Health effect

Usually the effects of solvents in paints and varnishes on health are dependent on concentration and exposure time. Adverse health effects may follow exposure to paints, varnishes and flieir solvents at the workplace. The conditions at paint and lacquer manufacturing sites (e.g., manufacturing mefliods, use of exhaust hoods, etc.) are responsible for the levels of evaporated solvents measured in the air. Adverse health effects depend on how the paint is applied, paint properties and working conditions (e.g., increased risk with spray painting). There is sufficient evidence to substantiate the fact that solvents to which painters have been exposed, are responsible for incidences of cancer. However, within paint manufacturing plants, this evidence is inadequate.  

Nevertheless, person working at home, occupants of painted rooms and children of parents which have been exposed are also at risk. Those involved with the abuse of solvents as a psychoactive substance (e.g., aromatic hydrocarbons in spray paints, mainly semi-volatile or nonvolatile components) are at a much higher risk. 

The main path of entry of solvents from paints and varnishes to the body is by inhalation. Volatile paint compounds present a particularly high risk as do some forms of paint application (e.g., spray painting with the risk of inhalation of even less volatile and nonvolatile paint components). Other pathways should, however, also be considered as dermal contact. 

In addition to solvents, other compounds from paints and varnishes can cause various diseases, often similar to the effects caused by solvents (e.g., asbestos as paint filler or in the construction and shipyard industry, silica, dusts, thermal decomposition products, contaminations of solvents, chromium, iron and lead compounds in paint pigments). It is often difficult to associate a particular components of paints and varnishes with adverse health effects. In most cases, the paint and varnish products were found to be a relevant cause of illness, but their individual compounds were not. 

The following symptoms involving the skin and mucose membranes may occm as a result 

There are two ways to determine if a chemical causes cancer—studies conducted on people and studies on animals. Studies on humans are expensive, hard to conduct, and very often not even possible. This type of long-term research is called epidemiology. Studies on animals are less expensive and easier to do. This type of research is sometimes referred to as toxicology. Results showing increased occurrences of cancer in animals are generally accepted to indicate that the same chemical causes cancer in humans. The alternative to not accepting animal studies means we would have a lot less knowledge about the health effects of chemicals. We would never be able to determine the health effects of the more than 100,000 chemicals used by industry. 

No level of exposure to cancer-causing chemicals is safe. Lower levels are considered safer. One procedure for setting health standard limits is called risk assessment. Risk assessment on the surface appears very scientific yet the actual results are based on many assumptions. The differences in these assumptions allow scientists to come up with very different results when determining an acceptable exposure standard. Following are major questions that assumptions are based on  

For exposures at the current permissible exposure limit (PEL), the risk of developing cancer from vinyl chloride is about 700 cases of cancer for every million workers exposed. The risk for asbestos is about 6400 cases of cancer for each million workers exposed. The risk for coal tar pitch is about 13,000 cases for each million workers exposed. PELs set for current federal standards differ because of these different risks. 

The dose of a chemical causing cancer in human or animal studies is then used to set a standard PEL below which only a certain number of people will develop illness or cancer. This standard is not an absolute safe level of exposure to cancer-causing agents, so exposure should always be minimized even when levels of exposure are below the standard. Just as the asbestos standard has been lowered in the past from 5 fibers/cm to 0.2 fibers/cm, and now to 0.1 fibers/cm (50 times lower), it is possible that other standards will be lowered in the future as new technology for analysis is discovered and public 

Once the radionuclide concentration in the air, and the ground deposition at a certain location liave been computed, the next step is to consider how the radiation reaches the people at that location. The four major pathways are  

For example, given a BWR-1 release (Table 8,2-1), typical weather conditions, no rain and less than one mile from the accident immersion, inhalation, and ground produce about the same magnitude doses for exposure times of several hours or less. The exposure from a cloud ceases once the cloud has passed, but exposure may continue from the ground until the area is decontaminated or evacuated. If the exposure time is long, the ground dose can eventually dominate. Tables 9-6 and 9-7 in NUREG/CR-2300 show examples of the relative importance of these pathways. 

The radiation dose from being in or near a cloud of aiibome radioactivity can be calculated if the radionuclide concentration in the cloud is known. While radioactive noble gases may be inhaled, they are not retained in the body, hence, most of their dose contribution is by cloud radiation. 

Ground radiation is from deposited radioactive particles. The deposition rate from a radioactive cloud without rain (dry deposition) is so low that the ground radiation dose is about the same as the inhalation dose. A heavy rain, however, may wash out enough particles from the plume to make ground radiation the dominant contributor to the total dose in a limited area. Rain will also attenuate radiation by leaching the radioactivity to be shielded by the soil and by moving it to streams for further removal. 

The ingestion pathway is much more complicated than the others since the radionuclides, except those in drinking water, have to be taken up by the plants and then consumed by humans in either vegetable or animal form. Of the various pathways, the milk pathway is particularly important because a dairy cow consumes a large amount of vegetation and concentrates radionuclides (e.g, 

Acute high-dose Cd toxicity in humans is now a rarity in Western countries. Its symptoms depend on the route of ingestion [123]. Toxicity also depends on the solubility of Cd compounds [2]. 

Acute intoxication mostly occurs by inhalation of fumes in an industrial setting [5]. There is usually a latent period of 4—12 hours between the exposure and the onset of symptoms [5]. In severe intoxication, patients develop a respiratory distress syndrome due to acute pneumonitis and pulmonary edema with respiratory failure, which can progress to death in 3-7 days [5,124,125]. Symptoms develop when CdO 

Apart from the kidneys, other organs are also affected by Cd, which may lead to damage and dysfunction as well (see Section 4.3). In fact, Cd exposure increases the risk of mortality in affected populations. This was recently demonstrated in 

There have been few studies on the fetal toxicity of Cd transported across the placenta, which acts as a barrier to Cd. Nevertheless, a small amount may reach the fetus. Cd is also transferred to neonates through lactation. Maternal hypertension and decrease in birth weight have been associated with elevated levels of Cd in the neonate [155]. A depletion of zinc with increasing number of births and a progressive increase in Cd in smokers negatively affect infant birth weight [156]. Moreover, Marlowe et al. [157] found an association between mental retardation and raised concentrations of Cd in hair in school age children. But overall, there is no substantial evidence that Cd has caused teratogenic effects in humans. 

Recent epidemiological studies have accounted for all these factors and endorse the role of exposure to Cd in the development of cancer of various organs in humans, such as female breast and endometrial [171,172], lung [173], pancreatic [174,175], and bladder cancer [176]. Though of 11 cohort studies, only 3 implied Cd as a cause 

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The objective of an EIA Is to document the potential physical, biological, social and health effects of a planned activity. This will enable decision makers to determine whether an activity is acceptable and if not, identify possible alternatives. Typically, ElA s will be carried out for... 

Proceedings of a Symposium on Potential Health Effects of Components ofPlantEoods and Beverages in the Diet, Aug. 14—15, 1992, University of California at Davis, p. 106. 

Announce. Index 12, 9—12 (1981). [A 121-page review of health effects Hterature primarily related to inhalation exposure.]... 

Receptors. The receptor can be a person, animal, plant, material, or ecosystem. The criteria and hazardous air pollutants were so designated because, at sufficient concentrations, they can cause adverse health effects to human receptors. Some of the criteria pollutants also cause damage to plant receptors. An Air QuaUty Criteria Document (12) exists for each criteria pollutant and these documents summarize the most current Hterature concerning the effects of criteria pollutants on human health, animals, vegetation, and materials. The receptors which have generated much concern regarding acid deposition are certain aquatic and forest ecosystems, and there is also some concern that acid deposition adversely affects some materials. 

G. D. Nelson, ed.. Health Effects of Dietay Fatty Acids, American Oil Chemists Society, Champaign, lU., 1991, pp. 136—167. 

When PET is extracted with water no detectable quantities of ethylene glycol or terephthaUc acid can be found, even at elevated extraction temperatures (110). Extractable materials are generally short-chained polyesters and aldehydes (110). Aldehydes occur naturally iu foods such as fmits and are produced metabohcaHy iu the body. Animal feeding studies with extractable materials show no adverse health effects. 

J. W. HoUeman, Health Effects of Haloalky I Phosphate Flame Retardants and Potential Metabolic Products, Oak Ridge National Laboratory, Term., 1984, DOE/NBM-4006848 (DE84 006848),... 

Hexane is classified as a flammable liquid by the ICC, and normal handling precautions for this type of material should be observed. According to the ACGIH, the maximum concentration of hexane vapor in air to which a worker may be exposed without danger of adverse health effects is 125 ppm benzene is rated at 10 ppm. 

Catalyst Molecular formula Possible health effects... 

Although thermal performance is a principal property of thermal insulation (13—15), suitabiHty for temperature and environmental conditions compressive, flexure, shear, and tensile strengths resistance to moisture absorption dimensional stabiHty shock and vibration resistance chemical, environmental, and erosion resistance space limitations fire resistance health effects availabiHty and ease of appHcation and economics are also considerations. 

For an excellent, comprehensive review of the chemistry, environmental, and anthropogenic release, environmental fate, and environmental and human health effects of lead, see Air Quality Criteria for Eead, Vol. I—IV, EPA-600/8-83/028a-dF, U.S. Environmental Protection Agency, Washington, D.C., June 1986, -Msd Air Quality Criteria for Eead Supplement to the 1986 Addendum, EPA-600/8-89/049F, U.S. Environmental Protection Agency, Washington, D.C., Aug. 1990. 

Health Effects Assessmentfor Eead, EPA-540/1-86/055, U.S. Environmental Protection Agency, Washington, D.C., Sept. 1984. 

Dentistry. Mercury is used in dental amalgams for fillings in teeth (see Dental materials). Dental uses have accounted for 2—4% of total U.S. mercury consumption since 1980 and generally 3—6% before that time (3). Dental amalgams used to fill cavities in teeth are approximately 50% mercury by weight. Dental use of mercury can be expected to continue to decrease, in part because of more effective cavity prevention as well as development and increasing use of alternative dental materials such as plastics and ceramics, and increasing awareness of the environmental and health effects of mercury. 

Oak Ridge Associated Universities Panel for the Committee on Interagency Radiation Research and PoHcy Coordination, Health Effects ofEow Frequemy Electric and Magnetic Fields, Washington, D.C., June 1992. 

M. Abdulla, B. M. Nait, and R. K. Chandra, eds.. Proceedings of An International Symposium, Health Effects and Interactions of Essential and Toxic Elements, Nutrition Research, Suppl. 1, Peigamon Press, New York, 1985. 

Most of the data on radiation health effects have come from medical monitoring of Japanese atomic bomb survivors. For survivors who received radiation exposures up to 0.10 Sv, the iacidence of cancer is no greater than ia the geaeral populatioa of Japanese citizens. For the approximately 1000 survivors who received the highest radiation doses, ie, >2 Sv, there have been 162 cases of cancer. About 70 cases would have been expected ia that populatioa from aatural causes. Of the approximately 76,000 survivors, as of 1995 there have beea a total of about 6,000 cases of cancer, only about 340 more cases than would be expected ia a group of 76,000 Japanese citizens who received only background radiation exposure (59). 

For radiation doses <0.5 Sv, there is no clinically observable iacrease ia the number of cancers above those that occur naturally (57). There are two risk hypotheses the linear and the nonlinear. The former implies that as the radiation dose decreases, the risk of cancer goes down at roughly the same rate. The latter suggests that risk of cancer actually falls much faster as radiation exposure declines. Because risk of cancer and other health effects is quite low at low radiation doses, the iacidence of cancer cannot clearly be ascribed to occupational radiation exposure. Thus, the regulations have adopted the more conservative or restrictive approach, ie, the linear hypothesis. Whereas nuclear iadustry workers are allowed to receive up to 0.05 Sv/yr, the ALARA practices result ia much lower actual radiatioa exposure. 

R. W. Gotchy, Health Effects Attributed to Coal andNuclearFuel Cycle Alternatives, Report NUREG-0332, U.S. Nuclear Regulatory Commission,... 

Health Effects Of Exposure to Row Revels oflonifing Radiation, Report of Committee on the Biological Effects of Radiation (BEIR Report V), National... 

Radian Corp., Plastics Processing—Technology and Health Effects, Noyes Data Corp., Park Ridge, N.J., 1986, pp. 317—338, Append. C. 

SolubiHty of the three commercial polysulfones foUows the order PSF > PES > PPSF. At room temperature, all three of these polysulfones as weU as the vast majority of other aromatic sulfone-based polymers can be readily dissolved in a few highly polar solvents to form stable solutions. These solvents include NMP, DMAc, pyridine, and aniline. 1,1,2-Trichloroethane and 1,1,2,2-tetrachloroethane are also suitable solvents but are less desirable because of their potentially harmful health effects. PSF is also readily soluble in a host of less polar solvents by virtue of its lower solubiHty parameter. 

Pyridine Chronic Toxicology. AH mutagenicity tests have been negative and (1) is not considered a carcinogen or potential carcinogen. There have been no reports of adverse health effects on long-term exposure to (1) at low concentrations. 

Inhalation of crystalline or fused vitreous silica dust, usually overlong periods, causes a disabling, progressive pulmonary disease known as silicosis (84). Amorphous siUcas have not been linked to siUcosis (85), but can cause respiratory irritation. The history and poHtics of siUcosis have been reviewed (86). Standards have been set or recommended for occupational exposures (87,88) and review articles on the health effects of siUca are available (83,89). 

Silver compounds having anions that are inherently toxic, eg, silver arsenate and silver cyanide, can cause adverse health effects. The reported rat oral LD values for silver nitrate, silver arsenate [13510-44-6] and silver cyanide are 500—800 (29), 200—400 (29), and 123 mg/kg (30), respectively. Silver compounds or complexes ia which the silver ion is not biologically available, eg, silver sulfide and silver thiosulfate complexes, are considered to be without adverse health effects and essentially nontoxic. 

In 1980, the EPA pubHshed ambient water quaHty criteria for silver. An upper limit of 50 f-lg/L in natural waters was set to provide adequate protection against adverse health effects (38). In 1992, EPA deleted the human health criteria for silver from the ambient water quaHty criteria to be consistent with the drinking water standards (39). 

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