stillbirths at 80 mg/kg bw per day. As summarized above, the survival rates of F₁ pups during lactation were decreased in all treated groups on days 4, 14, and 21 of lactation and in the F₂ generation at 5 mg/kg bw per day (days 14 and 21) and 80 mg/kg bw per day (days 4, 14, and 21); moreover, there was no dose–response relationship for the effect in the F₁ generation at day 4, although there was at days 14 and 21. It is arguable that the data, especially for days 14 and 21, indicate a dose-related effect, but there was clearly no dose-related effect in F₂ pups. There is no biologically plausible explanation for the difference between the two generations, and a statistical re-examination on a litter basis showed that the mortality rate was significantly increased only in the group at the highest dose. As hepatotoxicity was observed in F₀ males at the highest dose, the NOAEL for paternal toxicity was 20 mg/kg bw per day (Dirkx et al., 1992b; see also Janssen Pharmaceutica NV, 1994).

The developmental toxicity of imazalil (purity not stated) was studied in groups of 30 inseminated Cobs CD1 mice given a dose of 0, 40, 80, or 120 mg/kg bw per day by gavage on days 6–16 of gestation. Treatment did not affect the maternal mortality rate, but maternal body-weight gain and food consumption were decreased at the two higher doses. Litter size and the number of live pups were reduced in all treated groups. The number of resorptions was increased at the highest dose. No teratogenic effects were seen, and there were no differences between groups in mean pup weights. The NOAEL for maternal toxicity was 40 mg/kg bw per day; an NOAEL for fetotoxicity could not be established in view of the decreases in litter size and number of live pups at all doses (Gillardin et al., 1987).

A further study of the developmental toxicity of imazalil (purity, 99.3–99.5%) was carried out in groups of 30 inseminated Cobs CD1 mice given a dose of 0, 10, 40, 80, or 120 mg/kg bw per day by gavage on days 6–16 of gestation. Deaths were recorded during the study, and the animals were examined daily for abnormal clinical signs. Body weights were determined on day 1, daily on days 6–17, and on day 19 after copulation. Food consumption was recorded over days 1–5, days 6–16, and days 17–18. On day 19 after copulation and before killing, all survivors underwent a complete physical examination. The surviving dams were then killed, and macroscopic changes were recorded; the weights of the uteruses were recorded after removal of that organ in toto. The dams were examined for numbers of live and dead fetuses, implantation sites, and embryos undergoing resorption. All live fetuses were weighed, and live and dead fetuses were examined for external abnormalities. The pups were sexed and the fetuses examined radiographically. The fetuses were then dissected, and bones were stained with alizarin.

Fourteen mice died during the study: one control, four at 80 mg/kg bw per day, and nine at 120 mg/kg bw per day. At the highest dose, piloerection, excitability, convulsions, hypothermia, and prostration were observed. Body weights were decreased on days 17 and 19 in mice at the two higher doses in comparison with concurrent controls; moreover, the body-weight gain of these animals was decreased during days 6–17 after copulation, and that of animals at 40 and 120 mg/kg bw per day was decreased during days 17–19 after copulation. The total body-weight gain (uterine weight subtracted) over the whole period 1–19 days was decreased at doses of 40 mg/kg bw per day and more. Food consumption was decreased during dosing on days 6–16 in mice at 80 and 120 mg/kg bw per day and after dosing in those at 40 mg/kg bw per day and more. The pregnancy rates and number of implantations were comparable among groups, whereas fewer live fetuses were found in animals at the highest dose, and the number of resorptions was increased. The body weight of pups was decreased at the highest dose, but the sex ratio was similar in all groups. The frequency of minor changes in ribs was increased at 40 and 80 mg/kg bw per day but not at the highest dose; there was thus no clear dose–response relationship. The number of major abnormalities was comparable in all groups. The NOAEL for maternal toxicity was 10 mg/kg bw per day on the basis of decreased body-weight gain at 40 mg/kg bw per day and reduced food consumption after treatment. In addition, deaths occurred at doses of 80 mg/kg bw per day and more. The NOAEL for fetal toxicity was 80 mg/kg bw per day, as the number of live fetuses was reduced, the number of resorptions was increased, and the body weights of the pups were decreased at the highest dose. There was no evidence of teratogenicity (Levron et al., 1991).

If the results of the two studies of developmental toxicity in mice are taken together, the overall NOAEL for maternal toxicity was 10 mg/kg bw per day, but no NOAEL was identified for fetotoxicity.

The developmental toxicity of imazalil (sulfate; purity, 99.9%) was studied in groups of 24 pregnant Sprague-Dawley OFA.SD (IOPS Caw) rats treated by gavage at a dose of 0, 40, 80, or 120 mg/kg bw per day on days 6–16 of gestation. The dams were examined daily and weighed 1, 6, 17, and 22 days after copulation. Food consumption was recorded during days 1–5 (before dosing), 6–16 (during dosing), and 17–21 (after dosing). At the end of the study, on day 22 of gestation, the dams were killed and examined for live and dead fetuses, implantation sites, and resorptions. Live fetuses were weighed, and live and dead ones were examined for anomalies radiographically and by alizarin staining to visualize skeletal anomalies. One animal at 40 mg/kg bw per day died, but this death was considered to be unrelated to treatment as no others occurred during the study. Maternal body weight was reduced at the end of dosing at all three doses on day 17 and at the highest dose on day 22, in comparison with concurrent controls. Decreased body-weight gain was seen at the highest dose. Decreased food consumption was seen at all three doses throughout treatment. The rates of pregnancy and numbers of corpora lutea and implantations were similar in all groups. The number of live fetuses was decreased and the number of resorptions increased at 120 mg/kg bw per day. At the two higher doses, the birth weights of the pups were decreased. No teratogenic effects were seen. The NOAEL for fetal toxicity was 40 mg/kg bw per day, on the basis of reduced pup weight at the next higher dose. No NOAEL for maternal toxicity could be identified because of decreased maternal body weight at all doses (Gillardin et al., 1988).

The developmental toxicity of imazalil (purity, 99%) was studied in groups of 15 pregnant New Zealand white rabbits given a dose of 0, 1.2, 2.5, or 5 mg/kg bw per day by gavage on days 6–18 of gestation. The animals were weighed before the start of dosing, at day 19, and at termination. Food consumption was not recorded. On day 28 of gestation, the animals were killed and examined for the numbers of live and dead fetuses, implantation sites, and resorptions. Live fetuses were weighed, and dead and live fetuses were examined for anomalies radiographically and by alizarin staining. One rabbit at the low dose and one at the high dose died. There was no clear effect of treatment on body-weight gain or pregnancy rate. No differences were seen between groups in the numbers of live or dead fetuses or resorptions or in the birthweights of pups or 24-h survival rate. The NOAEL for both maternal and fetal toxicity was 5 mg/kg bw per day (Dirkx & Marsboom, 1985).

A further study of the developmental toxicity of imazalil was carried out in which groups of four pregnant albino rabbits were given imazalil sulfate (purity, 98.2–100%) by gavage at a dose of 0, 5, 10, or 20 mg/kg bw per day on days 6–18 of gestation. The animals were observed daily for ill health, abnormal behaviour, or other clinical effects. Body weights were recorded on the morning of day 0 and on days 6, 19, and 28 of gestation. Food consumption was recorded during days 0–5, 6–19, and 19–28. On day 28 of gestation, the surviving animals were killed and autopsied, the uterus was removed and the weight recorded, and the dams were examined for the numbers of dead and live fetuses and resorptions. The numbers of corpora lutea were determined, and the pups were sexed. Live fetuses were weighed, and both live and dead fetuses were examined externally by radiographic examination and alizarin staining. The fetuses were then dissected.

Eight animals at 20 mg/kg bw per day and one at 10 mg/kg bw per day died during the experiment. Five of those at the highest dose that died showed weight loss. No significant differences in clinical end-points were found in the survivors. On day 19 of gestation, the body weight of animals at 20 mg/kg bw per day was decreased in comparison with that of concurrent controls. Food consumption was reduced in animals at 10 mg/kg bw per day in comparison with concurrent controls during days 0–5, and in animals at 10 and 20 mg/kg bw per day during days 6–18. The pregnancy rates and numbers of corpora lutea were comparable between groups. Animals at 20 mg/kg bw per day had a decreased number of live pups, and those at 10 and 20 mg/kg bw per day had increased numbers of resorptions. Although these changes were not statistically significant, the numbers were small, and the decrease may be biologically significant. There was a significant decrease in the number of male fetuses at 5 mg/kg bw per day but not at higher doses. Fetuses of does at 20 mg/kg bw per day had an increased incidence of thirteenth rib and missing sternum in comparison with concurrent controls, but, especially in the latter case, there was no clear dose–response relationship, and the Meeting considered these findings to be coincidental. The NOAEL for maternal toxicity was 5 mg/kg bw per day on the basis of reduced food consumption at 10 mg/kg bw per day. The NOAEL for fetal toxicity was also 5 mg/kg bw per day on the basis of an increased number of resorptions and a decreased number of live pups at 10 mg/kg bw per day (Dirkx et al., 1992a).

A study of reproductive toxicity with measurement of neurobehavioural end-points was reported in which imazalil (purity, > 99%) was administered in the diet to groups of 10 Crj: CD-1 mice of each sex from 5 weeks of age in the F₀ generation to 9 weeks of age in the F₁ generation. The compound was given at a concentration of 0, 0.012, 0.024, or 0.048% (0, 120, 240, and 480 ppm, if % is assumed to equal w/w), resulting in intakes for the F0 generation of 0, 19, 31, and 79 mg/kg bw per day for males and 0, 26, 45, and 100 mg/kg bw per day for females before conception; 0, 18, 34, and 74 mg/kg bw per day during mating; 0, 21, 38, and 83 mg/kg bw per day during gestation; and 0, 65, 150, and 260 mg/kg bw per day during lactation. The intakes in the F₁ generation were 0, 21, 41, and 87 mg/kg bw per day for males and 0, 24, 49, and 93 mg/kg bw per day for females.

In the F₀ generation, there was no effect on the body weight of either sex before conception or on the body weights of dams during gestation or lactation. Food intake was increased in females at the low and high doses before conception but not in those at the intermediate dose. A number of indicators of exploratory behaviour were increased in males at the high dose. In the F₁ generation, litter size and weight and sex ratio at birth were unaffected by treatment. The mean body weight of animals at the two higher doses was reduced in early lactation. Indicators of behavioural developmental were affected, as follows. In males, surface righting was affected at the two higher doses at postnatal day 4 and at the intermediate dose at postnatal day 7. Swimming head angle was affected in males at the highest dose at postnatal day 4. In females, surface righting was affected in all treated F₁ offspring at postnatal day 7, without a clear dose–response relationship, and swimming head angle was affected in females at the highest dose at postnatal day 4. No convincing dose–response relationships were seen for other observations, such as on multiple water T-maze performance at week 7. By week 8, there were no effects on the exploratory behaviour of either sex. The doses used in this study were higher than those in other studies reviewed in this monograph. Furthermore, although the results suggest that neurobehavioural end-points can be adversely affected in mice exposed to imazalil in their diet during development, comparison with the study of Levron et al. (1991), described above, suggests that the lowest dose might have been almost maternally toxic. In view of the inconsistent results at the lowest dose, the many end-points measured, and lack of dose–reponse relationships in the adverse outcomes observed, the NOAEL was the lowest dose tested, about 20 mg/kg bw per day (Tanaka, 1995).

A 43-year-old female veterinary technician developed contact dermatitis to the veterinary antimycotic Imaverol, which contains imazalil (enilconazole). Patch testing showed sensitivity to several imidazoles, including imazalil (van Hecke & de Vos, 1983).

A case of palatal and nasal infection with Alternaria was treated with imazalil at oral doses up to 1200 mg/kg bw administered topically and orally. The drug was tolerated, but it was found to be bitter and unpleasant with an aftertaste lasting for hours, and nausea occurred at high doses (³ 800 mg). Very limited studies of pharmacokinetics were carried out: at a dose of 400 mg/day, the maximum serum concentration was about 2 µg/ml, while at a dose of 1200 mg, the maximum serum concentration was about 4 µg/ml. The half-time was about 2 h, and administration of 1200 mg/kg bw daily for 1 month did not result in accumulation. No changes in clinical chemical parameters were seen (Stiller & Stevens, 1986).

A study in volunteers was undertaken to examine the local effects of imazalil on the skin. Imazalil base 0.2%, imazalil base 0.2% ointment, imazalil sulfate (530 mg base/L), Fungaflor (68% w/w imazalil), and two control formulations not containing imazalil were applied under occlusive adhesive strips for 48 h. The skin was then examined for redness, oedema, irritation, or inflammation. There were no complaints of burning, itching, or pain, and the skin at the sites of application appeared normal in all cases (Desplenter & Verhamme, 1979).

After oral administration to rats, [¹⁴C]imazalil was rapidly and nearly completely absorbed. Most of the label was excreted within 96 h, predominantly in the urine but also in faeces. Nearly 50% of the radiolabel retained in the body was found in the liver. Very little imazalil was excreted unchanged, and the compound was metabolized to at least 25 metabolites. The main routes of metabolism were epoxidation, epoxide hydration, oxidative O-dealkylation, imidazole oxidation and scission, and oxidative N-dealkylation. No significant sex difference was seen in metabolism. The metabolic pattern was similar after oral and intravenous administration.

In a study of the hepatotoxicity of imazalil, the compound was found to affect liver morphology (vacuolation) when given in the diet to mice for up to 3 months. In rats, imazalil caused fatty infiltration of the liver and decreased serum concentrations of triglycerides, cholesterol, and phospholipids. Imazalil administered to mice by mouth induced the cytochrome P450 isoenzymes CYP1A, CYP2B, CYP2C, and CYP3A. Imazalil had no significant estrogenic effect when tested in vitro in an MCF7 cell proliferation assay or a yeast estrogen screen. Steroid 11beta-hydroxylation and 19-hydroxylation in the mitochondria of the gerbil were reported to be substantially suppressed in parallel by imazalil. Imazalil inhibited CYP19 aromatase activity in human placental microsomes.

The acute oral LD₅₀ of imazalil in rats was 200–350 mg/kg bw. Imazalil was not irritating to the skin of rabbits and was moderately irritating to the eye. It had weak sensitizing potential when tested according to the Magnusson and Kligman method. A single case report of contact dermatitis in humans in response to imazalil was found. A further report was considered, in which imazalil had been used orally at high doses by an individual to treat a fungal infection; it was well tolerated, the only adverse effect noted being nausea. Imazalil has been classified by WHO (1999) as moderately hazardous.

Studies in mice, rats, and dogs showed that the target organ of toxicity was frequently the liver. In addition, imazalil, like other azole fungicides, affects steroid synthesis, but there was little indication that this was manifested in vivo in the studies examined by the Meeting.

Imazalil was applied to the shaved backs of New Zealand white rabbits at a dose of 0, 10, 40, or 160 mg/kg bw per day for 6 h/day, 5 days/week for 3 weeks, on a porous gauze dressing. The highest dose reduced the creatinine concentration, specific gravity, and urobilinogen concentration in urine. The NOAEL was 40 mg/kg bw per day.

Imazalil was administered to groups of 10 rats of each sex at a dietary concentration of 0, 25, 100, or 400 ppm. The NOAEL was 100 ppm (equivalent to 5 mg/kg bw per day), on the basis of increased relative kidney weights in males and increased absolute and relative liver and kidney weights and increased absolute thymus weight in females at the highest concentration.

In a 1-year study of toxicity in beagle dogs, groups of four animals of each sex received imazalil at a dose of 0, 1.2, 2.5, or 20 mg/kg bw per day orally in gelatine capsules. The NOAEL was 2.5 mg/kg bw per day on the basis of clinical signs, decreased body-weight gain and food consumption, decreased serum calcium concentration, increased alkaline phosphatase activity, and increased liver weight at the highest dose.

In a 23-month study of carcinogenicity in mice, groups of 50 males and 50 females received imazalil at a dietary concentration of 0, 50, 200, or 600 ppm. Males at the two higher doses and females at the highest dose showed focal cellular changes, large and small vacuoles, and pigmented and swollen sinusoidal cells in the liver. Increased incidences of hepatic neoplasms were found in males at 200 and 600 ppm, with increased incidences of hepatic neoplastic nodules; a similar increase in the incidence of hepatic neoplasms was found in females at the highest dietary concentration. The hepatic neoplasms were evaluated three times, the last time by a pathology working group which concluded that the incidence of adenomas, but not that of carcinomas, was increased in males at the two highest doses. Therefore, the NOAEL for carcinogenicity was 50 ppm. The overall NOAEL for the study was 50 ppm, equal to 8.1 mg/kg bw per day, on the basis of morphological changes (adenomas, foci and nodules) in the livers of males at 200 ppm.

Imazalil was administered to groups of 20 male and 20 female rats at a dietary concentration of 0, 25, 100, or 400 ppm for 18 months. Decreased body-weight gain was observed in females at the highest dose, and males at this dose showed treatment-related gross (increase in the lobular pattern) and microscopic (periportal cytoplasmic vacuolation of hepatocytes) effects in the liver. There was no evidence of treatment-related neoplasia. The NOAEL was 100 ppm, equivalent to 5 mg/kg bw per day, on the basis of decreased body-weight gain in females, decreased plasma albumin concentration in males, and pathological changes in the livers of males at the highest dose.

Imazalil was administered to groups of 50 male and 50 female rats at a dietary concentration of 0, 25, 100, or 400 ppm for 30 months. The NOAEL was 100 ppm, equal to 3.6 mg/ kg bw per day, on the basis of decreased body-weight gain in males at the highest dose. No treatment-related histopathological effects were observed in the liver. There was no evidence that imazalil was carcinogenic.

Imazalil has been tested for genotoxicity in an adequate range of tests in vivo and in vitro. The Meeting concluded that imazalil is unlikely to have genotoxic potential. In view of the lack of genotoxicity and the finding of tumours only in mice, the Meeting concluded that imazalil is unlikely to pose a carcinogenic risk to humans. However, the Meeting was aware that the toxicological dossier supplied was incomplete.

A two-generation study of reproductive toxicity was conducted in rats, in which imazalil was administered in the diet at a nominal dose of 0, 5, 20, or 80 mg/kg bw per day. The NOAEL for maternal toxicity was 20 mg/kg bw per day on the basis of reduced maternal weight gain at 80 mg/kg bw per day. Decreased numbers of live pups and increased numbers of stillbirths were observed at this dose. The survival rate of pups during lactation was decreased in all test groups of the F₁ generation at days 4, 14, and 21 of lactation and in the F₂ generation, at 5 mg/kg bw per day (days 14 and 21) and 80 mg/kg bw per day (days 4, 14, and 21). However, when these data were evaluated on a per litter basis, the differences in survival were not significant. On this basis, the NOAEL for fetotoxicity was 20 mg/kg bw per day.

A study of reproductive toxicity in which neurobehavioural end-points were measured was conducted with dietary concentrations of 0, 120, 240, and 480 ppm. The lowest concentration used was high in comparison with the doses used in other studies that were reviewed. Nevertheless, the results suggest that neurobehavioural end-points in the offspring of mice exposed to imazalil in their diet, during pregnancy and perinatally, can be adversely affected. In view of the inconsistent results found at the lowest dose, the multiple end-points measured, and the lack of a dose–response relationship, the Meeting concluded that the NOAEL for developmental neurotoxicity was 120 ppm, equal to 20 mg/kg bw per day.

Two studies of the developmental toxicity of imazalil in mice were available for review. In the first, imazalil was administered by gavage at a dose of 0, 40, 80, or 120 mg/kg bw per day. The NOAEL for maternal toxicity was 40 mg/kg bw per day, on the basis of reduced body-weight gain and food consumption. No NOAEL was identified for fetal toxicity, as litter size and the number of live pups were decreased in all groups. In the second study, imazalil was administered by gavage at a dose of 0, 10, 40, 80, or 120 mg/kg bw per day. At the highest dose, the number of live fetuses was reduced, and the number of resorptions was increased. The body weights of pups at this dose were decreased, but the sex ratio was similar in all groups. The NOAEL for maternal toxicity was 10 mg/kg bw per day on the basis of decreased body-weight gain at 40 mg/kg bw per day and reduced food consumption after dosing. In addition, deaths occurred at doses of 80 mg/kg bw per day and above. The NOAEL for fetal toxicity was 80 mg/kg bw per day, as the highest dose reduced the number of live fetuses,increased the number of resorptions, and decreased the body weights of the pups. There was no evidence of teratogenicity. When the two studies were considered together, the Meeting concluded that the NOAEL for maternal toxicity was 10 mg/kg bw per day, but that a NOAEL for fetal toxicity could not be identified.

In a study of developmental toxicity in rats, imazalil was administered at a dose of 0, 40, 80, or 120 mg/kg bw per day by gavage. No teratogenic effects were seen, and the NOAEL for fetal toxicity was 40 mg/kg bw per day, on the basis of reduced pup weight at the higher dose. A NOAEL for maternal toxicity was not identified because of decreased maternal body weight in all the groups when compared with concurrent controls.

The developmental toxicity of imazalil in rabbits was studied at doses of 0, 1.2, 2.5, and 5 mg/kg bw per day. The NOAEL for both maternal and fetotoxicity was 5 mg/kg bw per day, the highest dose tested. In another study of developmental toxicity in rabbits, at doses of 0, 5, 10, and 20 mg/kg bw per day, the NOAEL for maternal toxicity was 5 mg/kg bw per day on the basis of reduced food consumption at 10 and 20 mg/kg bw per day. The NOAEL for fetal toxicity was also 5 mg/kg bw per day, on the basis of an increased incidence of resorptions and a decrease in the number of live pups at 10 and 20 mg/kg bw per day. In neither case was imazalil teratogenic.

The Meeting concluded that the existing database was adequate to characterize the potential hazard of imazalil to fetuses, infants, and children

The ADI of 0–0.03 mg/kg bw established by the 1991 Joint Meeting was reaffirmed. The ADI is based on a NOAEL of 2.5 mg/kg bw per day in a 1-year study of toxicity in dogs and a 100-fold safety factor.

The establishment of an acute RfD was considered unnecessary as no relevant end-point was identified.

    See Also:
       Toxicological Abbreviations
       Imazalil (ICSC)
       Imazalil (Pesticide residues in food: 1977 evaluations)
       Imazalil (Pesticide residues in food: 1980 evaluations)
       Imazalil (Pesticide residues in food: 1984 evaluations)
       Imazalil (Pesticide residues in food: 1984 evaluations)
       Imazalil (Pesticide residues in food: 1985 evaluations Part II Toxicology)
       Imazalil (Pesticide residues in food: 1986 evaluations Part II Toxicology)
       Imazalil (Pesticide residues in food: 1991 evaluations Part II Toxicology)
       Imazalil (JMPR Evaluations 2001 Part II Toxicological)
       Imazalil (JMPR Evaluations 2005 Part II Toxicological)