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| APPLIED AGRICULTURAL CHEMICALS
Summary Agricultural chemicals pose hazards to the respiratory system in a variety of ways, including direct irritation and constriction of airways, pulmonary edema, and respiratory depression. Three commonly used types of pesticides, fumigants, cholinesterase-inhibiting insecticides, and paraquat, can threaten life through their effects on respiration. Fumigants, commonly used in grain storage facilities, agricultural commodity storage and transport, and soil treatment, can cause laryngeal edema, bronchospasm, and/or pulmonary edema. Chloinesterase-inhibiting insecticides, the predominant agricultural insecticides used today, can cause systemic poisoning and death through respiratory depression, broncho-constriction, and bronchorrhea. Paraquat, a commonly used herbicide, can (when ingested) lead to a delayed proliferation of pulmonary connective tissue and death through asphyxiation. Prompt and specific management is crucial if victims are to survive severe poisonings by these agents. The large number of additional pesticides that affect the respiratory tract less commonly or less severely are listed in Table 3. Another agricultural chemical, the fertilizer anhydrous ammonia, may cause direct injury to the respiratory tract. Prevention of poisonings and injuries depends on safe usage and storage practices, good personal hygiene, monitoring of health status of frequently exposed workers, compliance with governmental regulations, and intelligent use of personal protective equipment. I. INTRODUCTION Since the Second World War, thousands of chemical products have been developed for use in livestock and crop production. Many of these products are injurious to human health. Indeed, the majority of such products are pesticides: products whose major purpose is to destroy life forms which have become "pests" to the farmer. (See Fig. 1) This unit focuses on pesticides that can kill through effects on the human respiratory system: fumigants, the organophosphate and carbamate cholinesterase-inhibiting insecticides, and the herbicide paraquat. Basic properties of these substances are listed in Table 1; they are discussed in detail in the following three sections. Numerous additional pesticides, and the fertilizer anhydrous ammonia, affect the respiratory tract either less severely or less commonly. Characteristics of these products are summarized in Section V. The final unit discusses prevention of pesticide injuries. Pesticides can cause injury either through contact with skin or mucous membranes, or through systemic effects after they have entered the body through inhalation, ingestion, or absorption through the skin. Fumigants, for example, injure the respiratory tract directly, causing irritation, bronchospasm, and/or pulmonary edema. When cholinesterase-inhibiting insecticides and paraquat are absorbed into the body, on the other hand, they cause systemic poisoning, the respiratory component of which may be fatal. Absorption may occur through the skin, but may also occur across alveoli following inhalation, or across the gut lining following ingestion. Workers must avoid eating or smoking with contaminated hands, and thus ingesting pesticides. Many types of agricultural workers, in addition to farmers, can be exposed to pesticides. Migrant or resident pickers may be exposed to residues when working in fields or harvesting crops. (See Fig. 2) Commercial formulators and applicators often handle the most highly toxic pesticides, sometimes in concentrated from; persons who dilute, mix, load, and apply the pesticides (including pilots) may be exposed. Those who provide agricultural support services, such as warehousemen, farm supply dealers, transportation workers, grain elevator operators, and those employed in storage facilities for perishable crops, all may work with pesticides. Manufacturers and formulators (those who prepare concentrated pesticide products for transportation and sale) routinely deal with highly concentrated pesticides. Farm families or nearby rural residents may become victims of drifting pesticide spray, pesticide spills, or accidental misapplication to their property. Although potential problems are great, statistics on pesticide poisonings are rare because of inadequate means of diagnosis and a lack of a comprehensive reporting system. We know that pesticide use is tremendous: In Iowa, in 1978, half of all corn fields were treated for above-ground insects and 95% were sprayed for weed control. Most application was done by the farmers themselves. Over seven million acres of crop land were treated with over seven million pounds of active pesticide ingredients. That same year, one and one-third billion pounds of synthetic organic pesticides were sold in the U.S. The University of Iowa Poison Control Center receives approximately 500 calls involving pesticides annually; many of these involve household products, rodent poisons, and the like. (Personal communication, Poison Control Center personnel, February 1985). Nationwide, an estimated average of 3,093 pesticide poisoning cases were admitted to hospitals each year, from 1974 through 1976, resulting in 40 deaths annually. Two hundred and thirty-two each year were occupational poisonings, with farmers being the most frequently poisoned occupational group, and organophosphates being the most frequently involved pesticides. These figures are thought to be gross underestimates of the actual total number of pesticide injuries and poisonings occurring annually, because of the inefficiency of reporting. II. FUMIGANTS Fumigants are biocides of low molecular weight, which have enormous powers of diffusion and penetration. They are either gases or volatile liquids above 40רF. Fumigants pervade an environment, be it space, soil, or a commodity storage area, from a few release sites. Most fumigants are nonspecific biocides, killing insects, insect eggs, nematodes, microorganisms, weed seeds, weeds, rodents, and even snakes and bats. Some fumigants, such as methyl bromide, are lethal to all plant and animal life and thus are classified as sterilants. Fumigants are formulated and packaged in various ways, as mixtures of liquids, liquified gases, aerosols, crystals, or slow-release tablets (the grain fumigant aluminum phosphide). Formulations often contain mixtures of compounds. This chemically diverse group of pesticides is classified in Table 2. Major agricultural fumigants include phosphine, methyl bromide, carbon tetrachloride, carbon disulfide, and chloropicrin. Registrations of a number of fumigants are being withdrawn mainly because of their potential for leaving residues in treated produce. PLEASE NOTE: THE FOLLOWING TABLE IS WIDER THAN THE SCREEN. USE THE RIGHT ARROW KEY TO VIEW THE RIGHT SIDE OF THE TABLE. TO
PRINT THE ENTIRE TABLE YOU MUST FIRST EXPORT THE TABLE
AND USE A WORD PROCESSOR OUTSIDE THE RETRIEVAL SYSTEM.
Table 1 Respiratory Effects of Fumigants, Cholinesterase Inhibitors, and Paraquat PESTICIDE REPRESENTATIVE POSSIBLE EFFECTS
TYPE COMMERCIAL PRODUCTS USE ON RESPIRATION
FUMIGANTS Methyl bromide. Used to kill insects, ש Irritation
phosphine (from microorganisms, weeds, ש Laryngeal edema
phosphide), chloropicrin rodents in agriculture, in- ש Bronchospasm
(see Table 2 for commercial dustry, homes ש Pulmonary edema
products) ש Respiratory depression
CHOLINESTERASE Parathion (Alleron, Insecticides, with ש Bronchoconstriction
INHIBITORS Paramar, Phoskil), widespread agricultural, in- ש Bronchorrhea
(Organophosphates phorate (Aarimet, dustrial, home use ש Pulmonary edema
and Carbamates) Thimet), fonofos ש Respiratory depression
(Dyfonate), aldicarb and death (due to inactiva-
(Temik), carbofuran tion of acetylcholin-
(Furadan) esterase)
PARAQUAT Paraquat (Crisquat, Herbicide, defoliant, widely ש Upper respiratory tract ir-
Esgram, mixtures used in agriculture and ritation
Weedol, Gramonol, elsewhere ש Following ingestion,
Pathclear) pulmonary fibrosis leading
to death
Table 2 Fumigant Compounds REPRESENTATIVE
CHEMICAL CLASS CHEMICAL COMPOUNDS
HALOCARBONS Methyl bromide (Brom-O-Gas, Kayafume,
Meth-O-Gas)
Chloropicrin (Acquinite, Chlor-O-Pic,
Pic-Clor)
Carbon tetrachloride
Chloroform
OXIDES AND Ethylene oxide (ETO, oxirane)
ALDEHYDES Acrolein (Aqualin)
SULFUR AND Phosphine (aluminum phosphide) (Phostoxin,
PHOSPHORUS Fumitoxin)
COMPOUNDS Carbon disulfide
Sulfur dioxide
Where are fumigants used? Because of the variety of available compounds and target organisms, fumigants are used in nearly every setting: home, industry, and farm. They can be injected into soil or released in warehouses, greenhouses, homes, poultry houses, grain elevators, other buildings with pest infestations, or stores of perishable commodities. Fumigants are applied to stores of grain, cereals, beans, perishables (such as citrus fruits, peaches, and grapes), and numerous other food commodities. Since most are highly toxic, application of many fumigants is restricted to licensed personnel. Agricultural use of fumigants in the Midwest primarily involves grain storage and transport. Most are applied at grain elevators by trained applicators; however, individual farmers occasionally use fumigants to preserve a bin of grain in long-term storage. Occasionally, poultry buildings are evacuated and fumigated to kill lice or other pests. In the Far West and in southern states, agricultural fumigants are used more commonly to preserve perishables in storage and to kill soil nematodes. Vehicles (including ships, trucks, barges, and trains) transporting perishables also are fumigated to destroy insects and microorganisms. Because fumigants are applied throughout the year, human poisoning is possible at any time. When does exposure to fumigants occur? In contrast to most other types of pesticides, most fumigants are restricted to use by licensed applicators, and most poisonings are occupational. Occupational risk groups include manufacturers, structural pest control operators, grain elevator workers, warehouse workers, transport workers (including truckers, sailors, and railroad personnel), commercial agricultural applicators, fruit and vegetable growers, and the occasional farm user. To protect these workers from the highly toxic and volatile products they handle, formulations and application techniques have been developed to contain these compounds and prevent human exposure. (See Fig.3) Grains are mixed with slow-release fumigant tablets (aluminum phosphide) as elevators are filled, or the tablets are injected deep into grain stores. Structures are tightly closed before fumigants are released. They remain closed for a period of hours to days to allow penetration and dissipation, and then are aerated before entering. Soil treatment is accomplished by injecting the chemicals deep into the soil, or treating soil and then covering it to retard fumigant escape; liquids also may be used to drench soil. Nevertheless, exposure has occurred, most commonly through inhalation. Such poisonings have resulted when workers have reentered fumigated structures before they had been adequately ventilated, or when structures or soil have been fumigated but not properly sealed. Fumigants also may escape into the air from the nozzles of soil injection equipment. Fumigants may remain with grain until it is removed from sealed storage areas; these fumigants may pose a hazard if they are allowed to concentrate within an enclosure as they desorb from the grain. Highway spills and other accidents have exposed persons nearby. Occasionally, fumigant liquid has been spilled on the skin. These compounds are rapidly absorbed across the skin, and such exposure can be life-threatening. Several factors make any exposure to fumigants unusually threatening. Some fumigants are colorless and odorless, and thus exposure is not readily detected. (For this reason, chloropicrin or "tear gas" often is mixed with other fumigants to aid detection.) Fumigants may penetrate rubber and plastics of protective clothing, but are excluded by most respirators with cartridges specifically selected for the fumigant in question. A self-contained breathing apparatus also is effective. However, use of a self-contained breathing apparatus can give a false sense of security which could easily be fatal in cases of equipment failure or human error. Thus, the only adequate protection from fumigant absorption is complete avoidance. Toxic effects on humans Fumigants cause more direct and serious injury to the respiratory system, more commonly, than any other class of agricultural chemicals. This injury typically occurs as respiratory tract irritation following exposure through inhalation. Cough, tearing, rhinorrhea, headache, nausea, and dizziness are early symptoms of exposure. Some agents, such as chloropicrin, irritate the upper respiratory tract so severely that a victim is unlikely to inhale enough fumigant to damage lung tissues. Irritants such as sulfur dioxide, acrolein, and chloropicrin may occasionally induce laryngeal edema and bronchospasm. Some other fumigants (methyl bromide, phosphine) are not so irritating to the upper respiratory tissues; these may be inhaled deep into the lungs, injure alveolar tissues, and induce pulmonary edema and death. Other fumigants (carbon tetrachloride, carbon disulfide, acrylonitrile) are less likely to injure the respiratory tract. Several nonrespiratory reactions can be induced by fumigants, with the likelihood and strength of reaction varying with the fumigant. Exposure of liquids to skin or eyes may result in injury ranging from a mild chemical burn and blistering to vesiculation and ulceration and possibly blindness. Depression of the central nervous system can lead to depression or cessation of respiration, unconsciousness, and convulsions. Early manifestations are tremors and drowsiness. Other effects of systemic poisoning include liver and kidney damage (carbon tetrachloride), peripheral neuropathy, and encephalopathy (carbon disulfide). Diagnosis Exposure to fumigants typically can be determined from the patient himself. Although rarely necessary, confirmation of absorption of certain compounds is possible. Certain fumigants also produce characteristic breath odors (e.g. phosphine like garlic or acetylene, cyanide like bitter almonds). At some large medical centers and in some chemical industries, expired air can be monitored for halocarbon absorption, blood tested for bromide concentrations, urine for carbon disulfide, and blood and tissues for cyanide. Treatment There are no specific antidotes for poisoning by fumigants. Treatment must be designed to combat the pathophysiologic effects of the specific fumigant to which the victim was exposed. If pulmonary edema occurs, it must be combatted vigorously: a semirecumbent position, positive pressure oxygen, rotating tourniquets, and other measures commonly are used to control pulmonary edema, whatever the cause. III. CHOLINESTERASE--INHIBITING INSECTICIDES The organophosphate and N-methyl carbamate insecticides poison insects and mammals by inhibiting acetylcholinesterase. Valued because of their rapid degradation in the environment, these compounds have largely replaced the persistent organochlorine insecticides, and today hundreds of products are used to control damaging insects. They are prepared as solutions in petroleum distillates, and then formulated as emulsions, wettable powders, suspensions, dusts, fogs, and granules. Most organophosphorus insecticides have a disagreeable skunk-like odor. Not all carbamate pesticides inhibit cholinesterase; certain thiocarbamate herbicides, for example, do not. They are mild respiratory irritants. These pesticides are listed in Table 3. A listing of representative insecticide products is given in Table 1. Where are these insecticides used? Widely used in homes, industry, and agriculture, organophosphate and carbamate insecticides kill insects and parasites on (and in the intestines of) livestock, poultry, and domestic pets; on forest, ornamental, fruit, and citrus trees; on vegetable and grain crops; on agricultural seeds; in soil (e.g. nematodes); in home flower and vegetable gardens; in houses and commercial buildings, including food storage facilities; and, in the general environment (e.g. mosquito control). A wide variety of insects in various stages of development are affected by these products. Use extends year-round and is worldwide. Most farmers use insecticides, and the majority of modern insecticides are cholinesterase inhibitors. Patterns of insecticide use are moving toward pyrethroids, which have minimal demonstrated toxicity in mammals. When are people exposed? These insecticides pose a threat to many types of users. In reality, the inherent toxicities of various products extend over a wide range, with those used in homes and gardens being least toxic, those used on livestock and pets being of intermediate toxicity, and some of those used to control crop pests being highly toxic. (See Fig. 4) Organophosphates generally cause more protracted poisoning than carbamates. A single drop of the discontinued organophosphate TEPP, absorbed through the eye, is usually fatal. The potential for serious poisonings among agricultural workers is great. These products are effectively absorbed across the skin, through inhalation, and by ingestion. Dermal absorption alone can lead to severe poisonings. The insecticides are applied by farmers in numerous ways: soils are injected, sprayed, or drenched; animals are immersed, powdered, or drenched through pouring; crops are sprayed from the ground or from airplanes. Serious spills are most likely to occur when transferring pesticide products, such as when loading hoppers or spray tanks. Inhalation of aerosolized dusts, dermal absorption from contaminated clothes or skin, or ingestion from contaminated hands are serious threats. Other potentially threatening situations include inhalation of drifting pesticide during application, inhalation of smoke when burning pesticide bags, and skin contamination during repair or calibration of contaminated application equipment. Field workers and harvesters may be poisoned by contact with pesticide residues. Formulators and commercial applicators are two additional major occupational groups at risk. Toxic effects on humans These pesticides inactivate acetylcholinesterase, an enzyme present at nerve synapses and neuroeffector junctions. Acetylocholinesterase is essential to normal transmission of nerve impulses. Inactivation allows accumulation of the neurotransmitter substance acetycholine at cholinergic neuroeffector junctions in glands, visceral smooth, and heart muscles (producing secretory effects, miosis, and bradycardia), at skeletal myoneural junctions (causing weakness and twitching), and in the brain (disturbing sensorium, motor function, behavior, and respiratory drive). Thus, effects on the respiratory system are secondary to systemic poisoning, and include respiratory depression, bronchospasm, and bronchorrhea. The usual cause of death is respiratory depression. Carbamate poisonings are usually less severe and protracted because of the relative lability of the carbamyl-cholinesterase bond. However, respiratory depression and pulmonary edema have occurred; dyspnea is a common symptom of poisoning. Symptoms are not evident before a certain mass of inactivated enzyme has accumulated at synapses. The speed with which this happens, and the severity of the toxic reaction, depend on the amount of pesticide ultimately absorbed, the rate of absorption, the rate at which the specific pesticide is metabolized and excreted from the body, the rate of reactivation of inactivated enzyme (or generation of new enzyme), and the individual's tissue stores of acetylcholinesterase prior to poisoning. Persons with genetically determined low levels (about 3% of the population), advanced liver disease, malnutrition, chronic alcoholism, dermatomyositis, and certain other rare conditions are at additional risk. Continued daily absorption of intermediate doses of these insecticides may lead to an influenza-like illness with anorexia, weakness, and fatigue; certain organophosphates have occasionally induced protracted peripheral neuropathy. Diagnosis ~ Symptoms of acute organophosphate poisonings develop from zero to six (usually less than four) hours after exposure, and include headache, dizziness, weakness, incoordination, muscle twitching, tremor, nausea, abdominal cramps, diarrhea, sweating, blurred or dark vision, confusion, toxic psychosis, and bradycardia. Fasciculations of facial and finger muscles, bradycardia, and miosis may help to differentiate these poisonings from other conditions. Respiratory symptoms include chest pain, rhinorrhea, bronchorrhea, tightness in the chest, wheezing, and productive cough; pulmonary edema may occur. Respiratory depression, together with airway obstruction, may be fatal. Symptoms may lead to misdiagnosis of acute alcoholism, asthma, heat prostration, influenza, exhaustion, pneumonia, encephalitis, or congestive heart failure. Carbamate poisonings frequently result in diarrhea, nausea, vomiting, abdominal pain, profuse sweating, rhinorrhea, salivation, blurred vision, weakness, and labored breathing, and may lead to respiratory depression or pulmonary edema. Diagnosis is confirmed by depression of plasma pseudocholinesterase and/or RBC acetylcholinesterase activities by 25% or more from preexposure levels. In the absence of preexposure measurements, activities below the minimum population norm probably indicate significant absorption. Depressed blood cholinesterases are found following absorption of considerably smaller dosages than those required to cause symptoms and signs. Blood cholinesterase monitoring is widely practiced among seasonally exposed workers. With organophosphate poisoning, depressed levels usually are evident within 0 to 24 hours of significant absorption, and persist up to a few weeks or months. Following carbamate absorption, enzyme activities revert to normal in a few minutes or hours, and thus the finding of normal blood cholinesterase levels does not rule out poisoning. Treatment~ Mild to moderately severe poisonings, wherein the patient remains conscious and cardiopulmonary function is not seriously impaired, can usually be treated by repeated intravenous administration of atropine, the specific antidote, for 2 to 12 hours. In this period of time, the toxicant is metabolized and excreted, and enzyme is regenerated. Complete decontamination (removal of contaminated clothes, bath, shampoo) is essential. The patient must not be released until he or she remains symptom-free after the atropine effect has worn off. Obtunded and unconscious patients must be treated vigorously with the following steps: ש Clear the airway; give positive pressure oxygen. ש Give atropine intravenously, slowly, in sufficient dosage to produce atropinization (dilated pupils, tachycardia, dry mouth, and dry lung bases). Doses of several milligrams may be necessary. ש Decontaminate: remove contaminated clothing, cleanse contaminated skin and hair. If pesticide was swallowed, evacuate the stomach; give activated charcoal and saline cathartic. ש If respiratory drive is depressed in organophosphate (not carbamate) poisonings, give pralidoxine (protopam) intravenously, slowly. ש Continue atropine intravenously as long as necessary at whatever dose is necessary to prevent reappearance of rales in the lungs or other cholinergic signs. IV. PARAQUAT A widely used herbicide, paraquat (1, 1-dimethyl -4, 4'-bipyridilium dichloride) rapidly kills many broadleaved plants and grasses on contact. Applied in aqueous solution as a spray, this herbicide is used in many agricultural situations. Both paraquat and its close relative, diquat, are highly toxic to humans; however, only paraquat has serious effects on the respiratory system. Where is paraquat used? Paraquat is used throughout the country in numerous agricultural and commercial settings, both singly and mixed with other herbicides. Depending on its intended purpose, it can be applied any time throughout the growing season. Sale and use of concentrated paraquat solutions is legally restricted to certified applicators who are commercial applicators and licensed farmers. In recent years, paraquat has found widespread acceptance by farmers as a " burndown" agent in no-till or minimum-tillage programs, where it is sprayed on to kill vegetation in a field before crop emergence. Paraquat is used for weed and grass control on plantations growing nut trees, bearing and nonbearing fruit trees, and ornamental trees. It is applied on fruit and vegetable croplands; for range improvement; for weed and grass control along highways and rights-of-way; and for grass seed preparation. Paraquat efficiently defoliates cotton plants and desiccates soybeans and potato vines prior to harvest. In warmer climates, it is applied under several tropical crops. Inactivation by adsorption occurs as soon as it contacts soil, eliminating the problem of a "carryover" herbicidal effect. When does exposure to paraquat occur? Health problems can result from contact with or inhalation of the spray or concentrate. However, the most serious threat is accidental or suicidal ingestion of the concentrate. Unfortunately, this has occurred occasionally, mainly in farm families. Commercial applicators are cautioned to wear full protective equipment (including proper gloves, shoes, goggles, respirator, and overalls or rubber suit) whenever working with paraquat. Occupational exposure can occur when these precautions are not taken, especially when transferring the compound from one container to another. A person also can be exposed to spills, or be caught in spray or drift. Occupational exposure has resulted primarily in topical injury, although there have been a few poisonings when careless work practices have allowed paraquat concentrate to be absorbed through ulcerated skin. Nine-tenths of all deaths from ingestion have been suicidal. Toxic effects on humans Topical exposure to paraquat concentrate or spray causes injuries, but these are not life threatening: irritation or fissuring of hand skin, cracking, discoloration or loss of fingernails, conjunctivitis or protracted corneal opacification, irritation of the nose and throat, and sometimes nosebleed. Ingestion of paraquat, on the other hand, frequently is fatal, causing death by inducing pulmonary fibrosis. (See Fig. 5) Following ingestion of paraquat (in some cases, reportedly no more than a teaspoon of the concentrate), the mouth and GI tract become inflamed and sometimes ulcerated, leading to pain, vomiting, and diarrhea. These reactions may be mild, even when the amount of paraquat ingested is sufficient to cause death. Once absorbed, paraquat damages parenchymal cells of the liver and tubule cells of the kidney. The patient usually survives these injuries. In the meantime, however, paraquat is actively concentrated in the pneumocytes of lung tissues, a delayed and poorly understood response that appears almost always to be irreversible. These cells die, and 4 to 14 days after ingestion, pulmonary fibrosis ensues. A few victims have survived, but death through asphyxiation usually results. In a few cases, protracted pulmonary edema and myocardial injury have occurred in the course of poisoning. Diagnosis Presence and quantity of ingested paraquat in blood and urine can be determined at certain toxicological laboratories (call your poison control center), and at the Chevron Environmental Health Center. Symptoms of ingestion of a toxic dose include burning pain in the chest (esophagitis) and abdomen, nausea, vomiting, and diarrhea (1-4 days after ingestion); indications of renal and hepatic insult such as elevated BUN and creatinine, oliguria, and jaundice (24-72 hours after ingestion); and appearance of pulmonary symptomatology. Cough, dyspnea, and tachypnea (usually 72-96 hours, but sometimes up to 14 days, after ingestion) are followed by progressive cyanosis, reflecting pulmonary fibrosis. In occasional cases, production of copious watery sputum indicates pulmonary edema. Treatment Skin contaminated by paraquat should be vigorously washed with water. If paraquat has contacted the eye, it should be flushed with clean water for 10 to 15 minutes. An opthalmologist should be consulted. Ingestion of paraquat represents a life-threatening emergency. If a substantial amount was swallowed less than 30 minutes before presentation, the stomach should be evacuated. A slurry of bentonite or activated charcoal should then be instilled as promptly as possible, and in as large a quantity as the patient can tolerate. If more than 30 to 45 minutes has elapsed since paraquat ingestion, omit stomach evacuation and give the adsorbent orally. The object should be to fill the entire gastrointestinal tract with bentonite or activated charcoal, thus limiting absorption. Once this has been accomplished, a saline cathartic should be administered. When catharsis is established, more bentonite should be administered. The Chevron Environmental Health Center will monitor blood and urine for absorbed paraquat, and advise as to subsequent treatment. Oxygen should not be administered to persons who have swallowed paraquat. Oxygen accelerates the injury to lung tissue induced by paraquat. If significant amounts of paraquat have been absorbed, hemoperfusion may be life-saving. This treatment ordinarily must be administered at a tertiary care hospital. V. ADDITIONAL FARM CHEMICALS INJURIOUS A large number of pesticides affect the respiratory system, but injury is limited to irritant effects that are rarely life threatening, or poisonings occur only infrequently for a variety of reasons. These pesticides are listed (along with their uses and the injury they may cause) in Table 3. When using this table, please realize that even if respiratory effects are minor, these substances may be major toxicants to other organ systems. One additional agricultural chemical threatens the respiratory system: anhydrous ammonia. (See Big. 6) Injected into soil throughout the U.S. in spring or fall, it is the most commonly used fertilizer today. Because of its low temperature as it escapes from orifices, its storage under very high pressure, its extraordinary affinity for water, and the high pH and corrosive power of the strongly alkaline hydrated form, anhydrous ammonia is capable of causing severe tissue damage. When inhaled, the ammonia dissolves in the mucous fluids of upper airways, and becomes a potent, severe irritant that occasionally even induces laryngospasm. Exposure usually is limited to these upper airways. However, massive exposure forcing inhalation deep into the lungs produces severe inflammation at all levels of the respiratory tract, and even pulmonary edema. This exposure could occur if large amounts of ammonia were released in a confined space. However, it is unlikely in a farm setting. Anhydrous ammonia also causes topical injury by freezing and desiccating tissues, and inducing severe alkali burns. If sprayed into the eyes, it penetrates the cornea and elevates pH to damaging levels in a few seconds, causing full or partial blindness. Eye exposure demands immediate and extended flushing with water; goggles should always be worn whenever working around anhydrous ammonia. Table 3 Respiratory Effects of Additional Pesticide Products ALIPHATIC ACIDS Representative Commercial Products:
Dichloropropionic acid
Use:
Herbicide
Effects on Respiratory Function:
Irritant
ALUMINOFLUORIDE SALT Representative Commercial Products:
Cryolite
Use:
Insecticide
Effects on Respiratory Function:
Mild irritant
ANTU Representative Commercial Products:
Krysid
Use:
Rodenticide
Effects on Respiratory Function:
If ingested, may cause dyspnea, cyanosis, rales,
pulmonary edema
Additional Comments:
Only one human poisoning known, resulting from large
suicidal dose. Less toxic than other rodenticides.
ARSENICALS Representative Commercial Products:
DSMA, MSMA, arsenic acid
Use:
Herbicide; crab grass control, particularly
Effects on Respiratory Function:
Subacute repeated intake causes upper respiratory
irritation, rhinorrhea. Excessive inhalation of dusts
can rarely cause bronchitis, pneumonia, increased
probability of lung cancer.
Additional Comments:
Widely used
BENZONITRILES Representative Commercial Products:
Chlorothalonil
Use:
Fungicide
Effects on Respiratory Function:
Moderate irritant, possibly sensitizer
BUTYL PHOSPHOROTHIOATES Representative Commercial Products:
Merphos, DEF, FOLEX
Use:
Herbicide
Effects on Respiratory Function:
Minor irritants
Additional Comments:
Produces extremely offensive butylmer-captan odor.
Moderate systemic toxicity.
CARBAMATES (noncholinesterase inhibiting) Representative Commercial Products:
Benomyl, chlorpropham
Use:
Herbicide, fungicide
Effects on Respiratory Function:
Mild irritants
Additional Comments:
Low systemic toxicity
CARBANILATE Representative Commercial Products:
Barban
Use:
Selective herbicide
Effects on Respiratory Function:
Potent sensitizer and irritant to skin and respiratory
tract
Additional Comments:
Used in western states only
CHLOROACETANILIDES Representative Commercial Products:
Propachlor, alachlor
Use:
Herbicide
Effects on Respiratory Function:
Irritant
Additional Comments:
Propachlor is a dermal sensitizer
CHLOROPHENOXY COMPOUNDS Representative Commercial Products:
2,4-D, 2,4,5-T, silvex, dicamba. Multiple salts and
esters are used.
Use:
Herbicides; formulated in various concentrations and
combinations into hundreds of weed control products.
Effects on Respiratory Function:
Moderate irritant to skin and respiratory tract. In the
U.S., 2,4,5-T products now used for rice and brush
control only
COPPER SALTS AND ORGANIC COMPLEXES Representative Commercial Products:
Citcop emulsifiable liquid copper fungicide
Use:
Fungicide
Effects on Respiratory Function:
Irritant
Additional Comments:
Widely used
DIATOMACEOUS EARTH Representative Commercial Products:
Diatomite, infusoral earth
Use:
Insecticide
Effects on Respiratory Function:
Can cause pulmonary granulomatosis
Additional Comments:
Hazardous mainly to producers
DITHIOCARBAMATE Representative Commercial Products:
Thiram
Use:
Fungicide
Effects on Respiratory Function:
Irritant. Inhalation may result in nasal stuffiness,
cough, (rarely) pneumonitis. Ingestion of large amounts
may lead to respiratory paralysis.
Additional Comments:
Substantial absorption of pesticide and ingestion of
alcohol can lead to "Antabuse" reaction: nasal
congestion, labored breathing, flushing, hypotension
ENDOTHALL Representative Commercial Products:
Endothal turf herbicide
Use:
Herbicide
Effects on Respiratory Function:
Irritant. Ingestion can lead to respiratory depression.
Additional Comments:
Widely used in agriculture
HALOGENATED URACILS Representative Commercial Products:
Bromacii, terbacil
Use:
Herbicide
Effects on Respiratory Function:
Irritant to respiratory tract and skin
METALLO ETHYLENE BIS DITHIOCARBAMATES Representative Commercial Products:
Maneb, zineb, dithane
Use:
Fungicides, sometimes combined with thiram and inorganic
salts of copper, manganese, zinc
Effects on Respiratory Function:
Mild irritant
Additional Comments:
Degrade to ethylene thiourea
NICOTINE SULFATE Representative Commercial Products:
Black Leaf 40
Use:
Insecticide
Effects on Respiratory Function:
Can cause respiratory depression or arrest
Additional Comments:
Widely used, highly toxic
ORGANOCHLORINES (SOLID) Representative Commercial Products:
DDT, dieldrin, aldrin, chlordane, toxaphene,
methoxychlor, perthane
Use:
Insecticide or acaricide, excepting HCB (a fungicide);
ingredients of various home, garden, agricultural and
structural pest control products.
Effects on Respiratory Function:
At high dosage, respiratory depression and convulsions
interfere with respiration
Additional Comments:
Stable persistent compounds; uses now limited by law
PENTACHLOROPHENOL Representative Commercial Products:
Penta, PCP
Use:
Herbicide, defoliant wood preservative, germicide,
fungicide, molluscicide, often one ingredient of
formulated mixtures for any of these uses.
Effects on Respiratory Function:
Irritant. At high dosage, increases metabolism,
respiration and heart rate
Additional Comments:
Ubiquitous substance. Small amounts present in human
blood and urine
PHOSPHONOMETHYL GLYCINE Representative Commercial Products:
Roundup
Use:
Herbicide
Effects on Respiratory Function:
Mild irritant
Additional Comments:
Extensively used; minimal toxicity
PICOLINIC ACID DERIVATIVE Representative Commercial Products:
Picloram
Use:
Herbicide
Effects on Respiratory Function:
Irritant to skin and respiratory tract
Additional Comments:
Widely used
PYRETHRINS, PYRETHROIDS Representative Commercial Products:
allethrin (Pynamin), fenvalerate (Belmark, Pydrin),
permethrin (Ambush, Pounce), resmethrin (Synthrin,
Chrysron), tetramethrin (NeoPynamin)
Use:
Insecticide, formulated into hundreds of products
Effects on Respiratory Function:
Most are minor irritants although some are strong
irritants
Additional Comments:
Crude pyrethrum includes potent irritants and sensitizers
RH-787 Representative Commercial Products:
Vacor, DLP-787
Use:
Rodenticide
Effects on Respiratory Function:
If ingested, may cause respiratory failure, acute and
chronic neurologic impairment
Additional Comments:
Highly toxic. No longer on the market, but existing
stores pose continued threat
SABADILLA Representative Commercial Products:
Pearson's Red Devil Dust
Use:
Insecticide
Effects on Respiratory Function:
Severe respiratory irritant
Additional Comments:
Limited use
SODIUM FLUOROACETATE Representative Commercial Products:
Ten-eighty
Use:
Rodenticide
Effects on Respiratory Function:
If ingested, a convulsant; causes respiratory depression,
contributing to death
Additional Comments:
Extremely toxic; use closely regulated
STRYCHNINE Representative Commercial Products:
Centerchem Strychnine Alkaloid
Use:
Rodenticide
Effects on Respiratory Function:
If ingested, causes convulsive interference with
pulmonary gas exchange and depression of respiration.
Additional Comments:
Extremely toxic convulsant
SULFUR (elemental) Representative Commercial Products:
Superior's Wettable Sulfur
Use:
Miticide, fungicide, bacteriocide
Effects on Respiratory Function:
Strong respiratory irritant
Additional Comments:
Low systemic toxicity. Widely used
THIADIAZIN (OL) Representative Commercial Products:
Basagran
Use:
Herbicide, fungicide
Effects on Respiratory Function:
Moderate irritant
Additional Comments:
Widely used
TIN (organic) Representative Commercial Products:
Fentin, Batasan
Use:
Fungicide
Effects on Respiratory Function:
Irritant
Additional Comments:
Widely used
UREA DERIVATIVES Representative Commercial Products:
Monuron, diuron, linuron
Use:
Herbicide
Effects on Respiratory Function:
Moderate irritant to skin and respiratory tract
Additional Comments:
Widely used on rights-of-way
YELLOW PHOSPHORUS Representative Commercial Products:
AFC Phosphorus Paste
Use:
Rodenticide
Effects on Respiratory Function:
Severe mucosal irritant
Additional Comments:
Extremely toxic; little used in U.S.
ZINC PHOSPHIDE Representative Commercial Products:
Phosvin, Zinc-tox
Use:
Rodenticide
Effects on Respiratory Function:
If ingested, causes chest tightness, dyspnea, cough,
production of frothy sputum, reflecting pulmonary edema
Additional Comments:
Extremely toxic; little used in U.S.
VI. PREVENTION OF PESTICIDE--INDUCED RESPIRATORY PROBLEMS Adherence to six general rules will help prevent pesticide-associated respiratory problems. These rules (discussed below) are:
Safe storage and usage includes storing pesticides in their original container, with labels intact, under lock and key. Choosing the proper pesticide, reading and following directions with care, applying the proper quantity to fields on calm days, handling all pesticides in well ventilated areas, keeping application equipment in good working order, and properly disposing of empty containers all are important safety practices for farm managers, and should be taught to all farm workers handling pesticides. (See Fig. 7) When fumigation of farm-stored grain becomes necessary, a professional fumigator should be hired. Avoiding areas for designated time periods ("reentry intervals") following spraying is the only way to avoid contact with organophosphate and other insecticide residues on foliage and fruit. Avoidance also is the only effective technique for preventing fumigant poisonings: fumigants must not be released until structures to be treated have been vacated; guards and warning signs should be posted around treated buildings. Slow release pellets and more efficiently enclosed application systems assist in this practice. Farmers can avoid fumigants by eliminating the need for their use (through storing good quality, dry grain in clean storage areas, which are monitored and aerated when necessary). Good personal hygiene requires frequent showering, hand washing, shampooing, and changing of work clothes whenever handling pesticides, especially before eating (to avoid ingestion) and after work. Contaminated clothes should be changed immediately; this is imperative when working with organophosphate insecticides or other substances that can be absorbed rapidly through skin. Work clothes should not be brought into living areas, and may require several launderings to rid them of residues. Spills should be cleaned up immediately, as should contaminated skin. Since cuts, abrasions, or dermatitis increase the absorption of pesticides, injured skin may require special protection. Personal protective devices include rubber suits, aprons, hats, boots, gloves, goggles, and face shields. (See Fig. 8) Inhalation of some pesticide dusts can be reduced to a minimum by using a disposable respirator (dust mask) or reusable mechanical filter respirator, but vapors require a chemical cartridge respirator with cartridge appropriate to the specific vapor. Vapor characteristics are printed on pesticide labels or material safety data sheets. All gear must be kept in good repair and scrupulously clean; respirator filters should be changed frequently. Protective gear is recommended when handling paraquat and cholinesterase-inhibiting insecticides even though this gear is hot and cumbersome. With fumigants, extreme care must be used to follow manufacturers' recommendations regarding use of the product and personal protective equipment. Precise recommendations are included with the fumigants. Failure to follow these recommendations or incorrect use of personal protective equipment can be deadly, since there are limits to the protection afforded by even self-contained apparatus, and some fumigants can penetrate protective clothing. Workers regularly exposed to highly toxic pesticides should be periodically examined by physicians. Some states require periodic measurement of blood cholinesterase activity in workers who regularly apply organophosphates. The federal government regulates many aspects of pesticide use, such as labeling containers, transporting and storing pesticides, establishing reentry intervals, and restricting application of certain pesticides to licensed, trained personnel. These regulations should be rigorously adhered to. However, physicians should be aware that farm supply companies do not always follow them, and that restricted pesticides may be sold to noncertified operators, extending the risk of exposure to any farm worker. i תתתתתתתתתתתתתתתתתתתתThe National Dairy Database (1992)תתתתתתתתתתתתתתתתתתתת תתתתתתתתתתתתתתתתתתתתת\NDB\OCCSAFE\TEXT2\OF200900.TXTתתתתתתתתתתתתתתתתתתתתתת %f TITLE;APPLIED AGRICULTURAL CHEMICALS %f COLLECTION;FARM AND OPERATOR
SAFETY |
