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Exposure data

Sections that indicate the extent of past and present human exposure, the sources of exposure, the people most likely to be exposed and the factors that contribute to the exposure are included at the beginning of each monograph. [Pg.12]

For chemical exposures, the Chemical Abstracts Services Registry Number, the latest Chemical Abstracts Primary Name and the lUPAC Systematic Name are recorded other S5mon5nns are given, but the list is not necessarily comprehensive. For biological agents. [Pg.12]

The dates of first synthesis and of first commercial production of a chemical or mixture are provided for agents which do not occur naturally, this information may allow a reasonable estimate to be made of the date before which no human exposure to the agent could have occurred. The dates of first reported occurrence of an exposure are also provided. In addition, methods of synthesis used in past and present commercial production and different methods of production which may give rise to different impurities are described. [Pg.13]

Data on production, international trade and uses are obtained for representative regions, which usually include Europe, Japan and the United States of America. It should not, however, be inferred that those areas or nations are necessarily the sole or major sources or users of the agent. Some identified uses may not be current or major applications, and the coverage is not necessarily comprehensive. In the case of drugs, mention of their therapeutic uses does not necessarily represent current practice, nor does it imply judgement as to their therapeutic efficacy. [Pg.13]


Vapor Toxicity. Laboratory exposure data indicate that vapor inhalation of alkan olamines presents low hazards at ordinary temperatures (generally, alkan olamines have low vapor pressures). Heated material may cause generation of sufficient vapors to cause adverse effects, including eye and nose irritation. If inhalation exposure is likely, approved respirators are suggested. Monoethan olamine and diethanolamine have OSHA TLVs of 3 ppm. [Pg.9]

Risk characterization is defined as the integration of the data and analysis of the above three components to determine the likelihood that humans wiU. experience any of the various forms of toxicity associated with a substance. When the exposure data are not available, hypothetical risk is characterized by the integration of hazard identification and dose—response evaluation data. [Pg.227]

Process hazard analyses, waste manifests, bills of lading, employee exposure data and other records may need to be maintained beyond the life of the toll. It is typically the toller s responsibility to maintain records of activities that occurred at their site although the client company may choose to keep duplicate records when deemed appropriate. Some of these documents may be proprietary and should be maintained as such. [Pg.138]

METROSOFT Metrosonics Rob Brauch P.O. Box 2307S Rochester, NY 14692 (716) 334-7300 Industrial hygiene information record system. Utilizes hand held monitoring system to record exposure data on computer. [Pg.298]

Employee and environmental health data records system. Maintains medical exposure data of employees. [Pg.308]

Health Hazards Information - Recommended Personal Protective Equipment Data not available Symptoms Following Exposure Irritating to skin and mucous membranes General Treatment for Exposure Data not available Toxicity by Inhalation (ThresholdLimit Value) Not pertinent Short-Term Exposure Limits Not pertinent Toxicity by Ingestion Grade 2 oral rat LDjq 3500 mg/kg Late Toxicity Not pertinent Vapor (Gas) Irritant Characteristics Not pertinent Liquid or Solid Irritant Characteristics Data not available Odor Threshold Not pertinent. [Pg.21]

The problems often encountered in retrospective cohort studies include poor exposure data and incomplete follow-up of all individuals. The accuracy of health outcome data may also be low. [Pg.242]

In risk characterization, the toxicology and exposure data are combined to obtain a quantitative or qualitative expression of risk. [Pg.297]

Hazard identification is defined as tlie process of determining whetlier human exposure to an agent could cause an increase in the incidence of a health condition (cancer, birtli defect, etc.) or whetlier exposure to nonliumans, such as fish, birds, and otlier fonns of wildlife, could cause adverse effects. Hazard identification cliaracterizes tlie liazard in terms of tlie agent and dose of the agent. Since tliere are few hazardous chemicals or hazardous agents for wliich definitive exposure data in humans exists, tlie identification of health hazards is often characterized by the effects of health hazards on laboratory test animals or other test systems. ... [Pg.299]

Toxicity and cancer dose-response data for tire constituents of the gasoline Estimated additional cancer risk for dwelling s occupants when exposure data me combined with cancer dose-response data... [Pg.433]

It is an accepted practice when assessing the environmental effects of pollution on man and his place of abode to use a divisor of 40 (some agencies may divide by 30) against the long-term exposure level in the Occupational Health and Safety Act (OSHA). Much lower exposure limits are necessary due to the much longer term of exposure in the domestic situation. The section of the population most likely to spend long periods of time in the home are those most susceptible to the detrimental effects of pollutants, i.e. the young, the elderly or the infirm. For short-term exposure the known data can be used directly from the list or from animal-exposure data. [Pg.754]

Stanners have designed a test rig (Fig. 19.12) which provides results that can be correlated with actual atmospheric exposure data. The rig has been designed to investigate a wide range of alloying elements in a development programme on slow-weathering steels for which it was essential to have a rapid, reliable and reproducible test that incorporated the specific atmospheric factors responsible for rust formation. [Pg.1028]

Lack of exposure data for most organotins together with limited toxicity information for marine organisms preclude the calculation of risk factors for the marine environment. For dibutyltin, measured concentrations in seawater reflect the use of tributyltin as a marine anti-foulant rather than the use of dibutyltin in plastics. It is therefore not possible to conduct a reliable risk assessment for the current uses of the compormd. [Pg.42]

The available evidence suggests that excretion of methyl parathion metabolites in humans and animals following acute oral exposure is essentially the same and occurs rapidly. Excretion occurs primarily via the urine. Methyl parathion can also be excreted in breast milk, although it has been detected only in a limited number of samples from women of central Asia, for which exposure data were not available (Lederman 1996) (see also Section 3.4.2.2). A study in rats also reported excretion of methyl parathion in the milk (Golubchikov 1991 Goncharuk et al. 1990). [Pg.96]

Information regarding inhalation exposure to endosulfan by humans was inadequate for derivation of inhalation MRLs (Aleksandrowicz 1979 Ely et al. 1967). Limitations associated with these reports include lack of quantitative exposure data, lack of data on the duration of exposure, the possibility of... [Pg.145]

Howard PH, et al. 1991. Handbook of environmental fate and exposure data for organic chemicals. Volume III. Lewis Publishers, 327-343. [Pg.299]

As with all statistical techniques the accuracy of any inference will improve with more data. Experiments are underway which will provide extensive data on several parameters for several coating types. These experiments will include both accelerated and outdoor exposure data. [Pg.98]

Renal Effects. Triehloroethylene may have effeets in the kidney however, studies in humans are limited by having poor or no exposure data and by concomitant exposure to other chemicals. There was no evidence of kidney damage in 250 neurosurgery patients who underwent prolonged trichloroethylene anesthesia (Brittain 1948), nor in 405 women who had caesarean sections and were exposed to trichloroethylene anesthesia (Crawford and Davies 1975). [Pg.45]


See other pages where Exposure data is mentioned: [Pg.509]    [Pg.554]    [Pg.555]    [Pg.309]    [Pg.263]    [Pg.70]    [Pg.248]    [Pg.399]    [Pg.286]    [Pg.110]    [Pg.123]    [Pg.124]    [Pg.43]    [Pg.119]    [Pg.145]    [Pg.166]    [Pg.659]    [Pg.667]    [Pg.816]    [Pg.60]    [Pg.94]    [Pg.152]    [Pg.170]    [Pg.184]    [Pg.222]    [Pg.227]   


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