Occupational exposure estimate

ECHA (2010) Guidance on information requirements and chemical safety assessment - Chapter R. 14 occupational exposure estimation. Version 2... 

Le Moual N, Orlowski E, Schenker MB, et al. 1995. Occupational exposures estimated by means of job exposure matrices in relation to lung function in the PAARC survey. Occup Environ Med 52 634-643. 

Maneb or mancozeb. Headley (1996) used an inductively coupled plasma-atomic emission spectrometry (ICP-AES) method for occupational exposure estimations that measures mancozeb by determining the elemental manganese portion of the pesticide in a sample. The method was successful in analyzing urine (0.02 mg/L), wash water (0.02 mg/L), tank mixes (0.02 mg/L), cellulose acetate filters (0.5 pg), and fabric from patches and clothing (0.5 pg), with detection limits in parentheses. However, ICP-AES methods cannot differentiate among various forms of manganese, so it is important that background... 

Chapter R.14 Occupational Exposure Estimation. ECHA-2010-G-09-EN. Available at http //echa.emopa.eu/documents/10162/13632/information require-... 

Heederik D et al. (1989) Chronic non-specific lung disease and occupational exposures estimated by means of a job exposure matrix the Zutphen Study. Int J Epidemiol 18(2) 382-389... 

Hawthorne, A., et al. (1987) Models for estimating organic emissions from building materials formaldehyde example. Atmos. Environ. 21, No. 2. Lewis, R. G., et al. (1986) Monitoring for non-occupational exposure to pesticides in indoor and personal respiratory air. Presented at the 79th Annual Meeting of the Air Pollution Control Association, Minneapolis, MN. 

Very few data are available on the effects of organotins in humans. Of the reported unintentional occupational exposures, none has an estimate of exposure concentration. Exposure was largely via the inhalation route, with some possibility of dermal exposure. Neurological effects were the most commonly reported, and these can persist for long periods. 

Where sufficient toxicologic information is available, we have derived minimal risk levels (MRLs) for inhalation and oral routes of entry at each duration of exposure (acute, intermediate, and chronic). These MRLs are not meant to support regulatory action but to acquaint health professionals with exposure levels at which adverse health effects are not expected to occur in humans. They should help physicians and public health officials determine the safety of a community living near a chemical emission, given the concentration of a contaminant in air or the estimated daily dose in water. MRLs are based largely on toxicological studies in animals and on reports of human occupational exposure. 

The National Occupational Exposure Survey (NOES), conducted by NIOSH from 1980 to 1983, estimated that 3,205 workers in the agricultural services industry were exposed to endosulfan in the workplace in 1980 (NIOSH 1984). The NOES database does not contain information on the frequency, concentration, or duration of exposure of workers to any chemicals the survey provides only estimates of the number of workers potentially exposed to chemicals in the workplace. 

The approach to developing metrics for process safety is analogous to those that might be used to assess Occupational Exposure risk. One can cite as well several indices that have been developed as metrics for estimating and ranking the safety of a given process or chemical reaction, such as the DOW fire and explosion index,the Stoessel index ° for hazard assessment and classification of chemical reactions, the Inherent Safety Index, the Prototype Index for Inherent Safety, amongst others. ... 

Information on occupational exposure to lead is obtained primarily from the National Occupational Exposure Survey (NOES) and industry surveys of workers. While occupational exposure is widespread, environmental monitoring data on levels of exposure in many occupations are not available. OSHA has established a permissible exposure limit (PEL) for lead of 50 pg/m3 for workplace air (OSHA 1991). NIOSH has estimated that more than 1 million American workers were occupationally exposed to inorganic lead in more than 100 occupations (NIOSH 1977a, 1978a). According to NOES, conducted by NIOSH between 1980 and 1983, an estimated 25,169 employees were exposed to tetraethyl lead (not used in gasoline since December 31, 1995) approximately 57,000 employees were exposed to various lead oxides mostly in non-ferrous foundries, lead smelters, and battery plants 3,902 employees were exposed to lead chloride and 576,579 employees were exposed to some other form of lead in the workplace in 1980 (NIOSH 1990). Workers who operate and maintain solid waste incinerators are also exposed to air lead levels as high as 2,500 pg/m3 (Malkin 1992). 

It has been estimated that over 100,000 workers are potentially exposed to acrylonitrile during production and use (NIOSH 1977, 1988). Occupational exposures include plastic and polymer manufacturers, polymer molders, polymer combustion workers, furniture makers, and manufacturers of fibers and synthetic rubber (EPA 1980a). Other populations who could have elevated exposure to acrylonitrile are residents in the vicinity of industrial sources or chemical waste sites. 

TABLE 5-1. Estimated Levels of Human Exposure to Acrylonitrile for Nonoccupational and Occupational Exposure... 

Workers in industrial facilities manufacturing or using hexachloroethane as an intermediate in the manufacture of other products may be exposed to the chemical by inhalation or dermal absorption. In addition, military or civilian personnel working with smoke or pyrotechnic devices may be exposed. Based on information collected for the National Occupational Exposure Survey, the National Institute for Occupational Safety and Health (NIOSH) estimates that 8,515 workers were potentially exposed to hexachloroethane (NOES 1991). 

In the debate about the toxic effects of dyes and chemicals, there is no doubt that carcinogenic effects are perceived by the general public as the most threatening. Chemicals remain a focus for this concern in spite of the weight of evidence that they make only a minor contribution to the incidence of cancer [60,67,83]. The generally accepted estimate of cancer causation, based on mortality statistics, indicates that only 4% of all cancer deaths are attributable to occupational exposure. Another 2% are considered to arise from environmental causes and 1% from other forms of exposure to industrial products. 

Although a great many deaths have occurred from accidental, intentional, or occupational exposures to HCN, in only a few cases are specific exposure concentrations known. In a review of human fatalities (ATSDR 1997), it was stated that exposure to airborne concentrations of HCN at 180 to 270 ppm were fatal, usually within several minutes, and a concentration of 135 ppm was fatal after 30 min. The average fatal concentration for humans was estimated at 546 ppm for 10 min. The latter data point is based on the work of McNamara (1976), who considered the resistance of man to HCN to be similar to that of the goat and monkey and four times that of the mouse. Fatal levels of HCN cause a brief period of central nervous system stimulation followed by depression, convulsions, coma with abolished deep reflexes and dilated pupils, and death. Several review sources, such as Dudley et al. (1942),... 

Effect of Dose and Duration of Exposure on Toxicity. No studies were located where -hexane concentration was measured in workplace air before workers became ill, so no dose-response relationship can be defined for human neurotoxicity as the result of -hexane exposure. Information on duration of exposure leading to toxicity is available from some case series reports. An occupational exposure caused sensory disturbances in the lower extremities after approximately 2 months (Herskowitz et al. 1971). A case of peripheral neuropathy after 7 months of exposure was reported among press-proofing workers in Taipei (Wang et al. 1986) a serious case resulting in quadriplegia after 8 months of exposure was reported among sandal workers in Japan (Yamamura 1969). Based on case reports, it can be estimated... 

Exposure Levels in Humans. Metabolism of endrin in humans is relatively rapid compared with other organochlorine pesticides. Thus, levels in human blood and tissue may not be reliable estimates of exposure except after very high occupational exposures or acute poisonings (Runhaar et al. 1985). Endrin was not found in adipose tissue samples of the general U.S. population (Stanley 1986), or in adipose breast tissue from breast cancer patients in the United States (Djordjevic et al. 1994). Endrin has been detected in the milk of lactating women (Alawi et al. 1992 Bordet et al. 1993 Dewailly et al. 1993), but no data from the United States could be located. Data on the concentrations of endrin in breast milk from U.S. women would be useful. No information was found on levels of endrin, endrin aldehyde, or endrin ketone in blood and other tissues of people near hazardous waste sites. This information is necessary for assessing the need to conduct health studies on these populations. 

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