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By: Joseph St. Geme, MD

  • Chair, Department of Pediatrics, Professor of Pediatrics and Microbiology, Perelman School of Medicine at the University of Pennsylvania
  • Physician-in-Chief, Leonard and Madlyn Abramson Endowed Chair in Pediatrics, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania


Inquire about the duration of symptoms gastritis diet абв order prilosec in india, whether the onset and termination of symptoms are subtle or abrupt gastritis diet paleo generic prilosec 20mg on line, and the factors associated with onset gastritis symptoms night sweats order 40mg prilosec with amex. Infants may manifest nonspecific symptoms of irritability and poor feeding; some cases may progress to chronic gastritis gastroparesis best 40mg prilosec congestive heart failure prior to identification of an abnormal rhythm. Special attention should be paid to a history of structural cardiac abnormalities or cardiac surgery because those factors increase the risk of both arrhythmias and adverse outcomes associated with them. A social history should investigate stress levels, caffeine intake, and tobacco use. Pallor on examination, a history of lethargy or easy fatigability, excessive blood loss, or a diet history suggestive of iron deficiency may be clues to anemia. If events are more intermittent, an incident or event recorder is preferable; these require activation by the patient when symptoms develop. If the history reveals any of these risk factors, an urgent cardiac evaluation is recommended. Occasionally it can be prominent; careful auscultation will identify the relationship to the respiratory phases and distinguish it from premature atrial contractions. It can also reveal abnormalities that may cause symptoms other than palpitations. When the complaint of palpitations is a minor one and is associated with a likely causative condition. They are often asymptomatic, although patients may describe a "skipped" beat followed by a strong beat or a sensation of the "heart turning over. They are usually asymptomatic; patients may occasionally complain of skipped beats or pauses in their heart rate. Otherwise healthy children experiencing atrial fibrillation should be evaluated for thyrotoxicosis, pulmonary emboli, and pericarditis. Reentrant tachycardias are characterized by an abrupt onset and cessation and tend to occur when the patient is at rest. It usually occurs in children with congenital heart disease, especially postoperatively, but may occur in neonates with normal hearts. It may be asymptomatic in children with normal hearts; children with structural heart disease are more likely to be symptomatic. The challenge to the practitioner is to ascertain which of these murmurs warrants additional evaluation. The clinical diagnosis of a normal or innocent murmur should be made only in the presence of a normal history and physical examination and characteristics consistent with a normal murmur. Despite the easy availability of echocardiography, the history and physical examination remain the accepted means of diagnosing normal murmurs. When the diagnosis of a murmur is unclear, it is generally more cost-effective to refer to a pediatric cardiologist than to order an echocardiogram. Hyperthyroidism is suggested by thyromegaly, tachycardia, a hyperdynamic precordium, slightly bounding pulses, and mild hypertension. Other physical examination findings that are worrisome include an abnormal rhythm, suprasternal thrill, prominent apical thrust, digital clubbing, wide or bounding pulses, and absent or weak femoral pulses. In older children, exercise or exertion can be assessed by inquiring about level of activity and tolerance to extended periods of play or activity. Inquiring about how well older children keep up with their peers or siblings regarding exercise tolerance may also be helpful. A history of fevers, lethargy, and recent dental work suggests possible endocarditis. Chronic mouth breathing, snoring, or obstructive sleep apnea may be clues to pulmonary hypertension. A maternal history of gestational diabetes, infection, and use of certain drugs or medications may be risk factors for congenital heart disease. A family history of sudden death, rheumatic fever, sudden infant death syndrome, and structural cardiac defects in a first-degree relative may be significant. A family history of hypertrophic cardiomyopathy is sufficient to mandate an echocardiogram because of the autosomal dominant pattern of inheritance. The cardiac examination should include assessment of pulses, palpation of the precordium, auscultation, and blood pressures in both arms (involvement of a subclavian artery [most commonly the left] in a coarctation would cause a lower blood pressure in the ipsilateral arm) and a leg. Lower extremity blood pressure is usually 10-20 mmHg higher than upper extremity pressure. Diminished femoral pulses or a delay between the radial and femoral pulses suggest coarctation of the aorta (the simple presence of a femoral pulse does not rule out coarctation). A history of fevers in the presence of a new or changing heart murmur should raise the suspicion for both rheumatic fever and endocarditis. The murmur is classically described as a loud, usually holosystolic murmur with a harsh or blowing quality and is best heard at the left sternal border; a thrill or lift may be palpable with moderate lesions. Small defects may have soft murmurs that become softer over time as the lesion closes. In large defects, the left-to-right shunting increases over the first few weeks of life as pulmonary vascular resistance falls. They are characterized by a hyperdynamic right ventricular impulse and a characteristic fixed and widely split second heart sound. Murmurs are not always audible, but large defects may manifest a mid-systolic pulmonary flow murmur at the left upper sternal border or a mid-diastolic rumble at the left mid or lower sternal border due to increased flow over the tricuspid valve. These murmurs are usually grade 1 to 3, short systolic murmurs with a slightly grating (rather than vibratory) quality. They are heard best over the left upper sternal border and may or may not transmit to the neck. The murmur can be accentuated by full exhalation and the supine position, and diminished by the upright posture and breath holding. It can occur in any age group (including neonates) but is most likely in older children and adolescents. Children not diagnosed in infancy can remain asymptomatic (even with severe coarctation) and often present with hypertension later in childhood. The classic physical findings are diminished or delayed arterial pulses in the lower extremities compared to the upper extremities, with corresponding lower blood pressures in the lower extremities. A short systolic murmur at the third or fourth left intercostal spaces may be detected with transmission to the left infrascapular area or neck. Large ones tend to be symptomatic, causing congestive heart failure and failure to thrive. The murmur characteristically becomes loudest during systole and softens during diastole. The lesion is one of the cardiac anomalies frequently associated with prenatal maternal rubella infection; it is also common in congenital hypothyroidism. The non-radiating murmur is usually a low-grade short systolic murmur heard best at the mid to lower left sternal border and also towards the apex. It has a characteristic vibratory or musical quality; commonly used descriptions include buzzing, a vibrating tuning fork, or a twanging cello string. Rarely, it can be surprisingly loud and ominous-sounding with transmission throughout the precordium. It may be heard best with the bell of a stethoscope, is usually loudest when the patient is supine and tends to diminish with an upright or a sitting position. The murmur is loudest at the left upper sternal border with good transmission to the axillae and back. It generally disappears between 3 and 6 months of life as the pulmonary branches increase in size; persistence warrants cardiology evaluation to rule out true stenosis or constriction of the pulmonary arteries. These are medium frequency continuous murmurs heard in the infraclavicular region (right more common than left) and neck; their intensity increases slightly during diastole. The murmur typically is heard when the patient is sitting or standing, and it diminishes or disappears in the supine position, when the patient turns his or her head far to one side, and when gentle pressure is applied to the jugular veins in the neck. They are presumed to be due to the turbulence created as the internal jugular and subclavian veins enter the superior vena cava. Cases may present acutely or insidiously with intermittent fevers (classically occurring in the afternoons) and vague symptoms of fatigue, myalgias, joint pain, headache, and nausea or vomiting. Echocardiography is helpful in identifying vegetations, although results may be normal early in the disease. Adding transesophageal echocardiography to the transthoracic approach improves the diagnostic yield.

Pretreatment of animals with this carcinogen enhanced biliary secretion of 14 C radiolabel gastritis diet 4 life order prilosec canada. A reduction in fertility in male and female offspring was observed in mice following exposure in utero gastritis diet киви purchase generic prilosec. There is some evidence that it causes skin gastritis diet барбоскины buy generic prilosec canada, lung gastritis loose stools purchase 20mg prilosec free shipping, and bladder cancer in humans and animals. Studies have noted increased lung cancer and a suggestion of increased gastrointestinal cancer incidence in the coal carbonization and coal gasification industries. Later skin changes include loss of color, reddish areas, thinning of the skin, and warts. On inhalation exposure, the patient should be moved to fresh air and monitored for respiratory distress. If cough or difficulty in breathing develop, evaluation for respiratory tract irritation, bronchitis, or pneumonitis should be performed. Humidified supplemental oxygen (100%) should be administered with assisted ventilation as required. On dermal exposure, the affected area should be washed thoroughly with soap and water. Patients developing dermal hypersensitivity reactions may require treatment with systemic or topical corticosteroids or antihistamines. Treatment of gastric, lung, or skin cancer is no different from that for the same cell type. Emergency shower facilities should be available if there is a possibility of skin exposure. On skin contact, affected skin should be washed immediately to remove the chemical. Workers in industries that produce coal or coal tar products and those who tar road surfaces and roofs are at maximum risk. The National Institute for Occupational Safety and Health occupational exposure recommendations are 0. It readily binds to soils and should not leach to groundwater, though it has been detected in some groundwater. If released into water, it will adsorb strongly to sediments and particulate matter. In most waters and sediments it will resist breakdown by microbes and reactive chemicals. Benzodiazepines are commonly used as anxiolytics, muscle relaxants, anticonvulsants, and to treat alcohol withdrawal, insomnia, and agitation. They are administered preoperatively for their anterograde amnesia effects and are combined frequently with other medications for conscious sedation before procedures. Exposure Routes and Pathways the most common route of exposure to the benzodiazepines is ingestion of oral dosage forms. Several of these agents are also available for parenteral administration (intramuscular or intravenous). Diazepam may be administered through an Benzodiazepines 261 endotracheal tube; aerosolized diazepam is under investigation. Toxicokinetics the benzodiazepines are generally well absorbed from the gastrointestinal tract. The benzodiazepines are all extensively metabolized by microsomal enzyme systems in the liver. The metabolites of many benzodiazepines are pharmacologically active and are biotransformed much more slowly than the parent compounds. The benzodiazepines that are not biotransformed to active metabolites include clonazepam, estazolam, lorazepam, nitrazepam, oxazepam, temazepam, and triazolam. The elimination half-lives of the benzodiazepines range from 1 to 70 h at therapeutic doses. These metabolites are ultimately conjugated, largely with glucuronic acid, to inactive compounds that are excreted primarily in the urine. When large doses of lorazepam have been infused chronically, there are multiple reports of the development of a syndrome consisting of a hyperosmolar state with metabolic acidosis and cardiovascular compromise. Chronic Toxicity (or Exposure) Animal Chronic dosing in pregnant rats has resulted in increased rates of cleft palate formation as well as decrease in serum thyroxine levels. Prenatal exposure to benzodiazepines in rats describes learning and memory deficits in pups as well as absence of usual startle responses. Benzodiazepine binding causes increased frequency of opening of the chloride channel. Chloride channel opening results in membrane hyperpolarization, thereby inhibiting cellular excitation. Tolerance and physical dependence may develop in persons who chronically use benzodiazepines. Abrupt discontinuation of chronic benzodiazepine therapy may result in a withdrawal syndrome consisting of anxiety, agitation, insomnia, tremors, headache, and myalgias. In more severe cases nausea, vomiting, diaphoresis, hyperpyrexia, psychosis, seizures, and death may occur. In Vitro Toxicity Data In vitro studies examining the effects of diazepam in the immune system have shown mixed results. Several cultured cell models have demonstrated diazepam-induced inhibition of cell proliferation. Obtunded patients with reduced gag reflex should be intubated to prevent pulmonary aspiration. Respiratory support, including oxygen and ventilation, should be provided as needed. If hypotension occurs it should be treated with standard Animals may be affected by the benzodiazepines much in the same way as humans. Lethargy, coma, shallow respirations, incoordination, and depressed reflexes may occur. Human There is a broad spectrum of signs and symptoms associated with acute benzodiazepine toxicity. Lethargy, 262 Benzyl Alcohol measures including intravenous fluids, Trendelenburg positioning, and dopamine by intravenous infusion. Forced diuresis, hemoperfusion, and hemodialysis are of no value in benzodiazepine toxicity. If withdrawal signs and symptoms develop, treatment should focus on either benzodiazepine or phenobarbital therapy with a gradual dose reduction. Because acute benzodiazepine overdoses generally result in only mild toxicity, it has limited clinical utility in this setting. This observation is necessary to be certain that reoccurrence of benzodiazepine toxic effects do not occur after flumazenil is metabolized. Flumazenil must be used with caution in mixed drug overdoses as seizures can develop, particularly if tricyclic antidepressants have been coingested. Also, it can induce potentially serious benzodiazepine withdrawal in dependent patients. Toxicokinetics Body tissue possibly takes up benzyl alcohol rapidly and releases it slowly into the bloodstream. Humans readily oxidize benzyl alcohol to benzoic acid, which, after conjugating with glycine, is rapidly eliminated as hippuric acid in the urine. If the dose is sufficiently high to allow the rate of formation of benzoic acid to exceed that of hippuric acid some of the benzoic acid is excreted as benzoylglucuronide.

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Associated with congenital diaphragmatic hernia (usually left-sided) gastritis breathing purchase prilosec 40 mg with visa, bilateral renal agenesis (Potter sequence) gastritis symptoms in pregnancy purchase discount prilosec line. Caused by abnormal budding of the foregut and dilation of terminal or large bronchi chronic gastritis support group order 40mg prilosec free shipping. Generally asymptomatic but can drain poorly chronic gastritis management 10mg prilosec, causing airway compression and/or recurrent respiratory infections. Secrete surfactant from lamellar bodies (arrow in A) alveolar surface tension, prevents alveolar collapse, lung recoil, and compliance. Surfactant synthesis begins around week 26 of gestation, but mature levels are not achieved until around week 35. Neonatal respiratory distress syndrome A Surfactant deficiency surface tension alveolar collapse ("ground-glass" appearance of lung fields) A. Risk factors: prematurity, maternal diabetes (due to fetal insulin), C-section delivery (release of fetal glucocorticoids; less stressful than vaginal delivery). Screening tests for fetal lung maturity: lecithinsphingomyelin (L/S) ratio in amniotic fluid (2 is healthy; < 1. Small airways consist of bronchioles that further divide into terminal bronchioles (large numbers in parallel least airway resistance). Warms, humidifies, and filters air but does not participate in gas exchange "anatomic dead space. Pseudostratified ciliated columnar cells primarily make up epithelium of bronchus and extend to beginning of terminal bronchioles, then transition to cuboidal cells. Airway smooth muscle cells extend to end of terminal bronchioles (sparse beyond this point). Lung parenchyma; consists of respiratory bronchioles, alveolar ducts, and alveoli. Mostly cuboidal cells in respiratory bronchioles, then simple squamous cells up to alveoli. Right lung is a more common site for inhaled foreign bodies because right main stem bronchus is wider, more vertical, and shorter than the left. If you aspirate a peanut: While upright-enters basal segments of right lower lobe. Pain from diaphragm irritation (eg, air, blood, or pus in peritoneal cavity) can be referred to shoulder (C5) and trapezius ridge (C3, 4). Pathologic dead space-when part of the respiratory zone becomes unable to perform gas exchange. Compliance-change in lung volume for a change in pressure; expressed as V/P and is inversely proportional to wall stiffness. Hysteresis-lung inflation curve follows a different curve than the lung deflation curve due to need to overcome surface tension forces in inflation. Hemoglobin 2 1 Heme 2 1 Hemoglobin (Hb) is composed of 4 polypeptide subunits (2 and 2) and exists in 2 forms: Deoxygenated form has low affinity for O2, thus promoting release/unloading of O2. Fetal Hb (2 and 2 subunits) has a higher affinity for O2 than adult Hb, driving diffusion of oxygen across the placenta from mother to fetus. Oxidized form of Hb (ferric, Fe3+) that does not bind O2 as readily, but has affinity for cyanide. Induced methemoglobinemia (using nitrites, followed by thiosulfate) may be used to treat cyanide poisoning. Causes oxygen-binding capacity with left shift in oxygen-hemoglobin dissociation curve. Nitrites (eg, from dietary intake or polluted/high altitude water sources) and benzocaine cause poisoning by oxidizing Fe2+ to Fe3+. Myoglobin is monomeric and thus does not show positive cooperativity; curve lacks sigmoidal appearance. When curve shifts to the right, affinity of Hb for O2 (facilitates unloading of O2 to tissue). With Hb there is O2 content of arterial blood, but no change in O2 saturation and Pao2. A in Pao2 causes a hypoxic vasoconstriction that shifts blood away from poorly ventilated regions of lung to well-ventilated regions of lung. With exercise (cardiac output), there is vasodilation of apical capillaries V/Q ratio approaches 1. Lifethreatening hemorrhages occur in posterior segment (sphenopalatine artery, a branch of maxillary artery). Common causes include foreign body, trauma, allergic rhinitis, and nasal angiofibromas. Field cancerization: carcinogen damages wide mucosal area multiple tumors that develop independently after exposure. Deep venous thrombosis A Blood clot within a deep vein swelling, redness A, warmth, pain. Use unfractionated heparin or low-molecularweight heparins (eg, enoxaparin) for prophylaxis and acute management. Use oral anticoagulants (eg, warfarin, rivaroxaban) for treatment (long-term prevention). Fat emboli-associated with long bone fractures and liposuction; classic triad of hypoxemia, neurologic abnormalities, petechial rash. Hypertrophy and hyperplasia of mucus-secreting glands in bronchi Reid index (thickness of mucosal gland layer to thickness of wall between epithelium and cartilage) > 50%. Smooth muscle hypertrophy and hyperplasia, Curschmann spirals F (shed epithelium forms whorled mucous plugs), and Charcot-Leyden crystals G (eosinophilic, hexagonal, double-pointed, needle-like crystals formed from breakdown of eosinophils in sputum). Diagnostic criteria: productive cough for > 3 months in a year for > 2 consecutive years. Findings: cough, wheezing, tachypnea, dyspnea, hypoxemia, inspiratory/ expiratory ratio, pulsus paradoxus, mucus plugging E. Exhalation through pursed lips to increase airway pressure and prevent airway collapse. Associated with bronchial obstruction, poor ciliary motility (eg, smoking, Kartagener syndrome), cystic fibrosis H, allergic bronchopulmonary aspergillosis. Bronchoscopy shows severe edema, congestion of bronchus, and soot deposition (A, 18 hours after inhalation injury; B, resolution at 11 days after injury). Granulomatous (noncaseating) on histology and therefore occasionally responsive to steroids. Prolonged coal dust exposure macrophages laden with carbon inflammation and fibrosis. Macrophages respond to silica and release fibrogenic factors, leading to fibrosis. A B Asbestos is from the roof (was common in insulation), but affects the base (lower lobes). Asbestos (ferruginous) bodies are golden-brown fusiform rods resembling dumbbells C, found in alveolar sputum sample, visualized using Prussian blue stain, often obtained by bronchoalveolar lavage. Anthracosis-asymptomatic condition found in many urban dwellers exposed to sooty air. Many causes and associations, including sepsis, pancreatitis, pneumonia, aspiration, trauma, shock. Initial damage due to release of neutrophilic substances toxic to alveolar wall and pulmonary capillary endothelial cells, activation of coagulation cascade, and oxygen-derived free radicals. Management: mechanical ventilation with low tidal volumes, address underlying cause. B Sleep apnea Repeated cessation of breathing > 10 seconds during sleep disrupted sleep daytime somnolence. Nocturnal hypoxia systemic/pulmonary hypertension, arrhythmias (atrial fibrillation/flutter), sudden death.

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In practice gastritis diet treatment discount 40 mg prilosec, the risk to chronic gastritis grading buy 20mg prilosec overnight delivery the mother and baby of paracetamol-induced liver damage probably far outweighs any potential risk of N-acetylcysteine gastritis zucchini order 40mg prilosec otc, and pregnancy should not be considered a contraindication to hcg diet gastritis buy discount prilosec 40 mg online the use of this agent. In Vitro Toxicity Data N-Acetylcysteine is negative in the Ames mutagenicity test and also reduces the mutagenic affect of chemical carcinogens in the same assay. Oral formulations of N-acetylcysteine are used intravenously in the clinical treatment of animals, although it has not been approved for this use. Basic and advanced life-support measures should be utilized as 718 Cytochrome P-450 necessary. Published by Cambridge University Press on behalf of the World Health Organization and of the Commission of the European Communities. Evolution of P-450s Cytochrome P-450 proteins are one of the largest superfamily of enzyme proteins. Sequence comparisons indicate that the diverse superfamily originated from a common ancestral gene some three billion years ago. The origin of the P-450 superfamily lies in prokaryotes, before the advent of eukaryotes and before the accumulation of molecular oxygen in the atmosphere. Humans have 57 different active P-450 genes and a similar number (58) of pseudogenes. There is particularly the large number of P-450 genes in the plants with 323 genes in the rice and 249 genes in the thale cress genomes. In the human genome, the P-450 genes are arranged into 18 families and 42 subfamilies. Biochemistry of P-450 Enzymes In vertebrates, the liver is the richest source of P-450 and is also the most active organ in the oxidation of xenobiotics. P-450 enzymes are expressed in the microsomal fraction (smooth endoplasmic reticulum) of the cell where they are anchored in the lipid bilayer. In addition to the liver, P-450s are also ubiquitously expressed in the lung, kidney, skin, nasal mucosal, gastrointestinal tract, placenta, bladder, nervous system, and blood platelets among other tissues. Although they are expressed in a variety of tissues, the function of P-450s seems to differ in each case. The liver, lung, and small intestine carry out mainly xenobiotic biotransformation. Placental P-450s are devoid of the ability to metabolize any appreciable xenobiotics but function mainly as a steroid hormone metabolizing system. Kidney P-450s are involved in some metabolism of xenobiotics, but are involved in cholecalciferol and salt balance regulation. Cytochrome P-450s are hemoproteins (iron-containing) of the b cytochrome type and derive the name P-450 from the wavelength (450 nm) at which the carbon monoxide derivative of the reduced cytochrome has an absorption maximum. Cytochrome P-450s, like other monooxygenases, carry out oxidation reactions in which one atom of molecular oxygen is reduced to water while another is incorporated into the substrate. Reactions Catalyzed by P-450s P-450s catalyze a large number of substrates that may be exogenous or endogenous compounds. Cytochrome P-450 719 P-450s carry out aliphatic and aromatic hydroxylations, aromatic epoxidations (leading to stable epoxides like dieldrin from aldrin, or arene oxides), O-, N-, and S-dealkylations and oxidations, oxidative deaminations, and desulfurations among other reactions. Although the primary evolutionary role of the P-450 enzymes is to convert hydrophobic xenobiotics into more hydrophilic compounds and enhance their removal from the body, P-450s also catalyze reactions that lead to more reactive (and hence toxic) compounds. Several xenobiotics are converted into potential carcinogens via the cytochrome P-450 system. Three important biological systems that are intrinsically regulated by several P-450 enzymes require special mention: 1. At least seven cytochrome P-450 enzymes play critical roles in the conversion of acetate into sterols and bile acids. The roles of each of these enzymes are beyond the scope of this article, but some excellent reviews and texts are available on the topic. The vitamin D3 system, which acutely controls calcium status in addition to a host of other physiological functions, is a classical example of P-450s in multiple tissues being involved in the biosynthesis of a biologically active metabolite. Most of the biological function is attributed to this metabolite, although recent studies suggest that even the 25-hydroxy metabolite may be exerting certain biological effects. Genes in this family are controlled by the aryl hydrocarbon (Ah receptor), which is activated most notably by components of incineration products and cigarette smoke. See also: Biotransformation; Genomics, Toxicogenomics; Mechanisms of Toxicity; Vitamin D; Xenobiotics. Further Reading Endogenous Functions of P-450s Following the sequencing of the human genome, all the human P-450s have been identified. However, the endogenous physiological role of the majority of P-450s remains unknown. The chief organs of deposition are kidneys, liver, and the central and peripheral nervous systems. Mechanism of Toxicity 2,4-D is a plant-growth regulator that stimulates nucleic acid and protein synthesis and affects enzyme activity, respiration, and cell division. Cl Uses 2,4-D free acids, esters, and salts are formulated in water suspensions or solutions, or in various organic solvents, for application as systemic herbicides. There are many commercial formulations available for weed and brush control, for certain agricultural uses, and for lawn and garden weed control. Acute and Short-Term Toxicity (or Exposure) Animal Exposure Routes and Pathways 2,4-D may be encountered as a vapor, liquid, or as a component of mixtures. It may cause damage at the point of contact (skin, eyes, lungs, and gastrointestinal tract). Occupational exposure may occur through inhalation and dermal contact when 2,4-D is produced or used. These results may account for slower learning in rats that were exposed to 2,4-D during postnatal development of the brain. Human Toxicokinetics Rapid and complete absorption of chlorphenoxy compounds from the gastrointestinal tract has been Acute ingestion can cause miosis, coma, fever, hypotension, emesis, tachycardia, muscle rigidity, possible respiratory failure, pulmonary edema, and rhabdomyolysis. Alteration in liver functions such as elevated lactate dehydrogenase and aspartate aminotransferase has also been reported. In humans, the 722 2,4-D (2,4-Dichlorophenoxy Acetic Acid) causal relationship between these effects and chlorphenoxy herbicides such as 2,4-D remains controversial and not yet proven. Environmental Fate 2,4-D has a relatively short half-life and is rather immobile in the soil. The acid form of 2,4-D, as well as the amine and ester chemical groups, metabolized to compounds of nontoxicological significance and ultimately to forms of carbon. Under normal conditions, 2,4-D residues are not persistent in soil, water, or vegetation. Chronic Toxicity (or Exposure) Animal Other Hazards To keep residues of 2,4-D out of meat or milk, dairy cattle should not be grazed on treated areas for 7 days after application. Also, hay should not be cut for 30 days and meat animals should not be slaughtered for 3 days. Inert ingredients found in 2,4-D products may include ethylene glycol, methanol, sequestering agents, petroleum hydrocarbons, and surfactants. Ethylene glycol is moderately toxic to humans; it may cause tearing, anesthesia, headache, cough, respiratory stimulation, nausea or vomiting, pulmonary, kidney, and liver changes. Methanol is moderately toxic to humans; it may cause damage to the optic nerve, tearing, headache, cough, difficult breathing, other respiratory effects, nausea, or vomiting. This indicates that these formulations may have considerably less acute toxicity than the acid form. However, exposure to these formulated products may have other health effects similar to those reported for 2,4-D alone or for inert ingredients in commercial formulations. Dibenzodioxins and dibenzofurans may cause disorders of the skin, blood, and gastrointestinal tract; they may also cause headaches, numbness, birth defects, or fetal toxicity. In 2-year dietary tests in mice and rats, 2,4-D was not oncogenic (tumor causing). Human Long-term exposure to 2,4-D has been reported to cause liver, kidney, digestive, muscular, or nervous system damage.

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