By William H. Hallenbeck, Kathleen M. Cunningham-Burns (auth.)
The impetus for this publication got here from quite a few requests through private and non-private businesses and voters for info in regards to the human overall healthiness results of pes ticide exposures. we've got attempted to collect a comparatively entire, concise sum mary of the intense and protracted overall healthiness results and the toxicology of insecticides in a layout that offers speedy and simple entry. This publication was once written to deal with the wishes of the next teams: clinical and public future health pros, tox icologists, environmentalists, business hygienists, regulators, manufacturers and clients of insecticides, public curiosity advocates, and the criminal occupation. Acknowledgments we're indebted to Mr. Christopher J. Wiant, leader of the Environmental Chemistry component of the Illinois division of Public health and wellbeing. The monetary help supplied by way of his place of work was once crucial in generating this publication. we're additionally indebted to Dr. Charles Benbrook, former employees member, and consultant George E. Brown, Chairman of the Subcommittee on go away ment Operations, learn and overseas Agriculture of the Committee on Agri tradition, usa apartment of Representatives, for his or her advice in receive ing pesticide toxicity information. within the Freedom of data place of work, place of work of Pesticide courses of the U.S. Environmental safety company, the endurance and counsel of Therese Murtagh and Virginia Salzman in acquiring files are preferred. Of the varied people who participated within the creation of this publication, the next advantage unique attractiveness for the standard in their study, enhancing, and demanding talents: Mark Loafman, Sue Ramirez, Steve Smith, Sally Burns, and Denise Steurer.
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Digestion disturbances eye: conjunctivitis, eyelid edema gastric ulcer hepatic: degeneration, jaundice joint pains meningismus metabolic acidosis mucous membrane irritation, atrophy, eruptions, dryness nausea renal: kidney tubule degeneration Boric Acid Chronic Exposure Effects (continued) tongue: red vomiting 29 weakness weight loss Suspected Effects ataxia 9(62) mutagenesis 27 prenatal damage reproductive system effects 27 5(168) Toxicology Boric acid is rapidly absorbed from the GI tract and skin.
The carbamyl-enzyme complex dissociates readily, which reduces the duration of toxic effects and limits the time during which the poisoning can be detected. Carbamates are metabolized by the liver and are mild inducers of mixed function oxidases. Carbamates alter several other enzyme systems. CNS depressants potentiate carbamate poisoning. Methomyl is potentiated by carbaryl and ronnel. Additional Information There is a rapid disappearance of the less severe exposure effects. Cholinesterase activities usually revert to normal within a few hours.
It acts on the nervous system, enzyme systems, carbohydrate metabolism, kidneys, liver, hormone functions, and cellular oxidation. Infants are more susceptible to boric acid than adults. The onset of symptoms may be delayed for hours in acute poisoning. 30 Carbamates Carbamates Class of Active Ingredients Use: fungicides, herbicides, insecticides, molluscicides, nematicides, plant growth regulators Acute Exposure Effects abdominal cramps aphasia ataxia bradycardia cholinesterase depression coma convulsions cyanosIs dermal irritation diarrhea disorientation dizziness epigastric pain eye: pain, blurred vision, loss of accommodation, dim vision, miosis/mydriasis, tearing, ciliary muscle spasm, unreactive pupils headache hypertension incontinence lassitude muscle twitching Chronic Exposure Effects anoreXIa cholinesterase depression muscle weakness nausea pallor paralysis of extremities (temporary) psychosis reflexes abnormal respiratory: pulmonary edema, cough, chest tightness, dyspnea, rales, orona sal discharge, bronchoconstriction salivation sleeping difficulty sweating tachycardia tremor unconSCIOusness vomiting weakness Death due to respiratory arrest, respiratory muscle paralysis, or bronchoconstriction renal/urinary: renal damage, albuminuria, glycosuria Carbamates Suspected Effects prenatal damage 1, 5( 171), 22, 23, 27, 36 reproductive system effects 5(343), 23, 27 Aldicarb: N-nitroso derivative is mutagenic 2(194) Benomyl corneal opacities 23 hepatic damage 23 mutagenesis 22, 36 Carbaryl: behavioral effects 36 carcinogenesis 20, 25 CNS lesions 8(111-81) heart defects 23 humoral immune response suppression 37 mutagenesis 22 N-nitroso derivative is carcinogenic 9(444) and mutagenic 2(193), 9(444) paraplegia 8(111-81) prostration 8(III-81) renal tubular damage 8(III-80) vasogenic edema 8(111-81) weight depression 23 Carbofuran: N-nitroso derivative is mutagenic 2(194) Chlorpropham: carcinogenesis 36 Methomyl: adrenal hypertrophy 23 bone marrow damage 33(87) breathing irregular 33(82) dermal: edema, erythema 33(95) eye: conjunctivitis 33(82), corneal opacity 33(95), exophthalmos 23, 31 Methomyl (continued) 33(82), tearing (bloody) 23, 33(82) hematocrit decrease 23 hemoglobin decrease 23 hepatic damage 33(87) N-nitroso derivative is mutagenic 2(194) prostrate enlargement 23 splenic damage 33(79) Mexacarbate: carcinogenesis 36 Phenmedipham: anemia 23 hematocrit decrease 23 hemoglobin decrease 23 spleen: histologic changes 23 Pirimicarb: anemia 23 blood dyscrasias 23 carcinogenesis 23, 36 growth retardation 22, 23 pituitary hypertrophy 23 spleen weight changes 23 Propham: carcinogenesis 36 Propineb: carcinogenesis 36 goitrogenesis 36 pituitary enlargement 36 Propoxur: N-nitroso derivative is mutagenic 2(194) Thiophanate-methyl: metabolite MBC is mutagenic 22 32 Carbamates Toxicology Carbamates cause reversible carbamylation of acetylcholinesterase.