Pub Date : 2001-04-16DOI: 10.1002/0471435139.TOX039
J. M. Davis
Manganese (Mn, atomic number 25) and rhenium (Re, atomic number 75) are group 7 (VIIB) transition elements. Before the discovery and confirmation of the existence of rhenium predicted by Mendeleev's periodic law, rhenium was provisionally termed dvi-manganese because of its expected resemblance to manganese. Manganese and rhenium share many of the general chemical characteristics of metals in the transition series, including multiple valency, the ability to form stable complex ions, paramagnetism, and catalytic properties. However, the second and third elements in the transition series generally have chemical properties more similar to each other than to the first member. Thus, in many respects, rhenium is chemically more similar to technetium than to manganese. Inhalation of particulate Mn constitutes the dominant route through which toxicity is expressed under most occupational conditions. Manganese is notably toxic to the central nervous system (CNS) and also has effects on the respiratory system and on reproductive function. Numerous clinical cases of frank Mn toxicity denote a characteristic syndrome that may include psychiatric symptoms, dystonia and rigidity, impaired manual dexterity, and gait disturbances. Several epidemiological studies provide a coherent pattern of evidence of neurotoxicity from occupational exposure to Mn at average concentrations around 1 mg/m3 or lower. The primary effects observed in such workers pertain to motor function, especially hand steadiness, eye–hand coordination, and rapid coordinated movements, which imply involvement of the CNS extrapyramidal system. Although a growing body of literature is devoted to medical applications of the radioactive isotopes 186Re and 188Re, very limited information is available on the toxicity of rhenium itself, which makes it difficult to characterize its toxicity with confidence. The few studies conducted thus far suggest that acute administrations of Re may have relatively low toxicity, at least by noninhalation routes. It has been described as “relatively inert” in the body and produces transient changes in blood pressure (both hypo- and hypertensive), tachycardia, sedation, and ataxia. In one comparative study, the lethal oral dose of Re was about eight times higher than that of molybdenum. However, one report suggests that it could be more potent as an inhalation toxicant. If true, rhenium and manganese might share the feature of having much greater toxicity by inhalation than by ingestion. Keywords: Manganese; Manganese compounds; Rhenium; Rhenium compounds; Nonhuman primates; Clinical cases; Edipemiology; Occupational exposure limits
{"title":"Manganese and Rhenium","authors":"J. M. Davis","doi":"10.1002/0471435139.TOX039","DOIUrl":"https://doi.org/10.1002/0471435139.TOX039","url":null,"abstract":"Manganese (Mn, atomic number 25) and rhenium (Re, atomic number 75) are group 7 (VIIB) transition elements. Before the discovery and confirmation of the existence of rhenium predicted by Mendeleev's periodic law, rhenium was provisionally termed dvi-manganese because of its expected resemblance to manganese. Manganese and rhenium share many of the general chemical characteristics of metals in the transition series, including multiple valency, the ability to form stable complex ions, paramagnetism, and catalytic properties. However, the second and third elements in the transition series generally have chemical properties more similar to each other than to the first member. Thus, in many respects, rhenium is chemically more similar to technetium than to manganese. \u0000 \u0000 \u0000 \u0000Inhalation of particulate Mn constitutes the dominant route through which toxicity is expressed under most occupational conditions. Manganese is notably toxic to the central nervous system (CNS) and also has effects on the respiratory system and on reproductive function. Numerous clinical cases of frank Mn toxicity denote a characteristic syndrome that may include psychiatric symptoms, dystonia and rigidity, impaired manual dexterity, and gait disturbances. Several epidemiological studies provide a coherent pattern of evidence of neurotoxicity from occupational exposure to Mn at average concentrations around 1 mg/m3 or lower. The primary effects observed in such workers pertain to motor function, especially hand steadiness, eye–hand coordination, and rapid coordinated movements, which imply involvement of the CNS extrapyramidal system. Although a growing body of literature is devoted to medical applications of the radioactive isotopes 186Re and 188Re, very limited information is available on the toxicity of rhenium itself, which makes it difficult to characterize its toxicity with confidence. The few studies conducted thus far suggest that acute administrations of Re may have relatively low toxicity, at least by noninhalation routes. It has been described as “relatively inert” in the body and produces transient changes in blood pressure (both hypo- and hypertensive), tachycardia, sedation, and ataxia. In one comparative study, the lethal oral dose of Re was about eight times higher than that of molybdenum. However, one report suggests that it could be more potent as an inhalation toxicant. If true, rhenium and manganese might share the feature of having much greater toxicity by inhalation than by ingestion. \u0000 \u0000 \u0000Keywords: \u0000 \u0000Manganese; \u0000Manganese compounds; \u0000Rhenium; \u0000Rhenium compounds; \u0000Nonhuman primates; \u0000Clinical cases; \u0000Edipemiology; \u0000Occupational exposure limits","PeriodicalId":19820,"journal":{"name":"Patty's Toxicology","volume":"22 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2001-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72963420","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2001-04-16DOI: 10.1002/0471435139.TOX100
L. Kheifets
Electric and magnetic fields (EMF) are ubiquitous. The earth has static electric fields, which produce lightning during thunderstorms, and geomagnetic fields created by electric currents within its core. Electric and magnetic fields are also produced during electric power generation, transmission, and use. Electric power has generally been considered safe during the more than 100 years of its use, although shocks and burns from direct contact with electrical conductors are a recognized health hazard. Of the approximately 1100 deaths from electric shock that occur each year in the United States, about three-fourths result from unsafe operation of household appliances; accidents in the workplace account for the rest. The possible health consequences of electric and magnetic field exposure are a much more recent concern. Power-frequency EMF exposure—unavoidable since the use of electricity has spread throughout the world—has been under investigation since the early 1970s. Investigations have included epidemiologic as well as in vitro and in vivo laboratory studies encompassing a wide range of diseases. The literature on EMF and health is vast, comprising over 1000 published studies, and has been reviewed in depth by several authoritative committees. Of note are reviews by the National Research Council of the National Academy of Sciences (NAS), the National Institute of Environmental Health Sciences (NIEHS) and the U.K. National Radiological Protection Board (NRPB). Electric power systems in the United States, Canada, and Mexico generate and transmit electricity as alternating current (ac), which oscillates at a frequency of 60 cycles per second, or 60 hertz (Hz). Most of the rest of the world generates power at 50Hz. Power-frequency 50- and 60-Hz fields occupy the extremely low-frequency (ELF), nonionizing range of the electromagnetic spectrum. The ELF range includes frequencies from 3 to 3000Hz. Above 3000Hz are, in order of increasing frequency or decreasing wavelength, radio waves, microwaves, infrared radiation, visible light, ultraviolet radiation, x-rays, and gamma rays. Microwaves have enough photon energy to heat tissue; ionizing radiation like x-rays and gamma rays can damage biological systems by breaking chemical bonds. Extremely low-frequency electric and magnetic fields can neither break bonds nor heat tissue, and the electric currents they induce in the body are very weak. Power-frequency fields have very long wavelengths of about 5000km. Exposure distances are much shorter than this wavelength; under these circumstances, electric and magnetic fields are independent. Electric field strength increases with increasing voltage, or electric potential; magnetic field strength increases with increasing current. Both electric and magnetic fields decline rapidly with distance from their source, with a faster decline of fields from point sources such as machinery and a slower decline of fields from power lines
{"title":"Electric and Magnetic Fields and Occupational Health","authors":"L. Kheifets","doi":"10.1002/0471435139.TOX100","DOIUrl":"https://doi.org/10.1002/0471435139.TOX100","url":null,"abstract":"Electric and magnetic fields (EMF) are ubiquitous. The earth has static electric fields, which produce lightning during thunderstorms, and geomagnetic fields created by electric currents within its core. Electric and magnetic fields are also produced during electric power generation, transmission, and use. \u0000 \u0000 \u0000 \u0000Electric power has generally been considered safe during the more than 100 years of its use, although shocks and burns from direct contact with electrical conductors are a recognized health hazard. Of the approximately 1100 deaths from electric shock that occur each year in the United States, about three-fourths result from unsafe operation of household appliances; accidents in the workplace account for the rest. The possible health consequences of electric and magnetic field exposure are a much more recent concern. \u0000 \u0000 \u0000 \u0000Power-frequency EMF exposure—unavoidable since the use of electricity has spread throughout the world—has been under investigation since the early 1970s. Investigations have included epidemiologic as well as in vitro and in vivo laboratory studies encompassing a wide range of diseases. The literature on EMF and health is vast, comprising over 1000 published studies, and has been reviewed in depth by several authoritative committees. Of note are reviews by the National Research Council of the National Academy of Sciences (NAS), the National Institute of Environmental Health Sciences (NIEHS) and the U.K. National Radiological Protection Board (NRPB). \u0000 \u0000 \u0000 \u0000Electric power systems in the United States, Canada, and Mexico generate and transmit electricity as alternating current (ac), which oscillates at a frequency of 60 cycles per second, or 60 hertz (Hz). Most of the rest of the world generates power at 50Hz. Power-frequency 50- and 60-Hz fields occupy the extremely low-frequency (ELF), nonionizing range of the electromagnetic spectrum. The ELF range includes frequencies from 3 to 3000Hz. Above 3000Hz are, in order of increasing frequency or decreasing wavelength, radio waves, microwaves, infrared radiation, visible light, ultraviolet radiation, x-rays, and gamma rays. Microwaves have enough photon energy to heat tissue; ionizing radiation like x-rays and gamma rays can damage biological systems by breaking chemical bonds. Extremely low-frequency electric and magnetic fields can neither break bonds nor heat tissue, and the electric currents they induce in the body are very weak. \u0000 \u0000 \u0000 \u0000Power-frequency fields have very long wavelengths of about 5000km. Exposure distances are much shorter than this wavelength; under these circumstances, electric and magnetic fields are independent. \u0000 \u0000 \u0000 \u0000Electric field strength increases with increasing voltage, or electric potential; magnetic field strength increases with increasing current. Both electric and magnetic fields decline rapidly with distance from their source, with a faster decline of fields from point sources such as machinery and a slower decline of fields from power lines","PeriodicalId":19820,"journal":{"name":"Patty's Toxicology","volume":"23 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2001-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88488054","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2001-04-16DOI: 10.1002/0471435139.TOX062
J. B. Reid
It is impossible to generalize on the saturated methyl halogenated aliphatic hydrocarbons discussed in this chapter. Physical properties and toxicological manifestations differ over a broad range depending on the particular halogen and the number of halogen atoms involved. As mentioned in the previous edition, the usefulness of these compounds has been significantly reduced because of the concern over stratospheric ozone depletion. On the other hand, toxicological interest in these compounds has increased because of concern over their production in chlorinated water systems. The USEPA (National Center for Environmental Assessment) and others are actively investigating the possible relationship between chlorination of drinking water sources and human cancer through many avenues, including sophisticated epidemiologic tools. Many of the compounds have been shown to produce cancer in animals, but their potency for humans is still under consideration, and the complex interactions with regard to human health are challenging. The other area of biochemistry that is of relevance to some of these materials is in regard to lipid peroxidation and its role in disease and in extrapolation from animal species to humans. As in the previous editions, this review relies extensively on information provided in earlier editions. Several online databases were utilized in searching for the most recent information in preparing the chapter. These included NTP (National Toxicology Program), IRIS (Integrated Risk Information Service), and the ATSDR (Agency for Toxic Substances and Disease Registry) websites. Most recent information was sought through MEDLINE, and, when possible, the original articles were reviewed. Debatably, IRIS was considered to be the last word with regard to cancer. Many of the compounds have been recently reviewed by the ATSDR and are reported in their toxicological profiles. Recent reviews were utilized in preparing this chapter. In addition, the Pocket Guide to Chemical Hazards and the ACGIH's TLV's and Other Occupational Exposure Values-1999 were utilized. Keywords: Methyl chloride; Refrigerant; Methyl bromide; Fire extinguishing agents; Methyl iodide; Methylene chloride; Cyanosis; Chloroform; Bromoform; Lacrimator; Iodoform; Carbon tetrachloride; Tetrabromomethane
{"title":"Saturated Methyl Halogenated Aliphatic Hydrocarbons","authors":"J. B. Reid","doi":"10.1002/0471435139.TOX062","DOIUrl":"https://doi.org/10.1002/0471435139.TOX062","url":null,"abstract":"It is impossible to generalize on the saturated methyl halogenated aliphatic hydrocarbons discussed in this chapter. Physical properties and toxicological manifestations differ over a broad range depending on the particular halogen and the number of halogen atoms involved. \u0000 \u0000 \u0000 \u0000As mentioned in the previous edition, the usefulness of these compounds has been significantly reduced because of the concern over stratospheric ozone depletion. On the other hand, toxicological interest in these compounds has increased because of concern over their production in chlorinated water systems. The USEPA (National Center for Environmental Assessment) and others are actively investigating the possible relationship between chlorination of drinking water sources and human cancer through many avenues, including sophisticated epidemiologic tools. Many of the compounds have been shown to produce cancer in animals, but their potency for humans is still under consideration, and the complex interactions with regard to human health are challenging. \u0000 \u0000 \u0000 \u0000The other area of biochemistry that is of relevance to some of these materials is in regard to lipid peroxidation and its role in disease and in extrapolation from animal species to humans. \u0000 \u0000 \u0000 \u0000As in the previous editions, this review relies extensively on information provided in earlier editions. Several online databases were utilized in searching for the most recent information in preparing the chapter. These included NTP (National Toxicology Program), IRIS (Integrated Risk Information Service), and the ATSDR (Agency for Toxic Substances and Disease Registry) websites. Most recent information was sought through MEDLINE, and, when possible, the original articles were reviewed. Debatably, IRIS was considered to be the last word with regard to cancer. Many of the compounds have been recently reviewed by the ATSDR and are reported in their toxicological profiles. Recent reviews were utilized in preparing this chapter. In addition, the Pocket Guide to Chemical Hazards and the ACGIH's TLV's and Other Occupational Exposure Values-1999 were utilized. \u0000 \u0000 \u0000Keywords: \u0000 \u0000Methyl chloride; \u0000Refrigerant; \u0000Methyl bromide; \u0000Fire extinguishing agents; \u0000Methyl iodide; \u0000Methylene chloride; \u0000Cyanosis; \u0000Chloroform; \u0000Bromoform; \u0000Lacrimator; \u0000Iodoform; \u0000Carbon tetrachloride; \u0000Tetrabromomethane","PeriodicalId":19820,"journal":{"name":"Patty's Toxicology","volume":"58 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2001-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87196228","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2001-04-16DOI: 10.1002/0471435139.TOX097
H. Mahar
The human body has the thermoregulatory capacity to maintain its body temperature within about 1°C of normal (i.e., 37°C) under a variety of external environmental temperatures. When the body's heat loss to the environment is greater than its ability to maintain its internal homeostatic temperature, the body undergoes cold strain in response to the external cold temperature stress. Prolonged exposure to any temperature less than normal body temperature to which the body's thermoregulatory capacity cannot accommodate may result in cold-related injuries to tissues or cause other systemic changes, including hypothermia and death. Those injuries may involve local tissue damage that results when the tissue actually freezes (e.g., frostbite) or that can result from nonfreezing conditions in tissue sufficient to cause temporary or permanent vascular damage (e.g., chilblain, immersion foot). Heat loss sufficient to overcome the body's thermoregulatory mechanisms can produce a critical drop in the body's deep-core temperature and eventually hypothermia and death. Exposure to cold stress may also produce physiological or metabolic changes or shifts in endocrine systems, affect judgment or behavior, or exacerbate existing medical conditions (e.g., cardiovascular disease). For acute exposures, the body's response to cold stress is a function of the rate of heat loss, the temperature to which the individual is exposed, and the duration of exposure. For chronic exposures which produce subtle endocrine and metabolic shifts, the diurnal or seasonal (e.g., circannual) periodicity of that exposure may be more important than the environmental temperature to which the person is exposed. In assessing the impacts of exposures to cold stress, one should differentiate between normal changes that result as the body accommodates to that stress (homeostatic response mechanisms) and actual damage or disruption that result when the body's homeostatic response mechanisms are exceeded. Keywords: Cold stress; Prevalence response; Thermoregulatory control; Delayed thermoregulatory control; Adaptation; Injuries; Freezing cold injuries; Nonfreezing cold injuries; Hypothermia; Manual performance; Cognitive function; Endocrine function; Respiratory system; Immunological responses; Carcinogenesis; Control; Exposure standards
{"title":"Cold Stress and Strain","authors":"H. Mahar","doi":"10.1002/0471435139.TOX097","DOIUrl":"https://doi.org/10.1002/0471435139.TOX097","url":null,"abstract":"The human body has the thermoregulatory capacity to maintain its body temperature within about 1°C of normal (i.e., 37°C) under a variety of external environmental temperatures. When the body's heat loss to the environment is greater than its ability to maintain its internal homeostatic temperature, the body undergoes cold strain in response to the external cold temperature stress. Prolonged exposure to any temperature less than normal body temperature to which the body's thermoregulatory capacity cannot accommodate may result in cold-related injuries to tissues or cause other systemic changes, including hypothermia and death. Those injuries may involve local tissue damage that results when the tissue actually freezes (e.g., frostbite) or that can result from nonfreezing conditions in tissue sufficient to cause temporary or permanent vascular damage (e.g., chilblain, immersion foot). Heat loss sufficient to overcome the body's thermoregulatory mechanisms can produce a critical drop in the body's deep-core temperature and eventually hypothermia and death. \u0000 \u0000 \u0000 \u0000Exposure to cold stress may also produce physiological or metabolic changes or shifts in endocrine systems, affect judgment or behavior, or exacerbate existing medical conditions (e.g., cardiovascular disease). For acute exposures, the body's response to cold stress is a function of the rate of heat loss, the temperature to which the individual is exposed, and the duration of exposure. For chronic exposures which produce subtle endocrine and metabolic shifts, the diurnal or seasonal (e.g., circannual) periodicity of that exposure may be more important than the environmental temperature to which the person is exposed. In assessing the impacts of exposures to cold stress, one should differentiate between normal changes that result as the body accommodates to that stress (homeostatic response mechanisms) and actual damage or disruption that result when the body's homeostatic response mechanisms are exceeded. \u0000 \u0000 \u0000Keywords: \u0000 \u0000Cold stress; \u0000Prevalence response; \u0000Thermoregulatory control; \u0000Delayed thermoregulatory control; \u0000Adaptation; \u0000Injuries; \u0000Freezing cold injuries; \u0000Nonfreezing cold injuries; \u0000Hypothermia; \u0000Manual performance; \u0000Cognitive function; \u0000Endocrine function; \u0000Respiratory system; \u0000Immunological responses; \u0000Carcinogenesis; \u0000Control; \u0000Exposure standards","PeriodicalId":19820,"journal":{"name":"Patty's Toxicology","volume":"138 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2001-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77521943","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2001-04-16DOI: 10.1002/0471435139.tox009
B. Cohrssen
Knowing where to go to get relevant up-to-date as well as state-of-the-art information about the health effects of a chemical is essential for effective protection of workers and the environment. The means to access information is changing every day and the amount of occupational health and safety information is expanding. Finding information to prepare a MSDS, to respond to an emergency, to meet legislative and regulatory requirements, to determine the cause of an illness, or to develop a health and safety program can be challenging, overwhelming, and time-consuming. Toxicological information and data are of interest to more than workers, toxicologists, industrial hygienists, lawyers, and regulators. The general public is increasingly interested in the health effects of industrial chemicals. Depending upon who wants the information and why they want it affects the use it will have and the amount of detail required about the chemical. For some, knowing that the basic health effects are respiratory or skin irritation is enough. For others, knowing the mechanics of the way the chemical works in the body will be of interest and required. For still others, the information is needed for an emergency so that whatever information is obtained must be gained quickly. The recency of the information may affect which information sources are used. Electronic data bases, which have become a fact of life and are probably now the first source of reference for most people looking for chemical information and toxicological data, may not be the best resource. Electronic data bases can include both CD-ROMs and on-line databases available either directly from the service provider such as DIALOG, MEDLINE, or CCOHS or via the Internet. The government sources of information are usually free; however, there are fees for many of the other services. Comprehensive information and data are necessary to develop regulations to protect people and the environment from the effects of exposure from a chemical; all of this information may not be available from an electronic source. But electronic data sources are the places to go to quickly to find current toxicological data. There are a number of different methods of finding electronic data sources, and they are discussed later in the chapter. There are a number of different types of safety, health, and toxicological information sources. These include traditional paper sources such as books, journals, and periodicals which were the typical sources of information before about 1970. There are also gray data. Gray data can include private or government research reports that have not been published, company catalogs, and material safety data sheets (MSDSs). These information sources are called gray data because they are difficult to find and are not always readily available. Still other sources of health and safety data are laws, standards, and patents in print. A preamble to a Federal OSHA health standard provide
{"title":"Toxic Chemical Information Sources","authors":"B. Cohrssen","doi":"10.1002/0471435139.tox009","DOIUrl":"https://doi.org/10.1002/0471435139.tox009","url":null,"abstract":"Knowing where to go to get relevant up-to-date as well as state-of-the-art information about the health effects of a chemical is essential for effective protection of workers and the environment. The means to access information is changing every day and the amount of occupational health and safety information is expanding. Finding information to prepare a MSDS, to respond to an emergency, to meet legislative and regulatory requirements, to determine the cause of an illness, or to develop a health and safety program can be challenging, overwhelming, and time-consuming. Toxicological information and data are of interest to more than workers, toxicologists, industrial hygienists, lawyers, and regulators. The general public is increasingly interested in the health effects of industrial chemicals. \u0000 \u0000 \u0000 \u0000Depending upon who wants the information and why they want it affects the use it will have and the amount of detail required about the chemical. For some, knowing that the basic health effects are respiratory or skin irritation is enough. For others, knowing the mechanics of the way the chemical works in the body will be of interest and required. For still others, the information is needed for an emergency so that whatever information is obtained must be gained quickly. \u0000 \u0000 \u0000 \u0000The recency of the information may affect which information sources are used. Electronic data bases, which have become a fact of life and are probably now the first source of reference for most people looking for chemical information and toxicological data, may not be the best resource. Electronic data bases can include both CD-ROMs and on-line databases available either directly from the service provider such as DIALOG, MEDLINE, or CCOHS or via the Internet. The government sources of information are usually free; however, there are fees for many of the other services. Comprehensive information and data are necessary to develop regulations to protect people and the environment from the effects of exposure from a chemical; all of this information may not be available from an electronic source. But electronic data sources are the places to go to quickly to find current toxicological data. There are a number of different methods of finding electronic data sources, and they are discussed later in the chapter. \u0000 \u0000 \u0000 \u0000There are a number of different types of safety, health, and toxicological information sources. These include traditional paper sources such as books, journals, and periodicals which were the typical sources of information before about 1970. There are also gray data. Gray data can include private or government research reports that have not been published, company catalogs, and material safety data sheets (MSDSs). These information sources are called gray data because they are difficult to find and are not always readily available. Still other sources of health and safety data are laws, standards, and patents in print. A preamble to a Federal OSHA health standard provide","PeriodicalId":19820,"journal":{"name":"Patty's Toxicology","volume":"4 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2001-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78744102","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2001-04-16DOI: 10.1002/0471435139.TOX025.PUB2
W. Boyes
Neurotoxicity is important to consider as a component of occupational and environmental safety and health programs. The failure to do so has contributed to a number of tragic cases in which workers, consumers of manufactured products, and people exposed in the environment were irreparably harmed by exposure to industrial compounds that proved toxic to the nervous system. The National Institute for Occupational Safety and Health (NIOSH) has listed neurotoxic disorders as one of the ten leading occupational problems in the United States. Many of the most severe environmental, industrial, and commercial human health disasters attributable to chemical exposure have involved neurotoxic effects. In Detroit, Michigan, in 1934, for example, an automotive redesign required grinding large amounts of excess lead solder from each car. Inhalation of the resulting lead dust produced between 2,700 and 4,000 cases of lead poisoning whose symptoms ranged from mild gastrointestinal upset to severe neurological deficits, including peripheral neuropathy and encephalopathy. As many as 12 people may have died. In another case that occurred during the Prohibition Era, a single batch of the popular ethanol-based elixir “Ginger Jake” was adulterated with tri-o-cresylphosphate (TOCP). This batch was then distributed throughout the southeastern and midwestern United States. As many as 50,000 people suffered peripheral neuropathy caused by degeneration of the large, long axons in the peripheral nerves of the legs and spinal cord. In a food contamination episode, 459 people were killed and more than 6,500 became ill in Iraq from methylmercury which was applied as a fungicide to seed grain intended for planting, but which was instead ground into flour and cooked into bread. Methylmercury was also the cause of environmental poisonings in Minamata Bay, Japan, in which industrial effluent discharged into the Bay bioconcentrated in the food chain and eventually led to exposure of thousands of inhabitants who consumed seafood from the bay. The effects on Minamata children exposed in utero were particularly severe. Since that time methlymercury poisoning has been referred to as “Minamata disease.” Fortunately, catastrophic disasters are relatively rare occurrences that typically involve exposures to high concentrations of neurotoxic compounds. A more common concern in occupational and environmental settings is exposure to lower levels of potentially neurotoxic compounds, for long periods of time. It is important to consider neurotoxicity in long-term, low-level exposure situations. Many occupational and environmental exposure standards have been established on the basis of effects on the nervous system. There is also concern that subtle neurotoxic damage might not be evident at the time of exposure due to the plasticity and functional reserve capacity of the nervous system but may become manifest later. Damage inflicted long ago may become evident as individuals age or under
{"title":"Neurotoxicology and Behavior","authors":"W. Boyes","doi":"10.1002/0471435139.TOX025.PUB2","DOIUrl":"https://doi.org/10.1002/0471435139.TOX025.PUB2","url":null,"abstract":"Neurotoxicity is important to consider as a component of occupational and environmental safety and health programs. The failure to do so has contributed to a number of tragic cases in which workers, consumers of manufactured products, and people exposed in the environment were irreparably harmed by exposure to industrial compounds that proved toxic to the nervous system. The National Institute for Occupational Safety and Health (NIOSH) has listed neurotoxic disorders as one of the ten leading occupational problems in the United States. Many of the most severe environmental, industrial, and commercial human health disasters attributable to chemical exposure have involved neurotoxic effects. In Detroit, Michigan, in 1934, for example, an automotive redesign required grinding large amounts of excess lead solder from each car. Inhalation of the resulting lead dust produced between 2,700 and 4,000 cases of lead poisoning whose symptoms ranged from mild gastrointestinal upset to severe neurological deficits, including peripheral neuropathy and encephalopathy. As many as 12 people may have died. In another case that occurred during the Prohibition Era, a single batch of the popular ethanol-based elixir “Ginger Jake” was adulterated with tri-o-cresylphosphate (TOCP). This batch was then distributed throughout the southeastern and midwestern United States. As many as 50,000 people suffered peripheral neuropathy caused by degeneration of the large, long axons in the peripheral nerves of the legs and spinal cord. In a food contamination episode, 459 people were killed and more than 6,500 became ill in Iraq from methylmercury which was applied as a fungicide to seed grain intended for planting, but which was instead ground into flour and cooked into bread. Methylmercury was also the cause of environmental poisonings in Minamata Bay, Japan, in which industrial effluent discharged into the Bay bioconcentrated in the food chain and eventually led to exposure of thousands of inhabitants who consumed seafood from the bay. The effects on Minamata children exposed in utero were particularly severe. Since that time methlymercury poisoning has been referred to as “Minamata disease.” \u0000 \u0000 \u0000 \u0000Fortunately, catastrophic disasters are relatively rare occurrences that typically involve exposures to high concentrations of neurotoxic compounds. A more common concern in occupational and environmental settings is exposure to lower levels of potentially neurotoxic compounds, for long periods of time. It is important to consider neurotoxicity in long-term, low-level exposure situations. Many occupational and environmental exposure standards have been established on the basis of effects on the nervous system. There is also concern that subtle neurotoxic damage might not be evident at the time of exposure due to the plasticity and functional reserve capacity of the nervous system but may become manifest later. Damage inflicted long ago may become evident as individuals age or under","PeriodicalId":19820,"journal":{"name":"Patty's Toxicology","volume":"8 1","pages":"35-74"},"PeriodicalIF":0.0,"publicationDate":"2001-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79959443","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2001-04-16DOI: 10.1002/0471435139.TOX021
D. Gardner
The genus Mycobacterium is one of the most widely distributed bacteria genera in nature and includes those organisms that cause two of the world's most prevalent infectious diseases in humans, M. tuberculosis, the agent of tuberculosis and M. leprae, the agent of leprosy. A large number of other species in this genera are widespread and occur as contaminants in soil, water, or organic debris. These organisms may be ingested or inhaled in dust particles and produce syndromes that are indistinguishable from classic tuberculosis. The term tuberculosis (TB) is commonly applied to all cases of mycobacterial infections except leprosy. Many of these infections are now being recognized more frequently in immunosuppressed patients who have organ transplants, individuals being treated for leukemia or cancer, and patients suffering from AIDS. In most cases of TB in humans, the lungs are the major organ affected but other tissues and organs such as bone, skin, and the digestive tract may also be infected. Although this chapter focuses primarily on tuberculosis, a discussion of a few of these other opportunistic organisms in this genus that are associated with human disease are also discussed. The bibliography provided will guide the readers to works which they can consult for more detailed information about these organisms. These references contain discussions on taxonomy, growth requirements, as well as the morphological characteristics, physiology, pathogenicity, and the metabolic activity of these organisms. Keywords: Tuberculosis; Organisms; Sources; Health issues; Risk factors; Prevention; Treatment
{"title":"Tuberculosis and Other Mycobacteria","authors":"D. Gardner","doi":"10.1002/0471435139.TOX021","DOIUrl":"https://doi.org/10.1002/0471435139.TOX021","url":null,"abstract":"The genus Mycobacterium is one of the most widely distributed bacteria genera in nature and includes those organisms that cause two of the world's most prevalent infectious diseases in humans, M. tuberculosis, the agent of tuberculosis and M. leprae, the agent of leprosy. A large number of other species in this genera are widespread and occur as contaminants in soil, water, or organic debris. These organisms may be ingested or inhaled in dust particles and produce syndromes that are indistinguishable from classic tuberculosis. The term tuberculosis (TB) is commonly applied to all cases of mycobacterial infections except leprosy. Many of these infections are now being recognized more frequently in immunosuppressed patients who have organ transplants, individuals being treated for leukemia or cancer, and patients suffering from AIDS. In most cases of TB in humans, the lungs are the major organ affected but other tissues and organs such as bone, skin, and the digestive tract may also be infected. Although this chapter focuses primarily on tuberculosis, a discussion of a few of these other opportunistic organisms in this genus that are associated with human disease are also discussed. \u0000 \u0000 \u0000 \u0000The bibliography provided will guide the readers to works which they can consult for more detailed information about these organisms. These references contain discussions on taxonomy, growth requirements, as well as the morphological characteristics, physiology, pathogenicity, and the metabolic activity of these organisms. \u0000 \u0000 \u0000Keywords: \u0000 \u0000Tuberculosis; \u0000Organisms; \u0000Sources; \u0000Health issues; \u0000Risk factors; \u0000Prevention; \u0000Treatment","PeriodicalId":19820,"journal":{"name":"Patty's Toxicology","volume":"22 1","pages":"747-761"},"PeriodicalIF":0.0,"publicationDate":"2001-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82097196","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2001-04-16DOI: 10.1002/0471435139.TOX086
R. Boatman, J. Knaak
There are currently seven U.S. manufacturers of ethers and other derivatives of ethylene glycol (EG), diethylene glycol (DEG), and higher glycols. Five of them are members of the American Chemistry Council (ACC) Glycol Ethers' Panel. The glycol ethers most commonly encountered industrially are colorless liquids that have mild ethereal odors. Alkyl glycol ethers are manufactured in a closed, continuous process by reacting ethylene oxide with an anhydrous alcohol in the presence of a suitable catalyst. Depending on the molar ratios of the reactants and other process parameters, the product mixtures obtained contain varying amounts of the monoethylene-, diethylene-, triethylene-, and higher glycol ethers. Typically, the products in these mixtures are separated and purified by fractional distillation. The miscibility of most of these ethers with water and with a large number of organic solvents makes them especially useful as solvents in oil–water compositions. Their relatively slow rate of evaporation also makes them useful as solvents and coalescing agents in paints. Other uses include inks, cleaners, chemical intermediates, process solvents, brake fluids, and deicers. The ethers of the higher glycols are used as hydraulic fluids. An estimate of the U.S. production and use of representative ethylene glycol ethers is presented. Production of ethylene glycol ethers (total) in Western Europe amounted to 245 thousand metric tons in 1995. Occupational exposure to glycol ethers occurs dermally and by inhalation. Ingestion is not a concern in industrial exposure, although some cases of intentional ingestion of consumer products containing ethylene glycol ethers have been reported. A number of analytical methods have been published that are suitable for detecting glycol ethers in environmental air samples. Glycol ethers generally have low acute, single-dose toxicity, and LD50 values generally range from 1.0 to 4.0 g/kg of body weight. In animals and humans, high-dose administrations (>350 mg/kg) result in central nervous system depression, although the results from many studies show no specific damage to neural tissues. Other toxicological effects attributable to glycol ethers are associated with metabolism to the corresponding alkoxyacetic acids. In the case of EGME, EGEE, and certain other glycol ether derivatives, significant reproductive, developmental, hematologic, and immunologic effects have been associated with the formation of either methoxyacetic (MAA) or ethoxyacetic acids (EAA). For other glycol ether derivatives substituted with propyl, butyl, or higher homologues, developmental effects secondary to maternal toxicity (without teratogenic effects), as well as hematologic effects, are observed. Ethylene glycol ethers and acetates may enter the environment from manufacturing effluents and emissions and as a result of their use in commercial products. Keywords: Ethylene glycol ethers; Analytical m
{"title":"Ethers of Ethylene Glycol and Derivatives","authors":"R. Boatman, J. Knaak","doi":"10.1002/0471435139.TOX086","DOIUrl":"https://doi.org/10.1002/0471435139.TOX086","url":null,"abstract":"There are currently seven U.S. manufacturers of ethers and other derivatives of ethylene glycol (EG), diethylene glycol (DEG), and higher glycols. Five of them are members of the American Chemistry Council (ACC) Glycol Ethers' Panel. \u0000 \u0000 \u0000 \u0000The glycol ethers most commonly encountered industrially are colorless liquids that have mild ethereal odors. Alkyl glycol ethers are manufactured in a closed, continuous process by reacting ethylene oxide with an anhydrous alcohol in the presence of a suitable catalyst. Depending on the molar ratios of the reactants and other process parameters, the product mixtures obtained contain varying amounts of the monoethylene-, diethylene-, triethylene-, and higher glycol ethers. Typically, the products in these mixtures are separated and purified by fractional distillation. \u0000 \u0000 \u0000 \u0000The miscibility of most of these ethers with water and with a large number of organic solvents makes them especially useful as solvents in oil–water compositions. Their relatively slow rate of evaporation also makes them useful as solvents and coalescing agents in paints. Other uses include inks, cleaners, chemical intermediates, process solvents, brake fluids, and deicers. The ethers of the higher glycols are used as hydraulic fluids. An estimate of the U.S. production and use of representative ethylene glycol ethers is presented. Production of ethylene glycol ethers (total) in Western Europe amounted to 245 thousand metric tons in 1995. \u0000 \u0000 \u0000 \u0000Occupational exposure to glycol ethers occurs dermally and by inhalation. Ingestion is not a concern in industrial exposure, although some cases of intentional ingestion of consumer products containing ethylene glycol ethers have been reported. \u0000 \u0000 \u0000 \u0000A number of analytical methods have been published that are suitable for detecting glycol ethers in environmental air samples. \u0000 \u0000 \u0000 \u0000Glycol ethers generally have low acute, single-dose toxicity, and LD50 values generally range from 1.0 to 4.0 g/kg of body weight. In animals and humans, high-dose administrations (>350 mg/kg) result in central nervous system depression, although the results from many studies show no specific damage to neural tissues. Other toxicological effects attributable to glycol ethers are associated with metabolism to the corresponding alkoxyacetic acids. In the case of EGME, EGEE, and certain other glycol ether derivatives, significant reproductive, developmental, hematologic, and immunologic effects have been associated with the formation of either methoxyacetic (MAA) or ethoxyacetic acids (EAA). For other glycol ether derivatives substituted with propyl, butyl, or higher homologues, developmental effects secondary to maternal toxicity (without teratogenic effects), as well as hematologic effects, are observed. \u0000 \u0000 \u0000 \u0000Ethylene glycol ethers and acetates may enter the environment from manufacturing effluents and emissions and as a result of their use in commercial products. \u0000 \u0000 \u0000Keywords: \u0000 \u0000Ethylene glycol ethers; \u0000Analytical m","PeriodicalId":19820,"journal":{"name":"Patty's Toxicology","volume":"12 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2001-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81715150","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2001-04-16DOI: 10.1002/0471435139.TOX080
R. M. David, R. H. Mckee, J. Butala, R. Barter, M. Kayser
The simple aliphatic esters of benzoic acid are liquids used as solvents, flavors, or perfumes. The arylbenzoate benzyl is used as a miticide or plasticizer. In general, these compounds have a low order of toxicity. The primary effect expected from ingestion of moderate amounts of benzoates is gastrointestinal irritation, gastric pain, nausea, and vomiting. Available data indicate a low order of skin absorbability, and the undiluted materials may be either slight or moderate skin irritants. In rabbits, the degree of skin irritation caused by alkyl benzoates increases with an increase in molecular weight. The salicylates are used as flavorants, perfumes, or analgesics. The most commonly used member of this class of compounds is methyl salicylate. Ingestion of relatively small quantities of methyl salicylate may cause severe, rapid-onset salicylate poisoning. The lower alkyl esters of p- or 4-hydroxybenzoic acid (C1 to C4), also named the methyl-, ethyl-, propyl-, and butyl parabens, are high-boiling liquids that decompose on heating. They are widely used in the food, cosmetic, and pharmaceutical industries as preservatives, bacteristats, and fungistats. Parabens also have been used therapeutically for the treatment of moniliasis, a Candida albicans infection. By the oral route, parabens are rapidly absorbed, metabolized, and excreted. The lower paraben homologues have low potential for acute or chronic systemic toxicity and are therefore approved as human food additives. The cinnamates (phenyl acrylates, phenylpropenoic acid esters) are mainly used as fragrances in the perfume industry. The cinnamates appear to have low to moderate toxicity in mammals. In humans, dermal exposure to allyl cinnamate may cause skin irritation. Some p-aminobenzoic acid (PABA) esters occur naturally, since the free compound, PABA, is an intricate part of the vitamin B complex and is utilized for its synthesis. PABA esters exhibit a low order of acute toxicity in experimental animals. In humans, cases of methemoglobinemia after topical benzocaine or procaine use have been reported. Sunscreen agents containing PABA esters may occasionally produce allergic photosensitization. The ortho-aminobenzoates (anthranilates) are less irritating and less likely to cause sensitization than the para-aminobenzoates, but have less therapeutic usefulness. They are used in some sunscreen lotions. Anthranilates have low toxicity potential. Long-chain fatty acids of glycerides may be replaced by one or more acetyl groups to produce mono-, di-, or triacetin. Acetins, propionates, and butyrates serve as food additives, solvents or plasticizers, and surface-active agents. Available evidence indicates that these agents exhibit a low order of toxicity. Normally, no irritant effects occur upon inhalation or direct dermal contact. The higher glycerides of fatty acids with odd-numbered carbon chains (C5 to C11) are found naturally in very sma
{"title":"Esters of Aromatic Mono‐, Di‐, and Tricarboxylic Acids, Aromatic Diacids and Di‐, Tri‐, Or Polyalcohols","authors":"R. M. David, R. H. Mckee, J. Butala, R. Barter, M. Kayser","doi":"10.1002/0471435139.TOX080","DOIUrl":"https://doi.org/10.1002/0471435139.TOX080","url":null,"abstract":"The simple aliphatic esters of benzoic acid are liquids used as solvents, flavors, or perfumes. The arylbenzoate benzyl is used as a miticide or plasticizer. In general, these compounds have a low order of toxicity. The primary effect expected from ingestion of moderate amounts of benzoates is gastrointestinal irritation, gastric pain, nausea, and vomiting. Available data indicate a low order of skin absorbability, and the undiluted materials may be either slight or moderate skin irritants. In rabbits, the degree of skin irritation caused by alkyl benzoates increases with an increase in molecular weight. \u0000 \u0000 \u0000 \u0000The salicylates are used as flavorants, perfumes, or analgesics. The most commonly used member of this class of compounds is methyl salicylate. Ingestion of relatively small quantities of methyl salicylate may cause severe, rapid-onset salicylate poisoning. \u0000 \u0000 \u0000 \u0000The lower alkyl esters of p- or 4-hydroxybenzoic acid (C1 to C4), also named the methyl-, ethyl-, propyl-, and butyl parabens, are high-boiling liquids that decompose on heating. They are widely used in the food, cosmetic, and pharmaceutical industries as preservatives, bacteristats, and fungistats. Parabens also have been used therapeutically for the treatment of moniliasis, a Candida albicans infection. \u0000 \u0000 \u0000 \u0000By the oral route, parabens are rapidly absorbed, metabolized, and excreted. The lower paraben homologues have low potential for acute or chronic systemic toxicity and are therefore approved as human food additives. \u0000 \u0000 \u0000 \u0000The cinnamates (phenyl acrylates, phenylpropenoic acid esters) are mainly used as fragrances in the perfume industry. The cinnamates appear to have low to moderate toxicity in mammals. In humans, dermal exposure to allyl cinnamate may cause skin irritation. \u0000 \u0000 \u0000 \u0000Some p-aminobenzoic acid (PABA) esters occur naturally, since the free compound, PABA, is an intricate part of the vitamin B complex and is utilized for its synthesis. PABA esters exhibit a low order of acute toxicity in experimental animals. In humans, cases of methemoglobinemia after topical benzocaine or procaine use have been reported. Sunscreen agents containing PABA esters may occasionally produce allergic photosensitization. \u0000 \u0000 \u0000 \u0000The ortho-aminobenzoates (anthranilates) are less irritating and less likely to cause sensitization than the para-aminobenzoates, but have less therapeutic usefulness. They are used in some sunscreen lotions. Anthranilates have low toxicity potential. \u0000 \u0000 \u0000 \u0000Long-chain fatty acids of glycerides may be replaced by one or more acetyl groups to produce mono-, di-, or triacetin. Acetins, propionates, and butyrates serve as food additives, solvents or plasticizers, and surface-active agents. Available evidence indicates that these agents exhibit a low order of toxicity. Normally, no irritant effects occur upon inhalation or direct dermal contact. \u0000 \u0000 \u0000 \u0000The higher glycerides of fatty acids with odd-numbered carbon chains (C5 to C11) are found naturally in very sma","PeriodicalId":19820,"journal":{"name":"Patty's Toxicology","volume":"85 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2001-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80463999","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2001-04-16DOI: 10.1002/0471435139.TOX110
D. Pedersen, Randy Young, Rose, E. Vernon
The practice of industrial hygiene and toxicology both involve recognition, as well as anticipation of the potential for occupational health problems. In the anticipation and/or recognition phase, an assessment of the risk to health or well-being resulting from exposure to an agent (chemical, physical, or biological) is made. This phase usually involves identifying the agents to which workers are or might be exposed; assessing the agents' properties, including toxicity; and understanding the conditions surrounding the use of, or interaction with, the agents. This information allows occupational health and safety professionals to make a preliminary assessment of occupational health risk based on the inherent properties of chemical, physical, or biological agents combined with the potential for contact or exposure under actual use conditions, including environmental level and in-use exposure control measures. The two basic applications of the anticipation/recognition process can be classified as either individual or aggregate. The individual process is used by occupational health and safety practitioners who apply anticipation and recognition techniques to the exposure and conditions of exposure prevalent in a single facility or group of facilities under his or her professional jurisdiction. In that process, the individual professional needs an understanding of the toxic properties of those agents associated with these specific workplaces or processes and an understanding of the conditions of exposure existing in those situations. The data necessary for the individual process have been available to the practitioner for quite some time, either through the scientific literature or through investigation in the workplaces under his or her jurisdiction, with the possible historical exception of accurate information regarding the formulation of trade-named products. The broader aggregate process of anticipation and recognition is applicable to definable industrial or occupational populations, and is an assessment of the potential risk of these populations for adverse health effects due to occupational exposure to chemical, physical, or biological agents in the workplace. The aggregate approach is common to occupational health and safety researchers, regulatory bodies, and others interested in the extent of exposure to a specific agent or list of agents with known adverse health effects. For example, in the initial stages of an epidemiologic study, researchers might wish to identify populations of workers who are exposed to a specific agent or group of agents. Government agencies need a measure of the potential impact of research or regulatory efforts based on the number of industries and workers impacted when they decide on the priorities to assign to research or regulatory efforts or the development of occupational health standards. This type of data was not available until after the implementation of the Occupational Safety and Health Act
{"title":"Populations at Risk","authors":"D. Pedersen, Randy Young, Rose, E. Vernon","doi":"10.1002/0471435139.TOX110","DOIUrl":"https://doi.org/10.1002/0471435139.TOX110","url":null,"abstract":"The practice of industrial hygiene and toxicology both involve recognition, as well as anticipation of the potential for occupational health problems. In the anticipation and/or recognition phase, an assessment of the risk to health or well-being resulting from exposure to an agent (chemical, physical, or biological) is made. This phase usually involves identifying the agents to which workers are or might be exposed; assessing the agents' properties, including toxicity; and understanding the conditions surrounding the use of, or interaction with, the agents. This information allows occupational health and safety professionals to make a preliminary assessment of occupational health risk based on the inherent properties of chemical, physical, or biological agents combined with the potential for contact or exposure under actual use conditions, including environmental level and in-use exposure control measures. The two basic applications of the anticipation/recognition process can be classified as either individual or aggregate. \u0000 \u0000 \u0000 \u0000The individual process is used by occupational health and safety practitioners who apply anticipation and recognition techniques to the exposure and conditions of exposure prevalent in a single facility or group of facilities under his or her professional jurisdiction. In that process, the individual professional needs an understanding of the toxic properties of those agents associated with these specific workplaces or processes and an understanding of the conditions of exposure existing in those situations. The data necessary for the individual process have been available to the practitioner for quite some time, either through the scientific literature or through investigation in the workplaces under his or her jurisdiction, with the possible historical exception of accurate information regarding the formulation of trade-named products. \u0000 \u0000 \u0000 \u0000The broader aggregate process of anticipation and recognition is applicable to definable industrial or occupational populations, and is an assessment of the potential risk of these populations for adverse health effects due to occupational exposure to chemical, physical, or biological agents in the workplace. The aggregate approach is common to occupational health and safety researchers, regulatory bodies, and others interested in the extent of exposure to a specific agent or list of agents with known adverse health effects. For example, in the initial stages of an epidemiologic study, researchers might wish to identify populations of workers who are exposed to a specific agent or group of agents. Government agencies need a measure of the potential impact of research or regulatory efforts based on the number of industries and workers impacted when they decide on the priorities to assign to research or regulatory efforts or the development of occupational health standards. This type of data was not available until after the implementation of the Occupational Safety and Health Act","PeriodicalId":19820,"journal":{"name":"Patty's Toxicology","volume":"2 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2001-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88630808","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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