Agrochemicals in peri-urban spraying and their effect on human health

Agrochemicals in peri-urban spraying and their effect on human health

By Jorge Kaczewer

Due to the vast amount of pesticides present in the environment and the vast amount of possible "target" tissues and final destinations that often differ depending on the stage of life in which the exposure occurs, the need to abandon the conditioning of any protective measure to the scientific demonstration of the safety of these substances based on the hazard criteria recommended by the WHO.

1. Introduction

In the Argentine Republic, there is a growing controversy regarding the long-term toxic effects of human exposure to agrochemicals for periurban aerial or terrestrial application. The extensive problem of pesticide dispersion in the air affects a diversity of communities throughout the country. In response to the request for advice from members of the Deliberative Councils and NGOs from various locations in the interior of Argentina, this paper explores recent scientific evidence and technical advances that reveal underestimations of potential negative health impacts and inadequacies of the protective value of strategies and local chronic toxicity assessment policies for licensed and illegally used pesticides. Both the review of various studies that have already documented health problems linked to this type of exposure, as well as the regulatory and productive alternatives later suggested, try to promote a precautionary attitude, less based on speculations about how much damage or risk a community must face in order to of progress and economic growth and more in guaranteeing its effective protection against pollution and exposures in the agro-urban interface.

2. Underestimation of the impact of exposure to pesticides on human health.

We know that agrochemicals produce acute and chronic toxic effects.
Long-term (chronic) impacts on human health can result both from a single exposure to high doses of pesticides, as well as from exposures over an extended period of time, even if the exposure levels are low. Although people may not know they were exposed, consequent problems can emerge many years after chronic exposure to low doses of pesticides.

Scientific advances in the investigation of the consequences of chronic poisoning are beginning to provide a level of information that until recently was inconceivable, especially regarding our ability to demonstrate exposure. Advances in analytical laboratory equipment and research procedures have facilitated the detection of very low concentrations of pesticides and their metabolites in almost all types of human tissue. From routinely detecting parts per million (milligrams per kilogram) and more recently as low as parts per trillion (peak grams per kilogram), some labs can now measure concentrations as low as parts per quintillion (femtograms per kilogram). The development of non-invasive sampling methods, such as the detection of pesticides and their metabolites in urine, made it possible to monitor pesticide exposure in infants and children. Today we can affirm with the utmost certainty that every child on the planet is exposed to pesticides from conception, throughout their gestation and until breastfeeding, regardless of their place of birth.

On the other hand, the quality and quantity of data on the risk posed to humans by individual pesticides vary considerably. Unlike obvious neonatal defects, most developmental effects cannot be discerned at birth or even later in life. In contrast, brain and nervous system disorders are expressed in terms of how an individual behaves and functions, which can vary considerably from birth and through adulthood.

Due to the vast amount of pesticides present in the environment and the vast amount of possible "target" tissues and final destinations that often differ depending on the stage of life in which the exposure occurs, the need to abandon the conditioning of any protective measure to the scientific demonstration of the safety of these substances based on the hazard criteria recommended by the WHO.

Functional deficiencies are not “on” and “off” conditions, but rather cover a spectrum that starts from the inconsistent, passes through the very mild, and goes to the very severe or totally debilitating. Consequently, it is difficult to quantify the degree of negative impact on neurodevelopment. Therefore, we face not only limitations in research techniques, but also the intrinsic incompleteness of all scientific evidence that does not include these findings when establishing criteria for the determination of safety. Because, if we do, our regulatory approach should be much more rigorous to protect human and environmental health in the absence of complete scientific certainty.

Neither the current nor the proposed strategies protect public health or the environment. To place pesticides in the different ranges of danger, the WHO is based on the toxicity of the pesticide, measured through Lethal Dose 50 (LD50). This parameter is defined as a statistical value of the number of milligrams of the poison per kilo of weight, required to kill 50% of a large population of exposed laboratory animals. It is usually expressed as a number, but in some cases it can be a range. The LD50 in the case of pesticides must be determined for the different routes of exposure (oral, dermal and respiratory) and in different species of animals. LD50 is usually expressed orally and for rats (UNEP, 2000).

The LD50 is exclusively related to the acute toxicity of pesticides. It does not measure its chronic toxicity, that is, that which arises from small daily exposures to the pesticide over a long period. In other words, a product with a low LD50 can have serious chronic effects due to prolonged exposure, such as causing cancer. Furthermore, in real life no one is exposed to a single pesticide but to several, and this is not covered by the LD50 either. In this case, the additive, synergistic or antagonistic effects that occur in our body when exposed to more than one pesticide must be considered (Albert, 2000).

The LD50 also does not fully reflect the short-term effects since it does not give an idea of ​​what percentage of the population under study felt dizzy or with coordination problems.

In the event that a pesticide causes damage to vital organs, has very marked cumulative effects, is particularly dangerous or allergenic, the WHO makes adjustments to its classification, placing it in a category that indicates greater danger. In this way, the classification is based on the LD50 of pesticides, but does not exclusively use this parameter (UNEP, 2000).

When the pesticide is prepared as an aerosol or fumigant gas, the criterion used to calculate the LD50 is the concentration level in the air.


We know that many cancers are caused by multiple genetic mutations in combination with damage to parts of the immune system, which normally destroy cancer cells, and exposure to both certain types of toxic substances and one or more types of viruses. For example, this conception applies especially to the case of lymphoma. The evidence gathered over the last two decades led to the suspicion that various combinations of these factors are involved in the genesis of lymphoma. The studies seem to involve a particular class of substances, chlorophenols. Chlorophenols are chlorine-containing substances that include dioxins, PCBs, DDT, and “phenoxy” herbicides, including 2,4-D and 2,4,5-T. A recent review of 99 human and one pet (dog) studies conducted by the Lymphoma Foundation of the United States (Susan Osburn, RESEARCH REPORT: DO PESTICIDES CAUSE LYMPHOMA? Http:// research / research report / rr_2000.pdf) found that 75 out of 99 human studies indicate a connection between pesticide exposure and lymphomas. And the dog study indicated a double chance of lymphoma after exposure to the popular 2,4-D herbicide.

Although this information is not enough to conclude that pesticide exposure causes cancer, we also know that science can never prove beyond a possible doubt that X causes Y. When it comes to toxic substances, humans and ecosystems, the complexity is enormous. , many important tools of science are still in full development and there is always more what is not known than what is. We must admit that science may never provide definitive answers to the most important questions we ask ourselves. But still, as individuals and as a human society, we need answers. At the very least, by reading these reviews we must decide whether we want to reduce our exposure to pesticides and question the alleged right of pesticide manufacturers to spread their products over our soil, water, air, and food.

Meanwhile, several very serious studies detected that exposure to agrochemicals has been associated with an increased risk of suffering from certain types of cancer among farmers and other agrochemical applicators (1-3). This has also been observed among families of rural workers and the general population living in agricultural areas (1, 2, 4–7), despite the fact that specific exposures were not evaluated in most studies.

(8). Table 1. Associations between different agrochemicals and different types of cancer



2,4-D, MCPA

Non-Hodgkin's lymphoma, soft tissue sarcoma, prostate carcinoma.
ORGANCHLORINATED INSECTICIDESLeukemia, non-Hodgkin's lymphoma, soft tissue sarcoma, pancreas, lung, breast.
ORGANOPHOSPHORATE INSECTICIDESNon-Hodgkin's lymphoma, leukemia.

Neurotoxicity :

Chronic exposure to agrochemicals may contribute to the increasing prevalence in the West of attention deficit hyperactivity disorder, autism, and associated neurodevelopmental and behavioral problems. There is exquisite embryonic and fetal sensitivity to any thyroid disturbance and sufficient evidence of intrauterine human exposure to contaminants that can interfere with the thyroid.

Since we may never be able to link prenatal exposure to a specific chemical with damage to the neurodevelopmental process in humans, alternative models in which associations are found between exposure to a specific chemical or types of substances should be explored. and developmental difficulties in laboratory animals, wild animals, and humans.

Definition of neurotoxicity: Neurotoxicity is defined as adverse effects on the structure or functioning of the central and / or peripheral nervous system resulting from exposure to chemical substances. Neurotoxic substances can cause morphological changes that lead to widespread nerve cell damage (neuronopathy), injury to axons (axonopathy), or destruction of myelin sheaths (myelinopathy). It has already been widely proven that exposure to certain agricultural and industrial toxic substances can damage the nervous system, with consequent neurological and behavioral damage. Symptoms of neurotoxicity include muscle weakness, loss of sensation and motor control, tremors, impaired cognition, and disorders in the functioning of the autonomic nervous system.

The central nervous system (CNS) is made up of the brain and spinal cord and is responsible for the higher functions of the nervous system (conditioned reflexes, learning, memory, judgment, and other functions of the mind). Chemicals toxic to the CNS can induce confusion, fatigue, irritability, and other behavioral changes, as well as degenerative brain diseases (encephalopathy).

The peripheral nervous system (PNS) includes all the nerves outside the brain or spinal cord. These nerves carry sensory information and motor impulses. Damage to nerve fibers in the PNS can disrupt communication between the CNS and the rest of the body. Substances that affect the PNS can cause symptoms such as lower limb weakness, paresthesias, and loss of coordination. Exposure to these toxins can also trigger a wide spectrum of adverse effects on the nervous system. It can alter the propagation of nerve impulses or the activity of neurotransmitters and cause a disruption in the maintenance of myelin sheaths or protein synthesis.

Neurotoxicity of the most used pesticides in Argentina:

- Most frequent neurotoxicity symptom: myotonia (the muscles cannot relax after their voluntary contraction).
- Peripheral neuropathy: unusual sensations, numbness and pain in arms and legs, gait disorders. Symptoms appear late and recovery may be incomplete. Wide variability in individual susceptibility to neuropathy.
- Behavioral disorders: changes in the daily rhythm of activity related to alterations in the brain level of the neurotransmitter serotonin and its metabolites.
- Neurotoxicity in children: reduction in brain size, alterations of components of the neuronal membrane. Infant exposure through breast milk: lower production of myelin (a fundamental component of the sheaths that line neuronal processes).
- At high doses, damage to the blood-brain barrier, allowing 2-4-D to penetrate into brain tissues.

Over the past 15 years, an Argentine research team produced a series of reports on 2,4-D. This team found that exposure during lactation to the herbicide 2,4-DBE (the butyl ester of 2,4-D) can alter brain production of 5-HT and its metabolite, 5-hydroxy-indoleacetic acid (5- HIAA), in adulthood (9).

The concentrations of both dopamine and serotonin changed transiently if the animals were exposed only throughout birth (399 µg / kg bw / day from the sixth day of gestation -GD6- until birth; 15 days) and permanently if it was administered to the offspring through breastfeeding as well as from GD6 to weaning (30 days). Duffard et al. (10) and Rosso et al. (2000) (11) found that 2,4-D interfered with myelination in the brain as a result of lactational exposure. This resulted in changes in behavior patterns that included apathy, reduced social interaction, repetitive movements, tremors, and immobility in infants exposed to 2,4-D (13,14). They also found that the serotonergic and dopaminergic effects occurred during postnatal brain development, somewhat similar to the effects of PFC. Bortolozzi et al. (14) and Evangelista de Duffard et al. (15) also found 2,4-D in the breast milk of 2,4-D-fed mothers and in the stomach, brain, and kidney contents of 4-day-old pups (Sturtz et al. 2000) (16 ).


The neurotoxicity of endosulfan is known. It blocks inhibitory receptors in the central nervous system, is a disruptor of ion channels, and destroys the integrity of nerve cells. Its acute toxic effects include dizziness and vomiting, hyperactivity, tremors, lack of coordination, seizures, and loss of consciousness. Chronic exposure can result in permanent damage to the nervous system manifested as various neurological diseases: cerebral palsy, epilepsy, mental retardation, brain cancer, etc. This insecticide is also a hormonal disruptor, being able to generate maternal exposure during pregnancy and neonatal and infant exposure through the presence of endosulfan in breast milk, various neurological effects of endocrine disruption such as mental retardation and, in later stages of life , behavioral disorders.

Cypermethrin and other synthetic pyrethroids

They are neurotoxic that act on the basal ganglia of the central nervous system, by prolonging sodium permeability during the recovery phase of the action potential of neurons, causing repeated discharges. These discharges can in turn cause the nerve to release the neurotransmitter acetylcholine, which stimulates other nerves. Some of them also affect the permeability of the membrane to chloride, acting inhibitory on type A receptors for gamma-aminobutyric acid, a fact that causes excitability and seizures.

Additionally, cypermethrin inhibits the incorporation of calcium in the nerves and inhibits mono-amino-oxidase, an enzyme that degrades neurotransmitters. It also affects an enzyme foreign to the nervous system, adenosine triphosphatase, involved in cellular energy production, transport of metal atoms, and muscle contraction. In all cases, the clinical picture is similar. Symptoms of human exposure include facial paresthesias, dizziness, headaches, nausea, anorexia, fatigue, and loss of bladder control. With increased exposure, symptoms include muscle contractures, vertigo, coma, and seizures.


Although glyphosate toxicity is not characteristically neurotropic, there is a history of neurotoxic adverse effects caused by the use of commercial herbicides based on this herbicide: After a fumigation accident in Brazil, a 54-year-old man suffered a syndrome Parkinsonian whose symptoms began one month after exposure (Barbosa, 2001) On the other hand, isobutane, an “inert ingredient” in commercial glyphosate-based formulas, has a clear neurotoxicity: It causes a depression of the nervous system.


The herbicide atrazine attaches to areas of the hypothalamus, a brain region involved with the regulation of levels of stress and sex hormones

Glufosinate ammonium

Glufosinate is a herbicide that kills plants by inhibiting the activity of an enzyme, glutamine synthetase, involved in the detoxification of ammonia and in the metabolism of amino acids. Glufosinate inhibits the same enzyme in mammals and reduces glutamine levels in the liver, brain, and kidneys.

In laboratory animals, exposure to this herbicide is irritating to the eyes and skin. In rats, skin exposure increased their aggressive behavior. Its intake in feeding studies produced, in addition to various harmful impacts on other organ systems, a decrease in the weight of the thyroid in dogs.

Endocrine disruption

Over the past decades, we have accumulated a large body of scientific evidence showing that some chemicals in food, water and the environment can mimic hormones and alter the development of fish, birds and mammals, including their development sexual. In some cases, the effects on wildlife were dramatic: male fish exposed to DDT and other chlorinated compounds developed female sex organs. Knowing that humans and animals share the same basic mechanisms of growth and development, more and more scientists are concerned about the possibility that humans may already be affected without recognizing it.

The following is a list of chemicals considered endocrine disruptors:

DDT and substances produced by its degradation
DEHP di (2-ethylhexyl) phthalate
HCB hexachlorobenzene
Lindane and other similar hexachlorocyclohexanes
Synthetic pyrethroids
Triazine-type herbicides
EBDC fungicides
PCB's and other congeners
2,3,7,8-TCDD and other dioxins
2,3,7,8-TCDF and other furans
Tributyltin and other organotin compounds
Alkylphenols (detergents and antioxidants present in modified polystyrene and PVC
Soy products (isoflavones)
Food products for laboratory animals and pets.

It is already known that all these substances, the majority introduced into the environment as a result of human activity and others of natural origin, exert harmful effects on the health of animal species. Some examples of observed effects are: thyroid dysfunction in birds and fish; decreased fertility in birds, fish, oysters and mammals; reduced successful mating in birds, fish and turtles; gross congenital malformations in birds, fish and turtles; metabolic abnormalities (disturbance or abnormality of energy management, tissue production, or metabolic waste management) in birds, fish, and mammals; behavioral disorders in birds; overculinization and feminization in fish, birds, and male mammals; defeminization and masculinization of female fish and birds; and compromise of the immune system of birds and mammals.

The type of effect varies according to the species and the causative substance. However, four characteristic general patterns were detected:

1- The substances in question exert totally different effects on the adult organism than those produced in the embryo, the fetus or the individual in the perinatal stage.

2- The effects are manifested much more frequently in the offspring than in the exposed parent.

3- The period in which the developing organism undergoes exposure is crucially determinant of the characteristics and the future potential of the effects.

4- Although critical exposure occurs during embryonic development, the effects may not manifest until the organism is mature.

Some disorders of human development are seen in adults descended from parents exposed to synthetic hormonal disruptors (agonists and antagonists) present in the environment.
Currently, the concentrations of various synthetic hormonal agonists and antagonists measured in the tissues of the human population of large cities coincide with the dose ranges within which effects were found in populations of wild animals. If the environmental burden of endocrine disruptors is not reduced and controlled, it can lead to large-scale dysfunctions in the human population. The spectrum and potential for harm to wildlife and the human population is enormous because of the likelihood of repeated and / or constant exposure to numerous disruptive chemicals. According to current predictive models, both exogenous and endogenous estrogens and androgens can alter the development of brain function. Any disturbance of the endocrine system of a developing organism can generate irreversible effects on it. For example, many sex-related characteristics are hormonally determined for a limited period of time in the early stages of development and can be altered by minimal changes in hormonal balance. Evidence indicates that sex-linked traits may be irreversible once they have been set. But in addition, there are three reasons why these predictions are still subject to great uncertainty: The effects of human exposure are not well understood, especially those of embryo exposure; there are data on reproductive problems in wildlife, but not enough information on behavioral disorders; and the potency of many synthetic estrogenic substances is not known with certainty (and there is still controversy regarding that of others of natural origin) (19).

Table I (Modified from ISTAS 2002 and Olea et al. 2002) (20)
Possible effects on human health of endocrine disruptors:


-Breast cancer


-Embryonic and fetal death

-Malformations in the


-Early puberty

-Vaginal cancer

-Higher incidence of cancers.

-Deformations in reproductive organs.

-Problems in the development of the central nervous system

-Low birth weight


-Learning problems

-Decrease in intelligence quotient and

reading comprehension

-Cryptorchidism or no testicular descent.


-Count reduction


-Decreased testosterone level

-Problems in the development of the central nervous system

-Low birth weight


-Learning problems

-Decrease in intelligence quotient and

reading comprehension

-Testicular cancer

-Prostate cancer

-Reduction of sperm count

-Reduction of sperm quality

-Decreased testosterone level

-Modification of the

thyroid hormone concentration

Currently, about 900 active ingredients registered as pesticides in the US have been formulated into 21,000 pesticide products, with herbicides being the most widely used. It has already been proven that more than 60% of herbicides are endocrine disruptors (21). Among the most widely used herbicides that interfere with the thyroid system is 2,4-D (see below).

We now recognize that just a slight difference in the concentration of thyroid hormones during pregnancy can lead to significant changes in intelligence in children. In pregnant women, normal thyroid hormones circulate bound to protein in parts per billion and as free hormone in parts per trillion.

In a long-term study by Haddow et al. (1999) (22), it was shown that chemicals that can interfere with the thyroid system would not have to be present in very high concentrations to affect the intellectual and behavioral development of embryos and fetuses. Their study unexpectedly demonstrates the fragile relationship between a mother and her developing offspring.

Briefly, there are chemicals that interfere with iodide uptake (the herbicides 2,4-D and man-cozeb) and with peroxidation at the molecular level (the herbicides aminotriazole and thioureas, the insecticides endosulfan and malathion).

Certain antagonists (the herbicides aminotriazole and dimethoate, and the insecticide fenvalerate) prevent the release of thyroid hormone from the cell and inhibit the conversion of T4 to triiodothyronine (T3). Several chemicals enhance the excessive excretion of thyroid hormones, some through activation of the cytochrome P450 system: dioxin, hexachlorobenzene, and fenvalerate)

During the organizational stages of gestation, responses to endocrine disruption are different from typical adult responses. Consequently, laboratory studies with mature animals do not cover organizational damage from prenatal exposure. Additionally, most traditional toxicology studies use doses between 1,000 and 1,000,000 times greater than the equivalent physiological range at which the endocrine system operates, and much higher than the concentrations of synthetic chemicals in the real world.

The high doses used in toxicological evaluations far exceed the threshold or peak concentrations at which the brain's homeostatic negative feedback control shuts down cellular responses. Consequently, other non-endocrine toxic effects could be expressed in adult animals but not the same ones that would occur if the exposure had occurred during its construction and programming. Therefore, in endocrine disruption, extrapolation from several high doses to determine the lowest safe dose or the no-effect dose of a chemical will not protect the fetus. Fortunately, many innovative and entirely new endocrine disruption detection protocols are in the early stages of validation and standardization in dozens of countries around the world, but unfortunately, it will take years before many are ready for use.

3. Growing doubts about the protective value of the current risk determination strategies for agrochemicals.

It is absurd to enter the debate on the effectiveness of the national health policy on chemical risks without acknowledging that it is still not possible to even control and prevent the consumption of phytosanitary products of already verified danger. But in countless areas of the Argentine interior, the commercialization of products whose use is prohibited, severely restricted or that have been withdrawn from sale persists. Obviously, the implementation of supervisory, preventive and corrective measures for these crimes should not fall on the civilian population but is the responsibility of the local authorities. However, the majority of complaints and proposals end up being the fruit of community participation or heroic individual efforts.

An example of this ecotoxicological chaos comes from the rural area of ​​three urban settlements, Huinca Renancó, in the South of the Province of Córdoba, and Realicó and Rancul, in the North of the Province of La Pampa. A teacher from Huinca Renancó detected disorders attributable to exposure to multiple combinations of pesticides in her neighbors and students and prepared a report addressed to authorities in her municipality. Its survey included a list of pesticides applied to crops near these locations:

Herbicides: Acetochlor, Aclonifen, Alachlor, Atrazine, Bromoxynil, Brominal, Dicamba, Diflufenicam, Flumetsulam, Flurocyioridone, Fluaxifop, Glyphosate, Haloxyfop-Methyl, Metolachlor, Metsulfuron, Nicosulfuron, Picloranural, Paraquat, 2, Quizranalofuron + Methosulfuron, 2, Prometrelofuron + Methosulfurine 4D, 2,4DB, 24D and Dicamba, Azetochlor + Promethrin.

Insecticides: Aficidas, Bacillius Thuringiensis, Chlorpyrifos, Cypermethrin, Dimethoate, Deltamethrin, Endosulfan, Lambdacia, Lotrin, Landacialothrin, Pirimicarb, Chlorpyrifos + Cypermethrin, Lindane, Carbaryl, Monocrotophos.

Fungicides: Flutriafol, Mancozeb, Triticonazde, Tebuconazde.

By comparing the agrochemicals used in your study area with the “Consolidated List of products whose consumption and / or sale have been banned, withdrawn, severely restricted or not approved by governments”, a consolidated list of products whose use is prohibited, severely restricted or that have been withdrawn from the sale issued annually since 1983 by the United Nations, an international organization of which Argentina is a member, this teacher detected that 12 agrochemicals from the international “black list” continued to be used in the surroundings of her city.

When it comes to protecting our population against substances of very high and already known toxicity, allowing the breach of laws is something inadmissible. As is the prevailing lack of scientific rigor and government irresponsibility regarding substances whose long-term toxicity is unknown.

Corrupt officials determine the risksAccording to a recent report issued by the Institute of Science in Society led by molecular biologist and geneticist Mae-Wan Ho, one of the world's leading regulatory agencies in Public Health, the US FDA (Food and Drug Administration). ., would be interfering politically in the process of science. Rampant conflicts of interest in its scientific advisory panels are undermining the ability to protect the public from the danger of numerous drugs. This body is already in the crosshairs of countless criticisms for recent controversies about experimental studies of drugs on sick children in Third World countries. Now, the Union of Concerned Scientists (UCS) has rekindled the fire by publishing a census that uncovers the widespread political influence on science at the FDA. UCS sent a questionnaire to 5,918 FDA scientists and received 997 responses. Almost a fifth of the scientists (18.4%) said they "had been asked for non-scientific reasons to improperly exclude, or alter technical information or their conclusions in scientific papers at the FDA."

Also the EPA (Environmental Protection Agency) was recently put under fire, and precisely with respect to the subject that concerns us here. Apparently, the EPA Pesticide Program would constitute a veritable “task force” of the “Pesticide Lobby”: a surprising number of senior officials from this Program have gone on to help manufacturers of toxic pesticides bypass and delay EPA efforts. for protecting public health. The complainant institution was the Environmental Working Group, a team of scientists, engineers, experts in regulatory policy, lawyers and computer programmers who, since 1993 and based in Washington DC, USA, are dedicated to Carefully study government information, legal documents, scientific studies, and own laboratory evaluations for the purposes of reporting threats to public health and the environment and finding solutions.

Some years ago, the EWG conducted a source-of-income analysis for top pesticide regulators at the EPA and found that, since the EPA's Pesticide Program began, two-thirds of them were then receiving EPA. less part of his salary from entities of the agrochemical industry. This included four of six former Assistant Administrators for Pesticides and Toxic Substances since 1977, and two of four former directors of the Office of Pesticide Programs since 1983. The EWG also tracked down a dozen former EPA members. who held important positions in pesticide risk assessment. All had continued their careers in the private sector representing interests in open fight against EPA actions to protect public health or the environment.

This investigation culminated in the complaint in December 2004 that objected to the appointment of two scientists to the EPA's advisory panel for perfluorooctanoic acid risk assessment by virtue of being "subsidized by the industry." Despite the fact that there were 99 industry-funded scientists among the applicants, EWG singled out these two because of their previous or current employment relationships with DuPont or 3M, companies that had a direct interest in the outcome of the committee's deliberation.

Fraudulent practices in the toxicological evaluation of pesticides by laboratories contracted by governments

In our country, government and provincial policy on biosafety is generally based on guidelines proposed by international organizations such as FAO, WHO, etc., which, in turn, base their regulations on the examples provided by the countries. more advanced in the matter (“mirror” policies). Among our government institutions involved in the approval, inspection and investigation of the health impact of agrochemicals are the General Coordination of Agrochemicals and Biologicals and the Coordination of Fertilizers, Formulated Pesticides and Chemical Contaminants of SENASA, the latter being the entity that supervises the verification of the suitability of the laboratories registered in the official SENASA network and verifies the standardization of analytical methodologies and controls the analytical protocols and their results. Regarding the health impact, the National Program of Chemical Risks of the Ministry of Health and its National Plan for Chemical Substances Management acts, with the goal of reducing the risks to human health associated with exposure to chemical substances in all stages of their life cycles and, in the present case, to determine vulnerability factors in the population exposed to pesticides. Its guidelines for the evaluation and risk management of pesticides in agricultural use arise from those issued by the WHO and PAHO. The last word regarding Biological Assessment is held by the Chair of Toxicology and Legal Chemistry of the Faculty of Pharmacy and Biochemistry of the UBA.

We wonder if, for example, your professionals are aware of antecedents such as that toxicology studies on glyphosate officially required in the US for registration and approval have been associated with fraudulent practices. In 1976, an audit carried out by the EPA discovered serious errors and deficiencies in studies conducted by one of the most important North American laboratories involved in the toxicological determination of pesticides prior to their official registration. The EPA publicly accused Industrial Biotest Laboratories (IBT), a laboratory that conducted 30 studies on glyphosate and commercial glyphosate-based formulas (including 11 of the 19 studies conducted regarding its chronic toxicity), of routine falsification of data and omission of reports of countless rat and guinea pig deaths. The EPA reported the episode 7 years late (1983) and with little media coverage. However, reports from the US Congressional Government Operations Committee and summaries from the EPA Office of Pesticides and Toxic Substances confirm in detail the fraudulence and poor scientific quality of the IBT studies.

In addition, the EPA denounced in 1991 that Craven Laboratories, a company that conducted determinations for 262 pesticide manufacturing companies, had falsified studies, resorting to “tricks” such as falsifying annotations of laboratory records and manually manipulating scientific equipment to produce results. false. Studies on round-up residues in potatoes, grapes and beets were part of the questioned tests. In 1992, the owner of Craven Laboratories and three of his employees were found guilty in 20 different criminal cases. The owner was sentenced to 5 years in prison and a fine of $ 50,000; the fine for Craven Laboratories was $ 15.5 million. Although the toxicological studies of glyphosate identified as fraudulent have already been superseded, these facts cast a shadow of doubt on the totality of the official pesticide registration procedures.

Suppression of dissent

In any area in which science intervenes to improve human life, the majority of discussions on risk assessment policies and regulation of the use of dangerous technologies are based on the belief that there are no systemic obstacles to the articulation of knowledge findings. scientific. However, today this "creed" suffers a progressive desertion of "faithful", disenchanted by the increasing incidence of avoidable negative health impacts and a lack of precaution of epidemic proportions.

Paradoxically, we live in a time dominated by an “official” scientific worldview that seems to shape the world to the detriment of the living beings that inhabit it. In fact, science did not prevent the world from entering such a serious crisis and caused many of the main problems that we must face today, in addition to its dangerous alliance with commercial interests, whose influence seems to generate in scientists a selective blindness that makes them ignore or misinterpreting the scientific evidence. An analysis of proposals from recently created international institutions reveals the existence of a complex system designed to prevent the publication of adverse findings, while the objective is advertised as "generating greater agreement between state-funded strategic research and the needs of the industry"; or "support the development of a broad platform for interdisciplinary research and academic training to help industry, commerce and government generate wealth."
And the subsidies are distributed "to enthuse the universities to" work more effectively in conjunction with the commercial sphere. Indeed, over the past two decades, gigantic companies began to impose the kind of science and scientific research that should be done, enriching themselves at our expense so that they can better exploit us and make greater profits later. The suppression of dissent is one of the most serious and visible signs of the existence of a "global academic-industrial-military complex" in full development and that threatens the very essence of what science is: the open and disinterested investigation of the causes of natural processes.

In other words, by implementing “mirror” regulatory policies, our authorities ignore their complicity with an invisible pattern of suppression of dissident information. There is a great bias in the citations and publications and in their analysis, which makes those with certain opinions and visions hopeless of any possibility of articulating them or even entering the field of research. Therefore, it is impossible to presume that the quality or strength of informed scientific opinion can be judged by reviews of publications in prestigious journals or by being conducted by scientists in senior positions. As long as some groups continue to have the power to suppress, they are sure to use it. To transform this situation it is necessary to change the balance of powers within and between scientific organizations and government agencies charged with protecting public health.

Returning to the emblematic example of glyphosate, we will see that there is already a great deal of evidence that the widespread use of glyphosate merits the issuance of severe health warnings and a new regulatory review. And in the meantime, their use should be kept to a minimum as a sign of prudence and caution. However, today in our country there are 15.5 million hectares dedicated to the cultivation of transgenic soybeans and an estimated annual consumption of 160 million liters of glyphosate. But local scientific warnings regarding the urgent need to multiply locally medium and long-term toxicological studies and dosages and bio-tests in water and soils are almost nil, not only with respect to the active principle and the product as it goes on sale. , but also on each of the coadjuvants.

An epidemiological study of rural Ontario populations showed that exposure to glyphosate nearly doubled the risk of late miscarriage (23). Professor Eric-Giles Seralini and his team of researchers at the University of Caen in France decided to do more research on the effects of glyphosate on human placental cells. They showed that glyphosate is toxic to placental cells, causing the death of a large percentage of them after 18 hours of exposure to concentrations well below those for agricultural use. Furthermore, RoundUp is always more toxic than its active ingredient, glyphosate; at least 200%. The effect increased over time, and was obtained with concentrations 10 times lower than those used in the cultures.

The aromatase enzyme is responsible for synthesizing the female hormones, estrogens, from androgens (male hormones). Glyphosate interacts with the active site of the enzyme but its effect on enzyme activity was minimal unless RoundUp was present. Interestingly, Roundup increased enzyme activity after one hour of incubation, possibly because its surfactant effect made the androgen substrate more available to the enzyme. But at 18 hours of incubation, Roundup invariably inhibited enzyme activity, which was associated with a decrease in messenger RNA synthesis, suggesting that Roundup caused a decrease in the rate of gene transcription. Seralini and his colleagues suggest that other ingredients in the Roundup formula enhance the availability or accumulation of glyphosate in cells.

There is actually direct evidence that glyphosate inhibits RNA transcription in animals at a concentration well below the level that is recommended for aerosol application. Transcription was inhibited and embryonic development delayed in marine shrimp after exposure to low levels of the herbicide and / or the surfactant polyoxyethyleneamine (POEA). Inhalation by aerosol application of the herbicide should be considered a health threat (24). New research reveals that brief exposure to commercial glyphosate-based formulas caused liver damage in rats, as indicated by the escape of intracellular liver enzymes. In this study, it was also found that glyphosate and its surfactant in Roundup act synergistically to increase liver damage (25).

Three recent case-control studies suggested an association between glyphosate use and NHL risk (27,28,29); while a prospective study in Iowa and North Carolina, USA that included more than 54,000 private and commercial licensed applicators suggested a link between glyphosate use and multiple myeloma (26).

And the list of findings that instead of being refuted or discussed should be reproduced in national laboratories continues: it was found that the children of those who had used glyphosate had a high degree of neurobehavioral alterations (27). Glyphosate caused delayed development of the fetal skeleton in laboratory rats (28). Other experimental and animal studies indicate that glyphosate inhibits steroid synthesis (29) and that it exhibits genotoxicity in mammals (30, 31), fish (32, 33) and frogs (34, 35). Exposure of worms at field doses caused at least 50 percent mortality and significant intestinal injury in surviving roundworms (36). A recent paper reported that Roundup caused alterations in cell division that could be associated with certain types of cancer in humans (37).

The following table summarizes a comparison of the assertions of Monsanto, the world's largest creator and marketer of glyphosate, with the findings of independent research.

Monsanto assertionsIndependent Research Findings
Roundup has a low potential for irritation to the eyes and skin and is also not a risk to human health.

- Roundup is among the most reported pesticides for causing poisoning incidents in several countries.

- Roundup causes a spectrum of acute symptoms, including recurrent eczema, respiratory problems, high blood pressure, and allergic reactions.

Roundup does not cause any adverse reproductive effects.- In laboratory tests on rabbits glyphosate has long-lasting harmful effects on sperm quality and sperm count.
Roundup is not mutagenic in mammals.- In laboratory experiments, damage to the DNA of mouse organs and tissues was observed.

The Roundup is

environmentally safe.

- In the agricultural environment, glyphosate is toxic to beneficial soil organisms and beneficial predatory arthropods, and increases the susceptibility to crop diseases.

- The use of glyphosate in forestry and agriculture generates harmful indirect effects on birds and small mammals by damaging their food supply and habitat.

- POEA content in Roundup is lethal to tadpoles of three species of terrestrial and arboreal toads in Australia. The Australian government has banned the use of these products near waters.

- Sub-lethal doses of glyphosate from drift damage wild plant communities and can affect some species up to 20 meters from the fumigator.

- The use of glyphosate in arable areas causes acronecrosis or regressive gangrene in perimeter trees.

- Glyphosate promotes the population growth of an aquatic snail that is the intermediate host of hepatic fasciolosis in mammals.

- Degradation of glyphosate by microorganisms in water can stimulate eutrophic effects

Roundup is quickly inactivated in soil and water.

- Glyphosate is very persistent in soil and sediments.

- Glyphosate inhibited the formation of nitrogen-fixing nodules in clover for 120 days after its application.

- Residues of glyphosate were found in lettuce, carrots and barley when they were planted one year after the application of glyphosate.

- Phosphate-based fertilizers can inhibit the degradation of glyphosate in soil.

Roundup is immobile and does not percolate on floors.

- Glyphosate can be easily desorbed from soil particles in a wide spectrum of soil types. It can be extensively mobile and percolates deeper into the soil.

- Glyphosate can be transported by soil particles in the form of secondary drift.

Roundup does not contaminate drinking water when used by local authorities on hard surfaces.- In England, the Welsh Water Company detected glyphosate levels above the limit set by the European Union every year since 1993. The Drinking Water Inspectorate recommends that glyphosate be monitored, especially in areas where it is used by local authorities on hard surfaces .
It is virtually impossible for glyphosate resistance to develop in weeds.- In 1996, a glyphosate resistant forage grass was discovered in Australia.
The shift of genes from transgenic crops to conventional species or weeds and horizontal transfer occur over a short distance and can be easily managed.- In those crops that have been examined, the pollen densities are much higher and their dispersion patterns differ from those of large fields compared to those found in experimental lots. Pollen dispersal by wind occurs at much greater distances and at higher concentrations than predicted by extrapolations from experimental crops. Genetic transfer from transgenic oilseed crops is inevitable.
Roundup Ready crops will reduce herbicide utilization levels.- Herbicide tolerant crops will intensify and increase dependence on agricultural use of herbicides rather than lead to significant reductions. A variety of herbicides will have to be reintroduced to control glyphosate-resistant volunteers and resistant weeds.

(Source: Health and Environmental Impacts of Glyphosate: The Implications of Increased Use of Glyphosate in Association with Genetically Modified Crops. July 2001. Report by David Buffin and Topsy Jewell, members of the Pesticide Action Network, UK. Table based on data from: Monsanto Company, 1985, Toxicology of Glyphosate and Roundup Herbicide. Monsanto Company, Department of Medicine and Environmental Health, Missouri, USA; Monsanto Company, Web Site: ., 18th January 1998; Monsanto Advertising Supplements in Farmers? S Weekly, Roundup 91, 7 June 1991, and Roundup 92, 5th June 1992; Pesticide Outlook, Dec. 1997, Royal Society of Chemistry, Vol. 8, No. 6, pp3-4.)

There are already national scientific studies that suggest the need for further research on the effects of chronic exposure to glyphosate (xx). Meanwhile, our country continues to boast of the surprising income from the agricultural sector, but avoiding the incorporation into the costs of calculating future expenses that the irresponsible use of pesticides will have on the health of the population.

(xx) Epidemiological and clinical status of commercial glyphosate in Argentina. Piola JC, Evangelista M, Ezpeleta DC, Prada DB. Toxicology Service of the Children's Sanatorium (Sertox) .Rosario. XIV Argentine Congress of Toxicology, Mendoza, October 2005

4. Effects on human health of drift of agrochemicals for aerial application.

Pesticide drift is unavoidable every time you spray. The magnitude of the drift is greatest from aerial spraying, in which typically about 40% of the applied pesticide is lost to drift. Drift from aerial applications is routinely observed hundreds of meters from the application site, and can reach several kilometers. Even land fumigation can drift considerable distances.

The effects of drift on human health are difficult to investigate, although there are several studies that have documented health problems linked to this type of exposure. Drift occurs wherever and whenever pesticides are used by aerial application. The magnitude of drift can vary between 5 and 60% although it is estimated that around 40% of an aerial application of pesticides leaves the “target area”. Various widely used pesticides are often found far away from the application site and in concentrations well above the acute or chronic exposure levels considered "safe" by regulatory agencies. In order for the agencies in charge to take responsibility for ensuring public health through a reduction and elimination of the use of pesticides susceptible to dispersal in the air, let's remember some facts:

The movement of any pesticide (insecticides, herbicides, fungicides, etc.) through the air away from its application site is considered dispersion and includes sprays, dusts, volatilized or vaporized pesticides, and contaminated soil particles. Sometimes the dispersion is obvious because it takes the form of a cloud of droplets or dust during fumigation, or sometimes it presents as an unpleasant odor after fumigation. It is often insidious, invisible and odorless, and can persist for days, weeks, or even months after application as volatile chemicals evaporate and pollute the air.

The regulatory definition of airborne dispersion excludes 80-95% of the total dispersion of volatile pesticides. The most obvious flaw in the regulatory process to control airborne dispersion is that they use too narrow a definition of pesticide dispersion. This definition does not include dispersion in all its forms in the air, and in some cases it comprises less than 5% of the total pesticides that are carried by the air outside the application site. Currently, they define dispersion as the movement of pesticides in the air to a place other than their application and that occurs during and immediately after their application. However, monitoring data indicates that in 45% of the cases of pesticides applied by various countries, the majority of dispersion occurs after application, when the pesticides volatilize (evaporate). Monitoring data shows that the concentration of pesticides in the air reaches its maximum level between eight to 24 hours after starting the application and then drops after a period of several days to several weeks.

Despite the need to apply controls during fumigation to reduce airborne drift associated with pesticide application, they are not sufficient to control drift that occurs after volatile pesticides are applied. In order to adequately address all the harmful effects caused by the dispersion of pesticides in the air, the dispersion must be regulated after application as it is regulated during application.

Dispersion controls are ineffective

The language used on the labels of pesticide products does not contribute to an adequate control of dispersion in the air during fumigation.

In 2000, the U.S. The North American EPA began a process to make the labels more consistent with all products and, initially, it was based on measures to protect health, prohibiting, through the labels, that the dispersion of pesticides in the air reached people, human-occupied buildings, property, and sites outside the fumigated field. Unfortunately, the agency produced enormous ambiguity by stating that a low level of dispersion, which they did not define, is inevitable and thus acceptable.

Current legislation does not regulate most airborne dispersion that occurs after pesticide applications

The dispersion of pesticides in the air results in many cases of poisoning each year. Between 1997 and 2000, the dispersion of pesticides into the air caused half of all reported cases of pesticide poisoning related to their use in agriculture, as well as a quarter of all reported cases of poisoning by all pesticide uses. Many of the cases of poisoning caused by the dispersion of pesticides in the air are not reported, because neither the victim, nor the doctor, associate the symptoms with the use of pesticides. In other cases, the doctor does not present the report or the affected person does not go to or does not have the financial resources for the necessary medical care.

Various chronic diseases are linked to pesticide drift.

The acute pathology resulting from drift is not easy to ignore, especially when it involves communities and large numbers of rural workers. But most of the consequences of pesticide drift are silent, and unknown to the general public. Most drift exposures come from the legal use of pesticides that does not result in apparent illness, leading to false safety assumptions. The most worrisome health problems are long-term effects that don't show up for months or years - too late to identify the source or do something about the exposure.
These chronic effects include cancer in children and adults, and reproductive and neurological problems, among others. Most studies on the chronic health effects of pesticides are of people exposed to pesticides in the workplace, such as farmers, rural workers, pesticide sprayers and formulators, and factory workers of these products. Non-occupational and environmental exposures are more relevant to the health risks of drift exposure. This work outlines the risks of living near cultivation areas or factories that emit pesticides into the environment, or of household or community exposures, not including occupational exposures of direct contact or those of accidental or suicidal ingestion.

The developing fetus, infants and young children are the most vulnerable to chronic health effects of drift. Clearly, they are not themselves involved in exposure and are affected by non-toxicologically significant exposures in an adult. The time span between exposure and chronic adverse effects is much shorter in children. They often do not have other exposures (eg, alcohol, tobacco, prescription / recreational drugs) that can make chronic adverse effects in adults more difficult to study. However, adults are also vulnerable, as the studies cited below show.

Child cancer: Pesticides are a risk factor for several types of cancer in children. Among the highest is the parental use of pesticides in the home, which can increase the risk of leukemia more than 11 times (1,100%) 10 and that of developing brain cancer more than 10 times (1,080) 11. Household pest extermination increases the risk of non-Hodgkin's lymphoma (NHL) 12, leukemia 13, and Wilm's tumor 14. Living on a farm increases the risk of bone cancer 15 and leukemia 16, 17. Having parents who are farmers or agricultural workers increase the risk of bone cancer 15, 18, 19, 20, brain cancer 21, soft tissue sarcoma 22, and Wilms tumor 23.

Cancer in adults: For adults, living in a growing area where pesticides are used increases the risk of NHL 24-27, leukemia 24-26, 28, brain cancer 24, 29, 30, nasal cancer 31, ovarian cancer 32, 33, cancer pancreatic 34, rectal cancer in men 34, soft tissue sarcoma 27, 35, stomach cancer 34, 36 and thyroid cancer in men 31, 34. There is a study that shows an increased incidence of soft tissue sarcoma and thyroid cancer in men living near a factory that emits pesticide air pollution 37.

Reproductive disorders: The effects on reproduction are difficult to study since the mother, father and developing child are all at risk. Most studies on reproductive disorders are done on women exposed to work during pregnancy, or men exposed occupationally. Being pregnant and living in an area of ​​intense pesticide use increases the risk of suffering from cleft lip and palate38, limb reduction malformations39, and neural tube defects (spina bifida, anencephaly) 40, and any type of congenital malformation43-45 . Even if the mother is not exposed to pesticides, the performance of the father in agricultural work can increase the risk of cleft lip / palate 40, hypospadias, or any type of congenital malformation 43-45.

Neonatal death: Environmental exposure to pesticides can increase the risk of stillborn babies. Mothers who live in pesticide use areas 42, 46, 47, or near a pesticide factory 48, or who use pesticides at home 49, 50 are at increased risk.

Spontaneous abortion: Many pesticides are embryotoxic or foetotoxic in animals, increasing the risk of premature death of the embryo or fetus in humans. A high percentage of normal human conceptions end in spontaneous abortion, making it difficult to study the impacts of environmental toxins. A heavy menstrual period or a missed period may not be recognized, even less documented, such as a miscarriage. An increased risk was found in two high-profile community exposure incidents: the ingestion of wheat grains treated with hexachlorobenzene in Turkey in the 1950s51, and a factory accident in Bohpal, India52. Several studies show an increased risk if the father, not the mother, is exposed to pesticides in floriculture53, in cotton fields54, or as an agricultural fumigator55, 56.

Fertility disorders: There was a lot of interest in the effects of pesticides on fertility, especially on sperm counts. The available studies in this regard relate only to occupationally exposed workers. There are none relevant to drift exposures.

Neurological disease: Most pesticides are neurotoxic and can damage the brain and nerves. The neurological disease most frequently linked to pesticide exposure is Parkinson's disease, a disorder of a specific area of ​​the brain (the basal ganglia). Most of the human studies are of occupationally exposed workers, especially to herbicides. There are reports of an increased risk of Parkinson's from exposure at home 57, living in a rural area 58-66, or drinking well water 63, 64, 67-70. However, some studies also describe risk reduction or no association with rural residence 71 or use of well water 71, 72.

An emerging research area is the study of pesticides as risk factors for other neurological diseases such as multiple systemic atrophy 73, amyotrophic lateral sclerosis (ALS, Lou Gehrig's disease) 74 and senile dementia or Alzheimer's disease 75. There are no studies. on pesticides as risk factors for developmental disorders in children such as autism, cerebral palsy and severe mental retardation, despite growing research interest

Children are at increased risk

Unborn fetuses, infants and young children are the most vulnerable to the health impacts of exposure to pesticides. Boys are still growing and developing, and they are less able to detoxify toxic chemicals. A fundamental saying of pediatric medicine that "children are not little adults." This observation is especially relevant to the discussion of childhood pesticide exposure. Children are at risk from pesticide exposure from different sources and at different levels than adults in the same exposure scenario.

Children play on the floor and put their hands and objects in their mouths, both of which may be covered in a layer of dust and dirt contaminated with pesticides. Because children breathe more air, eat more food, and drink more water per kilogram of body weight than adults, they are exposed to relatively higher amounts of pesticides. In one study, it was found that the levels of organochlorines in the offspring vary directly with the age of the mother (Lackman et al., 1999), pointing to the cumulative historical maternal exposure as the largest component of the total exposure of the child. For boys, the main route of exposure for these substances is through ingestion from milk and diet (Berlin et al., 2002; Fitzgerald et al., 2001; Koopman-Esseboom et al., 1995; Patandin et al., 1999; Sauer et al., 1994).

Many health risks are still unknown

We still don't know much about the health problems that can result from pesticide exposure. Most pesticides have never undergone a human risk assessment. And we know that this is something that no one would want, although controversy also recently broke out in the US due to an EPA program that was about to pay $ 1,000 to each family of children who would be exposed to pesticides and videotaped for two years. Still, EPA's risk assessment guidelines do not require observation of various testing hot spots such as developmental neurotoxicity or endocrine disruption. Neither is multiple exposure evaluated by this North American agency, that is, to several different pesticides simultaneously, even though this type of exposure occurs very frequently. On the other hand, non-active ingredients in commercial pesticide formulations (called "inert ingredients") can also be harmful, and are not identified on product labels.

It is necessary to establish a much wider sanitary protection strip .

Consequently with the information compiled in the present study, the discussion regarding how extensive the sanitary protection zone should be should start from an approach that measures its effectiveness in terms of the greatest possible precaution.

One of the best ways to begin to understand the complexities that this entails is to begin with a review of shortcomings and inadequacies in the current criteria. So far, the determination of a reasonable length is based on two types of data:

1 -the magnitude of drift from the last furrow treated taking into account the wind direction and
2- the toxicological characteristics of the pesticides used together with the exposure levels considered tolerable.

Assuming compliance with the prohibition of application of agrochemicals located within the toxicological classification as Class A, or in the one called 1a and 1b according to national provisions, something impossible to conceive given the evolution of the national pattern of use of Prohibited substances due to the appearance of glyphosate resistant weeds (paraquat, for example), the evaluation of the sanitary impact of permitted substances is based on acceptable exposure levels as they constitute a reasonable certainty of harmlessness.

Traditionally, the tolerable exposure level is called the “reference dose”, and represents the “NOAEL” (No Observable Adverse Effect Level) divided by a safety factor of 100. Once the residual levels have been determined , these must be translated toxicologically into the magnitude of the total body dose. Since drift is generally expressed as the mass of waste deposited on a given surface (in mg / m2), it is usually assumed that, knowing the body surface of a human being, and either the whole or a fraction of its body surface is As set forth, dividing by body weight would result in a dose in units of mg / kg. These units are the same as those used in the design of the reference dose. Clearly, the most conservative protective standard would be that of a child, because children have the greatest surface area per unit of body weight. Obviously, the calculation of the dermal absorption dose of pesticide residues resulting from drift is based on the dermal penetration efficiency in infants for each particular product. But we have previously analyzed the insufficiency of this requirement in the light of scientific and technical advances in this regard.

Therefore, we consider the current toxicological standards inappropriate for establishing the magnitude of the peri-urban sanitary protection strip, even when it was established at 500 m. for land fumigation and 2,000 m. for aerial fumigation.

5. Suggestions for minimizing human exposure to agrochemicals at the agro-urban interface

It is excessively frustrating to see that, despite the fact that our country has qualified scientists and sufficient technical resources to face this problem, effectively protecting the health of its population and the integrity of its environment, the current legislation is far from a true protective result. . An evaluation and a multidisciplinary analysis of environmental factors at the origin of human pathology are essential, including the implementation of measures such as:

-Integrated pest management.
-Biological control of pests.
-Ecological control of pests.
-Safe handling of agrochemicals
-Study of the effect of coarse particulate matter and other air pollutants on allergies, cancers, distress and other ailments.
-Study of the effect of contamination of water sources and soil.
-Studies on waste and quality of food consumed by the entire population. (healthy soil - healthy plant - healthy animal - healthy man).
-Forming integrated multidisciplinary teams where the causes and effects of the different factors that affect man in the agricultural sector are studied in parallel.
-Organization of specific conferences for the problems of the agricultural sector where professionals from different specialties related to agriculture, food and medicine interact.
-Awareness to start taking corrective measures, in which the objective pursued will be the mitigation of environmental risks.

(Source: Seminar on the evaluation and multidisciplinary analysis of environmental factors at the origin of human pathology, Universidad del Salvador, Ing. Agr. Gustavo Otamendi USAL

It is also imperative to eliminate the use of Category I pesticides, replacing them with pesticides of a lower toxicological category, organic and agroecological management practices.

In this regard, the legislation that prohibits the use of 2,4-D in the Province of Entre Ríos is provided as an example, which despite not being included in the category, has extremely harmful effects on human health.

Resolution No. 7 of the Secretary of Agriculture of the Province of Entre Ríos, according to Expdte. No. 402907 dated April 16, 2003:

That the application and use of the 2-4-D herbicide is causing severe damage to different agricultural, forestry and other crops, due to its high volatility, in different parts of the Province.
That the damages caused translate into low crop yields, causing considerable losses in the various plantations, as well as causing severe damage to the environment, people and property, and in view of the need to prevent future damage to third parties ...
… That the use of the 2-4-D component is highly harmful, as has been confirmed with the supporting documentation presented in different administrative files and from the reports issued by the Directorate of Agriculture and Soils, by the Directorate of Horticulture and Alternative Crops of the Secretary of State for Production and by SENASA ...
ARTICLE ONE: Restrict the use and application of the herbicide 2-4-D isobutyl ester of dichlorophenoxyacetic acid until August 31, 2003, authorizing the sale until the reported stocks are exhausted ……
SECOND ARTICLE: Suspend, until SENASA takes a definitive resolution, in the entire scope of the Province of Entre Ríos, the use and application of the aforementioned herbicide in its aerial and terrestrial application as of August 31, 2003, allowing its replacement. and application of the dimethylamine salt formulation of dichlorophenoxyacetic acid only in terrestrial form respecting the environmental conditions and the adjacent crops, the Agronomic recipe must be used in all cases.
THIRD ARTICLE: Those who cause damage to the environment and third parties and violate this Resolution will be liable to the sanctions provided for in the current Legislation ... "
Important resolution if it were more severe and if in any case Article Three will be respected.

And also a similar measure implemented in the Province of Tucumán:

DECREE 1610/3

Decree 1610/3 was recently signed by which the following herbicides are declared restricted sale and controlled entry to the province of Tucumán: 2,4-D formulated as an ester, Picloran, Dicamba and 2,4-DB. It also prohibits aerial application of 2,4-DB and 2,4-D esters.

The reference decree is inserted in the context of Law 6291 (Agrochemicals) and highlights the figure of the Technical Advisor, the only person who can authorize in Tucumán through the agronomic recipe, the sale of these herbicides with restricted commercialization and that are of use widespread.

This article explains the reasons that led to this decree and the role of the technical advisor. Some recommendations are also made to producers for a better use of herbicides, to prevent sanctions or extreme measures such as the prohibition of sale of products that damage third party crops.

Meaning of the restriction :

Law 6291 (art. 5), classifies herbal medicine into two classes: a) free sale and b) restricted sale. In this last classification, all the products classified toxicologically were grouped into the former categories A (extremely toxic) and B (highly toxic), currently designated 1a and 1b respectively. It also authorizes (art. 4), "to prohibit, limit, restrict or suspend in the territory of the province the introduction, manufacture, marketing, application, etc., of any pesticide", which in its opinion affect production, health, environment and others. On the other hand in its art. 8th establishes that the sale of agrochemicals and pesticides of restricted sale will be carried out by means of the written authorization of a Technical Advisor, drawn up in an Agronomic Recipe.
The herbicides now declared of restricted sale, do not belong to the toxicological categories mentioned above. Their new qualification for sale is established by making use of a power granted by law and is not related to a danger to human health, but to the damage caused to sensitive crops. From this measure, its sale, dosage and system with which it is applied, are subject to technical control.
In order to be able to compare the liters of product sold with a prescription, with those entered into the province, it is necessary to control their entry into the territory (in charge of phytosanitary barriers) and for vendors and large users to declare stocks of these products. Therefore, such considerations are part of the new decree.

Crop toxicity

In the 1996-1997 agricultural season, complaints of victims were received at the Directorate of Agriculture, due to the damage to their crops caused by herbicides of different types. In some cases the proximity of the treatment was indicated, but in others (cotton) the observed symptoms, characteristic of the toxic effects of 2,4-D, did not correspond to applications carried out in the vicinity.

The characteristic of producing toxic effects on sensitive plants and at considerable distances from the place where they were applied, is typical (but not exclusive) of the products now restricted due to their volatile characteristics.

Volatility involves the passage of the herbicide to the gaseous state, from where it is (spray fan, surface of the leaf or crop, soil, tank, etc.) towards the environment.
The factors that favor the volatilization of a product are the temperature and humidity of the air, size of the droplet, height of the boom, and the wind. The ease of evaporation is a characteristic of each product and may vary depending on the formulation with which it is manufactured.

If the product is volatile, it diffuses through the atmosphere in small amounts, but proportional to the area treated and the occurrence of climatic conditions that favor its evaporation. The wind moves these gases at a distance, which return to the ground level dissolved in raindrops, fogs, fixed in dust particles or condensed in the dew.

Since the air currents are the determinants of the place where the return of a vaporized herbicide occurs, it is not implausible to find references of damage occurrences at distances greater than 30 km. The protection perimeters (caution zones) that are set (figures 1 and 2) indicate an area of ​​greater probability for the new contact, but not its extreme limit and do not discriminate if they correspond to drift or volatility. From that limit, we should think about preventing a toxic accident.

Whether or not damage occurs in the return area of ​​the volatilized herbicide will depend on the amount of product diffused into the air (expressed in parts per million) and the sensitivity of the plant that receives and absorbs it, which is also variable. according to the stage of growth in which it is. Hence, not all applications produce toxic effects attributable to the volatility of the herbicide.

2,4-D formulated as an ester is very volatile, under favorable climate and application conditions. Picloran, Dicamba and 2,4-DB follow to a decreasing degree, but with higher toxic activity for certain vegetables. Cotton is an extremely susceptible crop to the effects of the aforementioned herbicides. Also vegetables such as peppers, tomatoes, aubergines, squash, watermelons, sweet potatoes, etc., are affected by the vapors of those, although not in a degree similar to cotton. Hence the need to restrict the sale and control the applications of these products, attentive to the increase in cases that represented the symptomatology of hormonal herbicides and that were reported as toxic accidents in crops. In general, there is an increase in the consumption of herbicides in our province and specifically in the case of 2,4-D, it is related to the incorporation of more than 70,000 hectares. of grain crops with direct sowing where their esters are used to carry out their chemical fallows. These treatments temporarily coincide with the 2,4-D weed controls carried out on sugar cane, where now their esters are largely used and not the amine salt, as was customary years ago. If we add its use in the conventional handling of corn, we see that its use is generalized in almost all the agricultural area of ​​Tucumán, thus configuring a system with high probabilities of occurrence of cases of toxicities caused by the products now restricted in their sale to the producer .

Herbicide drift damage:

The movement of the herbicidal droplet resulting from spraying outside the area where the desired target is found (weed, crop, insect, etc.) is called drift and is favored by the wind, height of the bar and size of the droplet.

The occurrence of herbicide drift damage is frequent, even in the same producer's field, as a consequence of the proximity of different crops or different growth stages for the same species.

If you proceed in a hurry and without taking precautions in the spraying operation and there is a neighboring crop sensitive to the applied herbicide, the chances of damage are high. It is exhausting to obtain an economic repair for the damage suffered. The noble intention of cultivating the land of both parties (injured and causing the toxic accident), is transferred to the field of legal studies and courtrooms. It is better to prevent this from happening.

Herbicide leak prevention :

No producer sprays his crop so that the product passes to the neighbor's field, although its effects are beneficial. The results of your investment you want in your field and therefore herbicide damage that occurs on third-party crops is not intentional, but careless without possible justification.

The basic recommendation since the dawn of herbicide development, to suspend spraying when wind speed, humidity and air temperature are not suitable, remains in full force. The size of the droplet resulting from spraying influences drift and volatilization. Lately looking for an economy of water not always necessary, nozzles with lower discharges per minute are used, which helps us with our objective of minimizing the risks of accidents. The development of ground spray contractors in the province was not proportional to that of its peer sprayers. The producer, in search of lower costs, does not develop its own spraying systems and its operational sowing capacity is lower than that of the workers who carry out their chemical fallows. IF the soils lose moisture, it is necessary to wait for the occurrence of a new rain and if it delays it is possible that the treatments should be repeated, thus contributing to the increase in the concentration of hormonal herbicides diffused in the air.

Aerial applications:

It is indisputable that the aerial application system favors the drift and volatilization of herbicides now declared of restricted sale and on the subject there were already similar antecedents in other provinces.

There are many hectares in the province of Tucumán, in which agrochemicals are applied with airplanes. As a result of the competition for work from the aerosol spray companies, even small batches that were not considered before are now sprayed by this means. The insertion of technical advisers in their companies is to help them in the proper management of herbal products.

The role of the technical advisor:

When it is said that 2,4-D ester, 2,4-DB, Picloran and Dicamba as of decree 1610/3 must be sold with an agronomic prescription, a simple bureaucratic measure should not be imagined, aimed at creating a new expense. This measure tends to formalize a relationship between the technical adviser and the producer for the management of some agrochemicals (it would be desirable with all of them), since the latter receives verbal and in writing a series of indicators for the proper use of the herbicide without this necessarily meaning an additional cost without return.

The provincial agrochemical law provides for the insertion of professionals trained in the handling of these products in different stages of the marketing and application process.

With the presence of a mandatory technical advisor in the businesses and application contracting companies, assistance and warning to the producer is intended to avoid the application of agrochemicals in risky or unnecessary situations that affect their economy and the environment.
The intervention of the technical advisor does not exempt those who use agrochemicals on their own or third parties from responsibilities for misuse. That is why you have to choose technicians with high professional responsibility and listen carefully to their recommendations. If possible, try to get him to repeat his advice and warnings to field personnel in charge of spraying.

The agronomic recipe (already sold to registered consultants) should be required to be carefully written. If they go directly to the archive, to justify compliance with standards that are considered useless, it will represent a defeat for all of us who in one way or another are involved with agrochemicals in the province.

Final thoughts:

In the search for the safe and effective employment of herbalists, in the province of Tucumán, regulations are dictated and controls are carried out, as well as training courses for all the people involved with their commercialization, sale and application.
No one who is involved in the use of agrochemicals can say that there is no more knowledge that is necessary and even less that he does not share the objective of Law 6.291: "regulate all actions related to agrochemicals in order to ensure their correct use to protect human, animal and plant health, improve agricultural production and reduce risks to the environment ".

By Ing. Ignacio Olea
EEAOC Weed Management Section
Agroindustrial Advance Magazine
No. 70 - October 1997

Other suggestions:

* Apply the first proposal gradually discouraging the use of Category I, through measures such as:
a) Require that they be applied by trained applicators and sell them only to these producers or applicators,
b) Avoid the registration of new Category I pesticides.

* Monitor strict compliance with current legislation. This will cause a more rational use of Category I pesticides since they will be sold exclusively under professional prescription.

* Apply a tax to Category I pesticides. The resources generated will be used to improve the control of compliance with current legislation, the implementation of a national plan for the collection of empty containers and the promotion of less toxic alternatives, prioritizing the organic agriculture.

* The Restricted Entry Interval must be listed on the label of all pesticides (especially Category I). In addition, the waiting times for pesticides (especially Category I) should be reviewed. Both proposals tend to improve the health protection of applicators and consumers.

* Measurement of pesticide levels in waterways (with emphasis on Category I) that cross agricultural areas with high pesticide use and that are key sources of drinking water or that flow into waterways where water is extracted for purify.

* Carry out control of pesticide residues in food where there is normally an intensive use of Category I pesticides.

* Promote research in alternative techniques such as organic and agroecological production at the national level as a way to increase the production of pesticide-free food.

(Source: We need them? Dangerous remedies. Analysis of the situation of the most toxic pesticides in Uruguay. Ing. Sebastián Elola, Uruguayan Studies Center for Appropriate Technologies)

We recommend the following specific actions:

Both at the provincial and national levels.

The actions they must take include:

1) The gradual elimination of the use of highly toxic fumigant pesticides with high consumption.
2) Advise agricultural producers during the transition towards the use of alternative less toxic products.
3) Define "airborne dispersion of pesticides" to include both windblown pesticides and any movement of the pesticide away from its application site.
4) Design easy-to-enforce regulations that are effective in preventing airborne dispersion.
5) Require the use of buffer zones, labeling and notification for all pesticide applications.
6) Consult with affected communities and create laws that protect them.
7) Require pesticide manufacturers to fund the costs of air monitoring as a condition of maintaining registration of their products.
8) Work with the agricultural inspectors of the municipalities to increase the amount of fines, as well as improve the application of existing regulations.
9) Work with municipal agricultural inspectors to establish and implement a uniform protocol in response to pesticide poisoning.

At the national level

As the entity responsible for the regulation of pesticides at the national level, the Chemical Risks program of the Ministry of Health, together with the corresponding departments of SENASA, must:
1) Maintain a “zero dispersion of pesticides in air” standard in the language used on pesticide labels.
2) Include exposure to airborne pesticides in risk assessments for all pesticides.
3) Reduce allowable application rates
4) Issue new regulations, under the Clean Air Act, to classify pesticide application sites as “polluting sources”.

A supported environmental justice fights by providing critical scientific information on health impacts that sustains and supports the experience lived by communities. Using the basic principle of "Do No Harm First," we support a precautionary approach to environmental regulations and restorations.

This implies:

* That we have an obligation based on the trust of the population to take precautionary actions to protect health and ecosystems even in the face of scientific uncertainty.
* To establish objectives. The precautionary principle promotes planning based on clear goals rather than future scenarios and risk calculations that can be fraught with error and bias.
* Undertake the search and evaluation of alternatives. Alternatives should aim to reduce or eliminate emissions, releases and exposures. The objective of regulatory actions should be to prevent pollution and exposures, not to determine the magnitude of harm or risk that a community must tolerate. The entire spectrum of alternatives will be taken into consideration including the evaluation of the proposed activity. Alternatives to a proposed potentially dangerous activity should be investigated as thoroughly as the activity itself.
* Change the test weights. Proponents of an activity should prove that their activity will not cause unexpected harm to human health or ecosystems.
* Increase democracy. Affected communities have the right to participate in decisions. The burden of proof on one activity should not be shifted to communities while another is filling their pockets. Debates on regulatory policies and polluting activities must be open, transparent and provide security to the voices of impacted communities.


1- Zahm SH, Ward MH, Blair A. Pesticides and cancer. Occup Med 12: 269–289 (1997).
2- Sever LE, Arbuckle TE, Sweeney A. Reproductive and developmental effects of occupational pesticide exposure: the epidemiologic evidence. Occup Med 12: 305-325 (1997).
3- Keifer M, Mahurin RK. Chronic neurologic effects of pesticide overexposure. Occup Med 12: 291–304 (1997).
4- Aschengrau A, Ozonoff D, Coogan P, Vezina R, Heeren T, Zhang Y. Cancer risk and residential proximity to cranberry cultivation in Massachusetts. Am J Public Health 86: 1289-1296 (1996).
5- Waterhouse D, Carman WJ, Schottenfeld D, Gridley G, McLean S. Cancer incidence in the rural community of Tecumseh, Michigan. Cancer 77: 763–770 (1996).
6- Gordon JE, Shy CM. Agricultural chemical use and congenital cleft lip and / or palate. Arch Environ Health 36: 213-220 (1981).
7- Schwartz DA, Lo Gerfo JP. Congenital limb reduction defects in the agricultural setting. Am J Public Health 78: 654–659 (1988).
8- Blair A, Zahm SH. Agricultural exposures and cancer. Environ Health Perspect 103 (suppl 8) 205–208 (1995).
9- Evangelista de Duffard AM, Bortolozzi A, Duffard RO. Altered behavioral responses in 2,4-dichlorophenoxyacetic acid treated and amphetamine challenged rats. Neurotoxicology. 1995; 16: 479–488.
10- Angelista de Duffard AM, de Alderete MN, Duffard R. Changes in brain serotonin and 5-hydroxyindolacetic acid levels induced by 2,4-dichlorophenoxyacetic butyl ester. Toxicology. 1990; 64: 265-270.
11- Rosso SB, Garcia GB, Madariaga MJ, Evangelist of Duffard AM, Duffard RO. 2,4-Dichlorophenoxyacetic acid in developing rats alters behavior, myelination and regions brain gangliosides pattern. 2000; 21: 155-163.
12- Bortolozzi AA, Duffard RO, Evangelist of Duffard AM. Behavioral alterations induced in rats by a pre- and post-natal exposure to 2,4-dichlorophenoxyacetic acid. Neurotoxicol Teratol. 1999; 21 (4): 451–465. [PubMed]
13- Bortolozzi A, Evangelista de Duffard AM, Dajas F, Duffard R, Silveira R. Intracerebral administration of 2,4-dichlorophenoxyacetic acid induces behavioral and neurochemical alterations in the rat brain. 2001; 22: 221–232.
14- Bortolozzi AA, Duffard RO, Evangelist of Duffard AM. Behavioral alterations induced in rats by a pre-and post-natal exposure to 2,4-dichlorophenoxyacetic acid.
15- Evangelista de Duffard AM, Bortolozzi A, Duffard RO.
16- Sturtz N, Evangelista de Duffard AM, Duffard R. Detection of 2,4-dichlorophenoxyacetic acid (2,4-D) residues in neonates breast-fed by 2,4-D exposed dams. 2000; 21: 147-154.
17- Barbosa, 2001.
18- Atrazine.
19- Synthesis of the conclusions of the Conference on Hormone Disrupters of Wingspread, 1996.
20- Endocrine disruption: environmental perspectives and public health
21- Short P, Colborn T. Pesticide use in the U.S. and policy implications: a focus on herbicides. Toxicol Ind Health. 1999; 15: 240-275).
22- Haddow JE, Palomaki GE, Allan WC, Williams JR, Knight GJ, Gagnon J, et al. Maternal thyroid deficiency during pregnancy and subsequent neuropsychological development of the child. N Engl J Med. 1999; 341: 549–555.
23- Arbuckle T, Lin Z and Mery L An exploratory analysis of the effect of pesticide exposure on the risk of spontaneous abortion in an Ontario farm population. Envir. Health Perspectives 2001, 109, 851-60.
24- arry V, Harkins M, Erickson L, Long S, Holland S and Burroughs B. Birth defects, seasons of conception and sex of children born to pesticide applicators living in the red river valley of Minnesota, USA. Health Perspectives (Suppl 3) 2002, 110, 441-9.
25- Marc J, Le Breton M, CormierP, Morales J, Belle´R and Mulner-Lorillo O. A glyphosate-based pesticide impinges on transcription. Toxicology and Applied Pharmacology 2005, 203, 1-8).
26- Benedetti AL, de Lourdes Vituri C, Trentin AG, Dominguesc MAC and Alvarez-Silva M. The effects of sub-chronic exposure of Wistar rats to the herbicide Glyphosate-Biocarb. Toxicology Letters 2004, 153, 227–32.
27- De Roos AH, Zahm SH, Cantor KP, et al. Integrative assessment of multiple pesticides as risk factors for non-Hodgkin’s lymphoma among men. Occup Environ Med 2003, 60, E11 28- Hardell L, Eriksson M, Nordstrom M. Exposure to pesticides as risk factor for non-Hodgkin’s lymphoma and hairy cell leukemia: pooled analysis of two Swedish case-control studies. Leuk Lymphoma 2002, 43, 1043-1049.
29- McDuffie HH, Pahwa P, McLaughlin JR, Spinelli JJ, Fincham S, Dosman JA, et al. 2001. Non-Hodgkin’s lymphoma and specific pesticide exposures in men: cross-Canada study of pesticides and health. 2001, Cancer Epidemiol Biomarkers Prev 2001,10,1155–63.).
30- De Roos AJ, Blair A, Rusiecki JA, Hoppin JA, Svec M, Dosemeci M, Sandler DP and Alavanja MC. Cancer incidence among glyphosate-exposed pesticide applicators in the agricultural health study. Environ Health Perspect 2005, 113, 49-54.
31- Garry V, Harkins M, Erickson L, Long S, Holland S and Burroughs B. 3) 2002, 110, 441-9.
32- Richard S, Moslemi S, Sipahutar H, Benachour N. and Seralini GE Differential effects of glyphosate and roundup on human placental cells and aromatase.Environ Health Perspect. 2005 Jun; 113 (6): 716-20.
33- A. Donna, P-G. Betta, F. Robutti, et al., Ovarian mesothelial tumors and herbicides: A case-control study, Carcinogenesis, 1984, 5: 941–42.
34- 2003
35- P. Lampi, T. Hakulinen, T. Luostarinen, et al., Cancer incidence following chlorophenol exposure in a community in southern Finland, Arch Env Health, 1992, 47 (3):
36- A. Paldy, N. Puskas, and I. Farkas, Pesticide use related to cancer incidence as studied in a rural district of Hungary, Sci Total Env, 1988, 73 (3): 229–44.
37- J.E. Gordon and C.M. Shy, Agricultural chemical use and congenital cleft lip and / or palate, Arch Env Health, 1981, 36: 213–21
38-39- D.A. Schwartz and J.P. LoGerfo, Congenital limb reduction defects in the agricultural setting, Am J Pub Health, 1988, 78: 654–57.

Long-term adverse impacts references

10 J.D. Buckley, L.L. Robinson, R. Swotinsky, et al., Occupational exposures of parents of children with acute nonlymphocytic leukemia: A report from the Children’s Cancer Study Group, Can Res, 1989, 49: 4030–37.
11 J.M. Pogoda and S. Preston-Martin, Household pesticides and risk of pediatric brain tumors, Env Health Persp, 1997, 105 (11): 1214–20.
12 J.K. Leiss and D.A. Savitz, Home pesticide use and childhood cancer: A casecontrol study, Am J Pub Health, 1995, 85 (2): 249–52.
13 X. Ma, P.A. Buffler, R.B. Gunier, et al., Critical windows of exposure to household pesticides and risk of childhood leukemia, Env Health Persp, 2002, 110 (9): 955–60.
14 A.F. Olshan, N.E. Breslow, J.M. Falletta, et al., Risk factors for Wilm’s tumor: Report from the National Wilm’s Tumor Study, Cancer, 1993, 72 (3): 938–44.
15 P.C. Valery, W. McWhirter, A. Sleigh, et al., Farm exposures, parental occupation, and risk of Ewing’s sarcoma in Australia: A national case-control study, Can Causes Contr, 2002, 13 (3): 263–70.
16 E.A. Holly, P.M. Bracci, B.A. Mueller, et al., Farm and animal exposures and pediatric brain tumors: Results from the United States West Coast Childhood Brain Tumor Study, Can Epid Biomark Prev, 1998, 7 (9): 797–802.
17 G.R. Bunin, J.D. Buckley, C.P. Boesel, et al., Risk factors for astrocytic glioma and primitive neuroectodermal tumor of the brain in young children: A report from the Children’s Cancer Group, Can Epid Biomark Prev, 1994, 3 (3): 197–204.
18 L. Hum, N. Kreiger, and M.M. Finkelstein, The relationship between parental occupation and bone cancer risk in offspring, Int J Epid, 1998, 27 (5): 766–71.
19 P. Kristensen, A. Andersen, L.M. Irgens, et al., Cancer in offspring of parents engaged in agricultural activities in Norway: Incidence and risk factors in the farm environment, Int J Can, 1996, 65 (1): 39-50.
20 E.A. Holly, D.P. Aston, P.K.A. Ahn, et al., Ewing's bone sarcoma, parental occupational exposures and other factors, Am J Epid, 1992, 135 (2): 122–29.
21 M. Feychting, N. Plato, G. Nise, and A. Ahlbom, Paternal occupational exposures and childhood cancer, Env Health Persp, 2001, 109 (2): 193–96.
22 C. Magnani, G. Pastore, L. Luzzatto, et al., Parental occupation and other environmental factors in the etiology of leukemias and non-Hodgkin's lymphomas in childhood: A case-control study, Tumori, 1990, 76 (5) : 413–19.
23 C.R. Sharpe, E.L. Franco, B. deCamargo, et al., Parental exposures to pesticides and risk of Wilm’s tumor in Brazil, Am J Epid, 1995, 141 (3): 210–17.
24 D. Godon, P. Lajoie, J.P. Thouez, et al., Pesticides and cancer in a Québec rural farming population: A geographical interpretation, Soc Sci Med, 1989, 29 (7): 819–33.
25 M. McCabe, M. Nowak, R. Hamilton, et al., Cancer of lymphatic tissues in cane-growing areas of Queensland, Med J Aust, 1984, 141 (7): 412–14.
26 D. Waterhouse, W.J. Carman, D. Schottenfeld, et al., Cancer incident in the rural community of Tecumseh, Michigan: A pattern of increased lymphopoietic neoplasms, Cancer, 1996, 77 (4): 763–70.
27 N. Hicks, M. Zack, G.G. Caldwell, et al., Life-style factors among patients with melanoma, South Med J, 1985, 78 (8): 903–8.
28 M.E. Loevinsohn, Insecticide use and increased mortality in rural central Luzon, Philippines, Lancet, 1987, 1: 1359–62.
29 A. Ahlbom, I.L. Navier, S. Norell, et al., Nonoccupational risk indicators for astrocytomas in adults, Am J Epid, 1986, 124 (2): 334–37.
30 A. Aschengrau, D. Ozonoff, P. Coogan, et al., Cancer risk and residential proximity to cranberry cultivation in Massachusetts, Am J Publ Health, 1996, 86 (9): 1289–96.
31 P. Vineis, F. Faggiano, M.Tedeschi, et al., Incidence rates of lymphomas and soft-tissue sarcomas and environmental measurements of phenoxy herbicides, J Nat Can Inst, 1991, 83 (5): 362–63.
32 A. Donna, P. Crosignani, F. Robutti, et al., Triazine herbicides and ovarian epithelial neoplasms, Scand J Work Env Health, 1989, 15: 47-53.
33 A. Robutti, et al., Ovarian mesothelial tumors and herbicides: A case-control study, Carcinogenesis, 1984, 5: 941–42.
34 D.M. Schreinemachers, Cancer mortality in four northern wheat-producing states, Env Health Persp, 2000, 108 (9): 873–81.
35 P. Luostarinen, et al., Cancer incidence following chlorophenol exposure in a community in southern Finland, Arch Env Health, 1992, 47 (3): 35 P. Luostarinen, et al., Cancer incidence following chlorophenol exposure in a community in southern Finland, Arch Env Health, 1992, 47 (3): 167–75.
36 A. Farkas, Pesticide use related to cancer incidence as studied in a rural district of Hungary, Sci Total Env, 1988, 73 (3): 229–44.
37 J.O. Grimalt, J. Sunyer, V. Moreno, et al., Risk excess of soft-tissue sarcoma and thyroid cancer in a community exposed to airborne organochlorinated compound mixtures with a high hexachlorobenzene content, Int J Can, 1994, 56 (2): 200–203.
38 J.E. Shy, Agricultural chemical use and congenital cleft lip and / or palate, Arch Env Health, 1981, 36: 213–21.
39 D.A. LoGerfo, Congenital limb reduction defects in the agricultural setting, Am J Pub Health, 1988, 78: 654–57.
40 G.M. Shaw, C.R. Wasserman, C.D. O'Malley, et al., Maternal pesticide exposure from multiple sources and selected congenital anomalies, Epidemiology, 1999, 10 (1): 60–66.
41 A.E. Czeizel, Pesticides and birth defects [letter], Epidemiology, 1996, 7 (1) 111.
42 E.M. Bell, I. Hertz-Picciotto, and J.J. Beaumont, A case-control study of pesticides and fetal death due to congenital anomalies, Epidemiology, 2001 12 (2): 148–56.
43 V.F. Garry, D. Schreinemachers, M.E. Harkins, et al., Pesticide appliers, biocides, and birth defects in rural Minnesota, Env Health Persp, 1996, 104 (4): 394–99.
44 M. Restrepo, N. Munoz, N.E. Day, et al., Birth defects among children born to a population occupationally exposed to pesticides in Columbia, Scand J Work Env Health, 1990, 16: 239–46.
45 A.M. Garcia, F.G. Benavides, T. Fletcher, et al., Paternal exposure to pesticides and congenital malformations, Scand J Work Env Health, 1998, 24 (6): 473–80.
46 F.M.M. White, F.G. Cohen, G. Sherman, et al., Chemicals, birth defects and stillbirths in New Brunswick: Associations with agricultural activity, Can Med Assoc J, 1988, 138: 117–24.
47 T.E. Taha and R.H. Gray, Agricultural pesticide exposure and perinatal mortality in central Sudan, Bull WHO, 1993, 71 (3–4): 317–21.
48 M.M. Ihrig, S.L. Shalat, and C. Baynes, A hospital-based case-control study of stillbirths and environmental exposure to arsenic using an atmospheric dispersion model linked to a geographical information system, Epidemiology, 1998, 9 (3): 290–94.
49 D.A. Savitz, E.A. Whelan, and R.C. Kleckner, Self-reported exposure to pesticides and radiation related to pregnancy outcome: Results from national natality and fetal mortality surveys, Public Health Reports, 1989, 104: 473–77.
50 L.M. Pastore, I. Beaumont, Risk of stillbirth from occupational and residential exposures, Occ Env Med, 1997, 54 (7): 511–18.
51 J. Jarrell, A. Gocmen, W. Foster, et al., Evaluation of reproductive outcomes in women inadvertently exposed to hexachlorobenzene in southeastern Turkey in the 1950s, Repro Toxicol, 1998, 12 (4): 469–76.
52 J.S. Bajaj, A. Misra, M. Rajalakshmi, et al., Environmental release of chemicals and reproductive ecology, Env Health Persp, 1993, 101 (Suppl 2): ​​125–30.
53 M. Day, et al., Prevalence of adverse reproductive outcomes in a population occupationally exposed to pesticides in Colombia, Scand J Work Env Health, 1990, 16: 232–38.
54 S.D. Rupa, P.P. Reddy, and O.S. Reddi, Reproductive performance in population exposed to pesticides in cotton fields in India, Env Res, 1991, 55 (2): 123–28.
55 G. Petrelli, I. Figa-Talamanca, R. Tropeano, et al., Reproductive malemediated risk: Spontaneous abortion among wives of pesticide applicators, Eur J Epid, 2000, 16 (4): 391–93.
56 V.F. Garry, M. Harkins, A. Lyubimov, et al., Reproductive outcomes in the women of the Red River Valley of the north. I. The spouses of pesticide applicators: pregnancy loss, age at menarche, and exposures to pesticides, J Toxicol Env Health, 2002, 65 (11): 769–86.
57 P.G. Butterfield, B.G. Valanis, P.S. Spencer, et al., Environmental antecedents of young-onset Parkinson’s disease, Neurology, 1993, 43 (6): 1150–58.
58 S.J. McCann, D.G. LeCouteur, A.C. Green, et al., The epidemiology of Parkinson’s disease in an Australian population, Neuroepidemiology, 1998, 17 (6): 310–17.
59 A.H. Rajput, R.J. Uitti, W. Stern, et al., Georgraphy, drinking water chemistry, pesticides and herbicides and the etiology of Parkinson's disease, Can J Neurolog Sci, 1987, 14: 414-18.
60 S.C. Ho, et al., Epidemiologic study of Parkinson’s disease in Hong Kong, Neurology, 1989, 39 (10): 1314–18.
61 C.M. Tanner, B. Chen, W-Z. Wang, et al., Environmental factors in the etiology of Parkinson’s disease, Can J Neuro Sci, 1987, 14: 419–23.
62 B. Ritz and F. Yu, Parkinson’s disease mortality and pesticide exposure in California 1984–1994, Int J Epid, 2000, 29 (2): 323–29.
63 A. Priyadarshi, S.A. Khuder, E.A. Schaub, et al., Environmental risk factors and Parkinson’s disease: A meta-analysis, Env Res, 2001, 86 (2): 122–27.
64 K. Marder, G. Logroscino, B. Alfaro, et al., Environmental risk factors for Parkinson’s disease in an urban multiethnic community, Neurology, 1998, 50 (1): 279–81.
65 W. Koller, B. Vetere-Overfield, C. Gray, et al., Environmental risk factors in Parkinson’s disease, Neurology, 1990, 40 (8): 1218–21.
66 G.F. Wong, C.S. Gray, R.S. Hassanein, et al., Environmental risk factors in siblings with Parkinson’s disease, Arch Neurol, 1991, 48 (3): 287–89.
67 C.H. Tsai, S.K. Lo, L.C. See, et al., Environmental risk factors of young onset Parkinson’s disease: A case-control study, Clin Neurol Neurosurg, 2002, 104 (4): 328–33.
68 M. Behari, A.K. Srivastava, R.R. Das, et al., Risk factors of Parkinson’s disease in Indian patients, J Neurol Sci, 2001, 190 (1–2): 49–55.
69 M. Zorzon, L. Capus, A. Pellegrino, et al., Familial and environmental risk factors in Parkinson's disease: A case-control study in north-east Italy, Acta Neurol Scand, 2002, 105 (2): 77– 82.
70 A. Smargiassi, A. Mutti, A. De Rosa, et al., A case-control study of occupational and environmental risk factors for Parkinson's disease in the Emilia-Romagna region of Italy, Neurotoxicology, 1998, 19 (4-5 ): 709–12.
71 a) A. Seidler, W. Hellenbrand, B.P. Robra, et al., Possible environmental, occupational, and other etiologic factors for Parkinson’s disease: A casecontrol study in Germany, Neurol, 1996, 46 (5): 1275–84.
b) K.M. Semchuk, E.J. Love, and R.G. Lee, Parkinson’s disease and exposure to rural environmental factors: a population based case-control study, Can J Neurol Sci, 1991, 18 (3): 279–86.
c) M. Stern, E. Dulaney, S.B. Gruber, et al., The epidemiology of Parkinson’s disease: A case-control study of young-onset and old-onset patients, Arch Neurol, 1991, 48 (9): 903–7.
72 a) A.M. Kuopio, R.J. Marttila, H. Helenius, et al., Environmental risk factors in Parkinson’s disease, Mov Disord, 1999, 14 (6): 928–39.
b) C.A. Taylor, M.H. Saint-Hilaire, L.A. Cupples, et al., Environmental, medical, and family history risk factors for Parkinson’s disease: A New England-based case control study, Am J Med Genet, 1999, 88 (6): 742–49.
c) J. Zayed, S. Ducic, G. Campanella, et al., Environmental factors in the etiology of Parkinson’s disease, Can J Neurol Sci, 1990, 17 (3): 286–91.
73 P.A. Hanna, J. Jankovic, and J.B. Kirkpatrick, Multiple system atrophy: The putative causative role of environmental toxins, Arch Neurol, 1999, 56 (1): 90–94.
74 a) C.J. Burns, K.K. Beard, and J.B. Cartmill, Mortality in chemical workers potentially exposed to 2,4-dichlorophenoxy-acetic acid (2,4-D) 1945–94: An update, Occ Env Med, 2001, 58 (1): 24–30.
b) M. Freedman, Amyotrophic lateral sclerosis and occupational exposure to 2,4-dichlorophenoxyacetic acid, Occ Env Med, 2001, 58 (9): 609–10.
c) V. McGuire, W.T. Longstreth, L.M. Nelson, et al., Occupational exposures and amyotrophic lateral sclerosis: A population-based case-control study, Am J Epid, 1997, 145 (12): 1076–88.
d) M. Poloni, A. Micheli, D. Facchetti, et al., Conjugal amyotrophic lateral sclerosis: Toxic clustering or change ?, Ital J Neurol Sci, 1997, 18 (2): 109–12.
75 a) A. Cannas, B. Costa, P. Tacconi, et al., Dementia of Alzheimer type (DAT) in a man chronically exposed to pesticides, Acta Neurol (Napoli), 1992, 14 (3): 220–23 .
b) E. Gauthier, I. Fortier, F. Courchesne, et al., Environmental pesticide exposure as a risk factor for Alzheimer's disease: A case-control study, Env Res, 2001, 86 (1): 37-45.
c) P.A. Schulte, C.A. Burnett, M.F. Boeniger, et al., Neurodegenerative diseases: Occupational occurrence and potential risk factors, 1982 through 1991, Am J Pub Health, 1996, 86 (9): 1281–88.
41 A.E. Tacconi, et al., Dementia of Alzheimer type (DAT) in a man chronically exposed to pesticides, Acta Neurol (Napoli), 1992, 14 (3): 220 23.
b) E. Boeniger, et al., Neurodegenerative diseases: Occupational occurrence and potential risk factors, 1982 through 1991, Am J Pub Health, 1996, 86 (9): 1281–88.

Video: Tyrone Hayes: The toxic baby: TED TALKS: documentary, lecture, talk: herbicide danger (July 2021).