Search

Insecticides are used to control diseases spread by arthropods, but theys vary greatly in toxicity. Toxicity depends on the chemical and physical properties of a substance, and may be defined as the quality of being poisonous or harmful to animals or plants. Poisons have many different modes of action, but in general cause biochemical changes which interfere with normal body functions. Toxicity can be either acute or chronic. Acute toxicity is the ability of a substance to cause harmful effects which develop rapidly following absorption, i.e. a few hours or a day. Chronic toxicity is the ability of a substance to cause adverse health effects resulting from long-term exposure to a substance. There is a great range in the toxicity of insecticides to humans. The relative hazard of an insecticide is dependent upon the toxicity of the pesticide, the dose received and the length of time exposed. A hazard can be defined as a source of danger. The great majority of insecticides are poisonous to man and his beneficial insects and animals and are carcinogenic agents particularly, the halogenated hydrocarbons containing benzene ring.

Methemoglobin levels more than 70% have almost always been reported to have been fatal. The case of a 4-year-old boy who survived with methemoglobin levels of 98% is presented here. He was brought to the emergency department with complaints of vomiting, pain abdomen, and altered sensorium following accidental ingestion of paint thinner mixed with "Holi" colors. On examination, the child was in altered sensorium, cyanosed with saturations of 55%, who did not respond despite positive pressure ventilation with 100% oxygen. A possibility of toxic methemoglobinemia was considered and confirmed by finding of elevated methemoglobin levels of 98%. The child survived with definitive therapy with methylene blue and aggressive goal-directed approach.

An 18-year-old man presented to a community emergency department with increasing shortness of breath and fever. His condition was diagnosed, and he was treated as an inpatient for bilateral pneumonia associated with hypoxemia. When his condition became worse, he acknowledged to deliberate inhalation of keyboard cleaner and to having hemoptysis. Before his death on hospital day 11, known causes of alveolar hemorrhage were excluded. We postulated a cause-and-effect relationship, adding alveolar hemorrhage to the known complications of inhalant abuse.

Previous research suggests that exposure to persistent organic pollutants (POPs) increases the risk of chronic diseases such as hypertension. We identified the zip codes of more than 800 waste sites contaminated with POPs and other pollutants, based on which we classified zip codes of upstate New York into three groups: "POPs sites", zip codes containing hazardous waste sites with POPs; "other waste sites", zip codes containing hazardous waste sites but not with POPs; and "clean sites", zip codes without any known hazardous waste sites. Age, gender, race, and zip code of residence of patients diagnosed with hypertension (ICD-9 codes 401-404) were identified using the New York Statewide Planning and Research Cooperative System (SPARCS) for the years 1993-2000. A generalized linear model, the negative binomial model, was used to assess the effect of living in a zip code with a hazardous waste site on the discharge rate of hypertension. After control for the aforementioned covariates, we found a statistically significant elevation of 19.2% (95% CI = 8.5%, 31%) in hypertension discharge rate for "POPs sites" and a 10% elevation in discharge rates for "other waste sites" as compared to "clean sites". In a subset of "POPs sites" where people have higher income, smoke less, exercise more and have healthier diets, there was still a 13.9% elevation of hypertension discharge rate as compared to "clean sites". The results support the hypothesis that living near hazardous waste sites, particularly sites containing POPs, may constitute a risk of exposure and of developing hypertension.

The kidney is the target of numerous xenobiotic toxicants, including environmental chemicals. Anatomical, physiological, and biochemical features of the kidney make it particularly sensitive to many environmental compounds. Factors contributing to the sensitivity of the kidney include: large blood flow, the presence of a variety of xenobiotic transporters and metabolizing enzymes, and concentration of solutes during urine production. In many cases, the conjugation of environmental chemicals to glutathione and/or cysteine targets these chemicals to the kidney where inhibition of renal function occurs through a variety of mechanisms. For example, heavy metals such as mercury and cadmium target the kidney after glutathione/cysteine conjugation. Trichloroethlene and bromobenzene are metabolized and conjugated to glutathione in the liver before renal uptake and toxicity. In contrast, renal injury produced by chloroform and aristolochic acids is dependent on renal cytochrome P450 metabolism to toxic metabolites. Other compounds, such as paraquat or diquat, damage the kidney via the production of reactive oxygen species. Finally, the low solubility of ethylene glycol metabolites causes crystal formation within the tubular lumen and nephrotoxicity. This chapter explores mechanisms of nephrotoxicity by environmental chemicals, using these example compounds. What remains to be accomplished and by far the most difficult process is the elucidation of the detailed mechanisms of tubular cell injury after toxicant uptake and metabolism. The large number of individuals experiencing a decline in renal function with age makes the search for these mechanisms very compelling.

The potential association between fetal death and residential proximity to agricultural pesticide applications was examined in 10 California counties for 1984. A case-cohort analysis utilized 319 cases of selected causes of fetal death other than congenital anomalies and 611 non-cases. A statewide database of all applications of restricted pesticides was linked to maternal address; residential proximity within 1 mile (1.6 km) provided a surrogate for daily exposure. Pesticides were grouped by chemical class and mechanism of acetylcholinesterase inhibition. Multivariate proportional hazards models using time-dependent exposure variables were fit for each pesticide grouping. Overall, pesticides showed no strong association with fetal death. Slightly elevated risks were observed for women who resided near applications of halogenated hydrocarbons, carbamates, estrogenic pesticides, and carbamate acetylcholinesterase inhibitors during the second trimester, with hazard ratios of 1.3 (95% confidence interval (CI): 1.0, 1.8), 1.3 (95% CI: 1.0, 1.8), 1.4 (95% CI: 0.8, 2.5), and 1.3 (95% CI: 1.0, 1.8), respectively. In a month-by-month analysis, elevated risks were observed when exposure occurred during gestational months 3 and 4 for carbamates and carbamate inhibitors and during months 4 and 5 for halogenated hydrocarbons. Since previous studies have relied on personal recall of exposure, major strengths of this study were the objective source for environmental pesticide exposure assessment and the use of data on the timing of exposure.

This report describes an acute intentional trichloroethylene exposure that developed neurological and cardiovascular toxicity. The patient presented with palsies of the third, fifth, and sixth cranial nerves. Clinical manifestations, laboratory values, and treatment plans are discussed. Emergency physicians should be aware of the complications of trichloroethylene exposure and consider the diagnosis in patients with similar symptoms.

In 13 patients (2 males, 11 females, 15-70 years of age) on account of severe intoxications with hypnotics sedatives, psychopharmaca, in most cases mixed intoxications, with propranolol and halogenized hydrocarbons a 4--8-hour haemoperfusion treatment with amberlite XAD-4-Resin was performed. 11 patients survived, 1 patient died in irreversible cardiogenic shock of a propranolol intoxication, another patient of the sequels of a crotylbarbital and methaqualone intoxication. The curves of the course of the blood concentration of the individual substances showed a good elimination for phenobarbital and crotylbarbital, methaqualone, meprobamat and didropyridine as well as trichlorethylene, a less good elimination for nitrazepam, propranolol and tetrachlorethylene, Altogether the effectiveness of the detoxication clearly higher in the time unit, compared with the dialysis.

Clinical and experimental data accumulated within the past 2 decades explain the relationship between fat embolism and osteonecrosis, which now appears to be more causal than coincidental. Evidence for fatty liver, coalescence of endogenous plasma lipoproteins, and/or disruption of depot or marrow fat, all resulting in continuous or intermittent fat embolism, is related to 13 different clinical conditions associated with osteonecrosis, most recently including pregnancy, carbon tetrachloride poisoning, and possibly Legg-Calvé-Perthes disease. Intraosseous fat embolism, then, appears to trigger a three-phase thrombotic process of focal intravascular coagulation that results in osteonecrosis.

This article summarizes the state of the art in research on cardiovascular diseases (CVD) and occupational exposure. The major chemical and physical agents are considered and the methodological difficulties of epidemiological surveys are discussed. Work-related CVD, like all occupational disorders, are changing continuously as a consequence of modifications in industrial processes, improvements in preventative measures, and the tertiarization of the economy. The cornerstones of a preventative strategy of CVD are still based on environmental monitoring and medical surveillance, but at the same time on multidisciplinary and multicentred scientific research. Where possible, health promotion will include more general programmes directed at changing personal risk factors.

Fatal chemical pneumonia occurred in a worker following exposure to an unidentified gas in a salvaged cylinder. Inspection of the tank revealed a scrawled chemical formula for 1,1,2,3,3-pentafluoro-3-chloropropene, a suspected pulmonary irritant. The report underscores the potential hazards which salvaged cylinders pose to individuals who use or refill them. The population at risk includes scuba divers, emergency rescue personnel, and workers in the compressed gas industry.

This case documents postmortem tissue concentrations of fluorocarbons in an individual whose inhalation of cooking spray vapors was well documented. The data presented here should contribute to the information base which will assist the pathologist in determining the cause of death in cases related to inhalation of these fluorocarbons.

Epidemiologic studies have suggested factors in drinking water influence on the human cardiovascular system. A clear identification of the factors involved requires more invasive techniques and more strict experimental controls than can usually be applied in epidemiologic studies. Consequently laboratory animals are often used to expand and support epidemiologic data. For laboratory purposes cardiovascular toxicology must be broken down to effects on the myocardium, the vasculature and the kidney. Further division may be necessary to take into account the influence of the neuroendocrine system or other systems that influence the function of the cardiovascular system. Since environmental influences upon the cardiovascular disease are relatively subtle (versus the acute effects of some drugs) it is assumed that major difficulties are chronic in nature. Accordingly, it is suggested that laboratory experimentation focus on either chronic toxin exposure or short-term exposure to stressed or genetically susceptible animals. A variety of in vivo and in vitro tests may be necessary to relate the toxicity realized in animals to what might be expected in man. Wide species differences with respect to the susceptibility of particular target tissues must be taken into account to clearly apply the results to man. Similarly, special characteristics of stressed and genetically susceptible animals must be understood to avoid deceptive results.

The agriculturally important nematocide 1,2-dibromo-3-chloropropane (DBCP) has been implicated as a cause of human male sterility. A survey at the Michigan Division of The Dow Chemical Company included measurements of semen samples, testicular size, and serum follicle-stimulating hormone (FSH), luteinizing hormone (LH), and testosterone in 232 chemical workers with past potential exposures to DBCP and in 97 nonexposed comparison employees. Potentially exposed groups showed significantly higher, although not abnormal, mean levels of FSH and LH. In the subgroup with the highest potential exposure ending subsequent to 1972, greater duration of exposure correlated with lower sperm count, higher FSH level, and smaller testicular volume. Mean values for this latter time-divided subgroup were not abnormal. The findings are consistent with a testicular effect of DBCP and also with reversibility of that effect over time.

This article offers a brief introduction to the general principles of toxicology, followed by a discussion of the toxicology of heavy metals, solvents, halogenated hydrocarbons, and alcohols. It concludes with an overflow of pesticide toxicology.

With the removal from the general marketplace of volatile hydrocarbons which have been previously abused by "thrill-seekers", new and often unlikely products are now being exploited by those who whish to escape reality. Many of these products have proven harmful. An example of such an unusual product is reported in this case of a sixteen-year-old male who inhaled Arrid Extra-Dry aerosol deodorant and subsequently died following ventricular fibrillation. The only findings at autopsy were cerebral edema, pulmonary edema and generalized visceral congestion.

In poisoning animals with various aliphatic series haloid-hydrocarbons (LK99 and LD99) free cysteine was found to be a group antidote in rats poisoned with monohaloid-hydrocarbons. It was established that the therapeutic activity of cystein depends not on the nature of haloid and double bonds, but on the number of the haloid atoms in a molecule, the length, ramification and nature of the radical. A good durative action are shown by such cystein derivatives as acetyl-cysteine, glutathione and cystein salts. In poisoning with haloid-alkyls dithiol antidotes (unithiol, mecaptide, BAL) and other drugs proved ineffective.

During the period 1969-71 samples of human body fat were taken during routine necropsies on 201 subjects over 5 years old and 20 stillborn babies and infants under 5 years old, and analysis was carried out for organochlorine pesticide residues. By comparing the results from this period with those from similar studies undertaken in 1963-4 and 1965-7, it is clear that a downward trend continues.

After inhaling fluoroalkane gases, which are used as aerosol propellants, some people have died suddently and unexpectedly. Seeking an explanation, we had 14 monkeys inhale these gases. All developed ventricular premature beats, bigeminy, or tachycardia, which began at an average of 39 (SE +/-4.2) sec. Fluoroalkanes were present in blood, but arterial hypoxemia or hypercapnia was absent, and arterial pressure was reduced only slightly. In contrast, without fluoroalkanes, 3 min of asphyxia or anoxia caused arrhythmias in only one monkey whose arterial oxygen tension had fallen to 16 mm Hg. The ventricular arrhythmias caused in well oxygenated monkeys by fluoroalkane gases may either be mediated through beta adrenergic receptors, since propranolol abolished these arrhythmias, or result from a nonadrenergic, direct, toxic effect of these gases on the heart. These results suggest that some deaths after propellant inhalation may be caused by ventricular tachycardia or fibrillation.