Exposure study

In a cross-sectional study, exposure and effect are studied simultaneously. This approach contains an inherent problem because exposure must precede the effect. However, it can he used to investigate acute effects and also mild chronic effects (which do not force people to leave their jobs) if exposure has remained rather stable for a long time. When the prevalence of the effects studied are compared with the prevalence in other worker groups (controls or references) which correspond otherwise with the study group but are not exposed to the agent investigated, indicative evidence of possible causality may be obtained. For example, cross-sectional studies have been applied successfully to reveal the associations between mild neurotoxic effects and exposure to organic solvents. ... 

In Swager s study, exposure of 2 to Hay conditions also failed to yield 1 or the corresponding tetrameric PDM (76, R=H). Preparation of the latter molecule, however, was reported almost simultaneously. Starting with known o-iodo-... 

In another study exposure of water containing NDEA to sunlight caused a raoid decrease in the NDEA concentration (to near zero after 16 h)2Q. Wolfe, et al. 2fi found Ji-nitrosoatrazine to be photolabile in natural water with both denitrosation and dealkylation being identified as decomposition pathways. 

Cancer is the major latent harmful effect produced by ionizing radiation and the one that most people exposed to radiation are concerned about. The ability of alpha, beta, and gamma radiation to produce cancer in virtually every tissue and organ in laboratory animals has been well-demonstrated. The development of cancer is not an immediate effect. In humans, radiation-induced leukemia has the shortest latent period at 2 years, while other radiation induced cancers have latent periods >20 years. The mechanism by which cancer is induced in living cells is complex and is a topic of intense study. Exposure to ionizing radiation can produce cancer at any site within the body however, some sites appear to be more common than others, such as the breast, lung, stomach, and thyroid. 

Respiratory Effects. In most case reports of acute accidental exposure to hydrogen sulfide and occupational studies, exposure concentrations and duration were not reported. However, acute inhalation exposure to >500 ppm hydrogen sulfide is considered to result in respiratory failure. Death is often the result of respiratory depression as a result of the action of hydrogen sulfide on the respiratory center in the brain. Respiratory distress was reported in 2 workers exposed to >40 ppm hydrogen sulfide for... 

Each of the main risk analysis elements consists of three interactive studies. Exposure estimates result from the integration of pollutant dispersion patterns and human population patterns. The dispersion patterns, in turn, result from the joint action of emissions and dispersion processes. 

Cohen J. 1988a. Dietary lead estimates for case-study exposure analyses. Memo to the files. Research Triangle Park, NC U.S. Environmental Protection Agency, Office of Air Quality Planning and Standards. May 16, 1988. 

Data for humans show that adverse effects occur at concentrations in air >1.0 mg PCP/m3 and in tissues at more than 8 mg/kg fresh weight (Table 23.7). No adverse effects were noted at daily intakes of 2.1 mg per 70-kg adult or 30 pg/kg BW, up to 1.01 mg/L in drinking water, <0.5 mg/m3 in air, <0.5 mg/L in blood plasma, and <1.0 mg/L in blood (Table 23.7). It is noteworthy that the recommended PCP air concentration of 0.5 mg/m3 results in a daily intake of 2.5 to 3.8 mg (based on 15 to 23 m3 of air inhaled daily, 8-h exposure), equivalent to 42 to 63 pg/kg BW for a 60-kg female. These levels are higher than the currently recommended no-adverse-effect level of 30 pg/kg BW daily (Table 23.7), and overlap or exceed the 58 to 74 pg/kg BW daily range — a level recommended by Williams (1982). Air concentrations >1.0 mg PCP/m3 can produce respiratory irritation in unacclimatized individuals, but concentrations as high as 2.4 mg/m3 can be tolerated by conditioned individuals (USEPA 1980). The biological tolerance value of <1000 pg PCP/L in blood, recommended by Ziemsen etal. (1987), is based on occupational air exposure studies exposure to maximum average air concentrations of 0.18 mg PCP/m3 for up to 34 years produced blood PCP residues of 23 to 775 pg/L, with no measurable adverse effects. The authors concluded... 

Few data were available that met the definitions of AEGL end points. One inhalation study with 20 human subjects described headaches and slight loss of balance at exposure concentrations of 0.1 to 1.5 ppm for exposure durations of up to 8 h (Stewart et al. 1974). Acute exposure of monkeys for 6 h at concentrations ranging between 70 and 100 ppm resulted in severe signs of toxicity including convulsions but no deaths (Jones et al. 1972). In the same study, exposure of rats at a higher concentration, 189 ppm for 4 h, resulted in no toxic signs. Examination of the relationship between exposure duration and concentration for both mild and severe headaches in humans over periods of 1 to 8 h determined that the relationship is C xt=k. 

In a dominant lethal test, treatment of male mice with a single oral dose of 5 mg/kg disulfoton had no effect on male fertility (Herbold 1980). In a three-generation reproductive study, exposure of male and female rats to disulfoton in the diet at 0.5 mg/kg/day resulted a "slight" reduction of litter sizes in... 

Disulfoton induced the liver MFO system in animals (Stevens et al. 1973). In the same study, exposure to disulfoton orally for 3 days also increased ethylmorphine N-demethylase and NADPH oxidase activities, but had no effect on NADPH cytochrome c reductase. Thus, the induction of the MFO system required repeated dosing with relatively high doses. Furthermore, these changes are not specific for disulfoton exposure, and these subtle liver effects require invasive techniques in humans to obtain liver tissue for performance of these enzyme assays. 

The Guidelines for Developmental Toxicity Risk Assessment (US-EPA 1991) outline principles and methods for evaluating data from animal and human studies, exposure data, and other information to characterize risk to human development, growth, survival, and function because of exposure prior to conception, prenatally, or to infants and children. 

In an early range-finding study, exposure of rats to 1000 ppm for 4 hours was lethal to 5 of 6 animals. In a more recent study, the LCso for 4 hours in rats was 2730ppm. Behavior of the animals suggested irritation of the eyes, nose, and respiratory tract, with labored breathing. At necropsy, there were no discernible gross abnormalities of the major organs. 

In a proportional mortality study, exposure to butyl mercaptan, a degradation product of cotton defoliants, did not account for a higher respiratory mortality in cotton-growing areas of California. ... 

Exposure of rats to 800 ppm for 15 minutes was fatal, but nearly all survived when exposed for 13 minutes. There was severe inflammation of all exposed mucosal surfaces, resulting in lacrimation, corneal ulceration, and burning of exposed areas of skin. In another study, exposure of rats to 480 ppm for 40 minutes or to 96ppm for 3.7 hours was fatal in the latter group, effects were pulmonary edema and marked irritation of the bronchial mucosa. Chronic exposure of dogs and rats to about Ippm, 6 hours/day for up to 6 months caused severe pulmonary irritation and some deaths. ... 

In animal studies, exposure to 3 mg demeton/m for 2 hour resulted in no illness in rats during the first exposure, tremors during the second exposure, lacrimation and tremors during the third exposure, and death in 10 of 17 animals during the fourth exposure. ... 

In another study, exposure of rats and male hamsters hy inhalation induced a high incidence of nasal tract carcinomas. ... 

Reproductive effects at the time of the incident included a 44% loss of fetuses in 865 pregnant women (15% expected), and the neonatal death rate increased from 3% to 15%. Reproductive toxicity of MIC has been confirmed in animal studies exposure has caused increased resorptions, reduced pup weight, and reduced neonatal survival. Terato-logical anomalies including wrist drop, everted claw, syndactyly, cleft palate formation, and unequal ribs were observed in rats exposed to concentrations of up to 0.353 ppm during gestation. ... 

In a range-finding study, exposure for 4 hours to 5700ppm was fatal to rats. The oral LDso for male rats and mice was 3200mg/kg. Signs of intoxication included weakness, prostration, and ataxia. 

The acute oral LDso in rats was 530mg/ kg. In a 4-week inhalation study, exposure to... 

In experimental human studies, exposure to 4500ppm for 30-100 minutes resulted in significant impairment in tests of manual dex-... 

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