Because of a lack of health effects data on human exposure to azamethiphos, we could not make a comparative risk evaluation.

Because of a lack of health effects data on human exposure to azamethiphos, caution should be exercised when using this pesticide until epidemiological and toxicological studies become available.

A.  Acute Health Effects

Methomyl is a carbamate pesticide initiating cholinesterase (ChE) inhibition. The acute toxic action of methomyl is characterized by signs of anticholinesterase action such as lacrimation, profuse salivation, tremor, and pupil constriction. Methomyl has a well-known mechanism of toxic action with particular toxicity by the acute oral and inhalation routes. As with other carbamate pesticide active ingredients, methomyl is excreted rapidly and does not accumulate in mammalian tissue. If exposure is suspended, ChE inhibition and its symptoms rapidly reverse.

1.  Oral Exposure

Accidental and suicidal poisonings provide the bulk of human exposure data for methomyl. One instance of accidental poisoning comes from five Jamaican fishermen who added methomyl to their meal instead of salt. Methomyl had been stored in an unlabeled tin can and was mistakenly used in preparing "roti," an Indian dish. Only minutes passed before three of the men began twitching, trembling, and frothing at the mouth. All died within 3 hours of ingestion. Estimations from food samples show that the individuals consumed between 12 mg/kg and 15 mg/kg methomyl, which is considered a lethal dose.^[809]

In nonfatal cases, illness generally lasts less than 24 hours. Based on qualitative and quantitative methomyl toxicity characteristics, 0.03 mg/kg/d is unlikely to cause adverse effects in humans by any exposure route. Accidental and intentional human poisoning data identify similar acute levels of methomyl toxicity in humans to that found in laboratory animals.^[810]

The deaths of a 31-year old woman and her son concur with the previously cited lethal methomyl dose. Examination after their deaths identified 15.4 mg/kg methomyl concentrations. The estimated doses for the son and his mother were 13 mg/kg and 55 mg/kg, respectively.^[811]

A 79-year-old man and his 73-year-old wife attempted double suicide by ingesting methomyl powder. The woman died 19 hours after ingestion despite intensive care. An autopsy revealed a large number of miliary hemorrhages found in both thalami of the brain. Her husband recovered after 10 days of treatment. Analysis revealed the methomyl concentration was 44 �g/g in the wife’s serum sample collected 1 hour after ingestion, and 0.2 �g/g in the blood sample collected at autopsy. The methomyl concentration in the husband’s blood sample collected 28 hours after ingestion was 0.01–0.1 �g/g. An estimated 11 g methomyl were ingested between the 2 of them. Methomyl powder, weighing approximately 5 g, amounts to approximately 30 mg/kg.^[812]

2.  Dermal Exposure

Because of the slower absorption phase of methomyl, acute dermal toxicity is low. Acute dermal exposures allow for recovery time from toxic action; therefore, the effect is never fully exerted.^[813]

3.  Inhalation Exposure

A health surveillance study in 22 healthy spraymen showed significant T-wave changes (including inversion) following a 5-day exposure to methomyl. Significant changes in plasma ChE and lactic dehydrogenase activities were also noticed. This is the first reported type of change in occupationally exposed subjects following exposure to a carbamate compound. Study results indicate that these changes are probably related directly to methomyl rather than its toxicity through ChE inhibition. The study identifies significance of these changes and the need for further investigation.^[814]

In an unpublished document, more than 225 poisonings were reported between 1972 and 1973 following inhalation exposure to dry formulations of methomyl. Some exposure incidences resulted in serious acute reactions, but none were fatal. After this compound was reformulated as a liquid, cases decreased to fewer than 10 per year.^[815]

In another case, methomyl was found in the blood of a pilot who died when his aircraft crashed while he was spraying methomyl. Circumstances of the pilot’s case suggest that the methomyl poisoning probably occurred by inhalation and dermal absorption. The pesticide active ingredients in his blood were measured by gas chromatography with flame photometric detection and the results confirmed by mass spectrometry with direct liquid injection through a liquid chromatography interface. The whole blood methomyl concentration was 570 ng/mL.^[816]

Specific dosage-related acute human inhalation studies were not found in the research literature. For this reason, data from the acute oral human studies will be used for making comparisons to the Health Risk Assessment (HRA) exposure estimates.

1.  Oral Exposure

Human health effects studies providing toxicology benchmark dosages for this exposure route were not found in the research literature.

2.  Dermal Exposure

Human health effect studies providing toxicology benchmark dosages for this exposure route were not found in the research literature.

3.  Inhalation Exposure

Human health effect studies providing toxicology benchmark dosages for this exposure route were not found in the research literature.

1.  Oral Exposure

Human health effect studies providing toxicology benchmark dosages for this exposure route were not found in the research literature.

2.  Dermal Exposure

Human health effect studies providing toxicology benchmark dosages for this exposure route were not found in the research literature.

3.  Inhalation Exposure

One study identified chronic inhalation exposure in a plant manufacturing methomyl. The workers’ average employment duration was 2 years. Eleven workers were hospitalized for illnesses related to methomyl exposures. The highest hospitalization rates occurred in areas involved with chemical packaging (27 percent), production (22 percent), and plant maintenance (9 percent). Clinical evaluation revealed 46 percent of the 11 packaging workers experienced the highest frequency of acute cholinergic symptoms, including miosis, blurred vision, nausea or vomiting, muscle weakness, fatigue, and increased salivation. No precise dose response or chronic health effects were determined and reliable ChE measurements were not made.^[817]

Human health effects studies providing specific toxicology benchmark dosages for this exposure route were not found in the research literature.

Please refer to the reference table(s) in Section B.4.C.1.b of Other Toxicity Benchmarks from Human Data..

Table 146. Methomyl, comparison of HRA doses to benchmarks (application exposure)