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Indoor exposure

Chronic lead poisoning seems to remain an important social issue in the United States with regard to certain groups of children (low income, urban, afro-American). The primary lead source for nearly all of the children is leaded paint in deteriorated housing stock (Mushak et al. 1989, Roberts et al. 2001). Indoor problems are often different in developed countries when compared with developing countries. [Pg.423]


Occupational and environmental exposure to chemicals can take place both indoors and outdoors. Occupational exposure is caused by the chemicals that are used and produced indoors in industrial plants, whereas nonoccupa-tional (and occupational nonindustrial) indoor exposure is mainly caused by products. Toluene in printing plants and styrene in the reinforced plastic industry are typical examples of the two types of industrial occupational exposures. Products containing styrene polymers may release the styrene monomer into indoor air in the nonindustrial environment for a long time. Formaldehyde is another typical indoor pollutant. The source of formaldehyde is the resins used in the production process. During accidents, occupational and environmental exposures may occur simultaneously. Years ago, dioxin was formed as a byproduct of production of phenoxy acid herbicides. An explosion in a factory in... [Pg.255]

It is primarily for testing materials to be used in products subject to indoor exposure and to sunlight. Exposure in the Fadeometer cannot be related directly to exposure in direct sunlight, partially because other weather factors are always present outdoors. [Pg.332]

Pentachlorophenol concentrations in urine and serum can be used as biomarkers of internal dose (Colosio et al., 1993a). PCP concentrations up to about 30 mg/L were detected in urine samples of exposed workers, while concentrations lower than 0.3 mg/L were detected in the general population. The presence of PCP in biological samples of the general population is attributable to indoor exposure to the compound released from treated materials (furniture, leather, paints, etc.). [Pg.15]

Pesticide exposure assessment Jazzercize activities to determine extreme case indoor exposure potential and in-use biomonitoring... [Pg.97]

In 1985, Berteau and Mengle (1985) of the California Department of Health Services and Maddy of the Department of Food and Agriculture conducted a preliminary review of pesticides used indoors. They noted several cases (six) from the Pesticide Illness Surveillance system in which illness was reported after structural pest control. Hypothetical exposure estimates for infants, children, and adults following label use for propoxur, DDVP, and chlorpyrifos were sometimes greater than toxic levels. In 1987, Berteau et al. (1989) reiterated the concern about the potential magnitude of indoor exposures, particularly for children. [Pg.98]

Studies in indoor environments of dermal contact transfer required an estimate, and a tight-fitting whole-body dosimeter was adopted and initially considered as a surrogate for skin (Krieger et al., 2000). Contact with treated surfaces was limited to feet, hands, limbs, and torso. Standardized Jazzercize to represent daily human activities and maximum contact was incorporated into protocols for indoor exposure studies (Ross et al., 1990,1991). Comparative studies will be reported elsewhere (Krieger et al., 2000). [Pg.99]

Jacobi, W. and Paretzke H.G. 1985, Risk Assessment for Indoor Exposure to Radon Daughters, In Proceedings, Seminar on Exposure to Enhanced Natural RAdiation and Its Regulatory Implications, Maastricht, the Netherlands, March 25-27, Elsvier Science Publisher, Amsterdam. [Pg.88]

James, A.C., Dosimetric approaches to risk assessment for indoor exposure to radon daughters, Rad. Prot. Dos. 7 353-366 (1984)... [Pg.324]

Low level Rn-d exposure-effect studies that may be relevant to the general indoor exposure situation, at least as far as lifetime exposure is concerned, are available for miners in CSSR, US, Canada,... [Pg.434]

The nature and behavior of free Rn-d ions or atoms, i.e. not attached to atmospheric condensation nuclei, is still subject of controversy, particularly with regard to the influence of environmental atmospheric conditions, such as humidity and presence of other gases (Busigin et al., 1981). Free Rn-d atoms are one of the most critical parameters for the exposure-dose conversion. This can be of particular importance in indoor exposure situations with a large ratio of unattached to attached Rn-d. [Pg.437]

Due to the superposition of various other biological, physiological and physical parameters used in modelling, the published exposure-dose conversion factors range from 2 to 120 mGy per WLM. However, a sensitivity analysis indicated that for most indoor exposure situations compensatory effects can reduce this range to about 5 to 10 mGy/WLM for the indoor situations occurring most frequently (OECD/NEA, 1983). [Pg.437]

Figure 2. Mean bronchial dose to basal cells, standardized for 1 WLM exposure to free radon 222 daughter atoms for different physical activities (assuming typical indoor exposure with equilibrium factor F = 0.4) ... Figure 2. Mean bronchial dose to basal cells, standardized for 1 WLM exposure to free radon 222 daughter atoms for different physical activities (assuming typical indoor exposure with equilibrium factor F = 0.4) ...
Using the miner data for this purpose may be overestimating the risk due to indoor exposure, since it includes risks from simultaneous exposure to external gamma radiation, long lived alpha emitters. This effect, however, may be outweighed by the fact... [Pg.441]

From the above it can be concluded that the risk for lung cancer induction from chronic indoor exposure to Rn-d is unlikely to be higher than 1.10 4/mSv. in order to understand the magnitude of this risk it has to be emphasized that man can be exposed to a multitude of different hazardous materials in the indoor atmosphere besides Rn-d, such as formaldehyde, nitrogen dioxide, carbon monoxide, nitrosamines, polyaromatic hydrocarbons, volatile organic compounds, asbestos and pesticides (Gammage and Kaye, 1985). [Pg.441]

Martell, E. A., a-Radiation dose at bronchial bifurcations of smokers from indoor exposure to radon progeny, Proc. Natl. Acad. Sci. USA, 80 1285-1289 (1983a). [Pg.461]

Radon 222 and its decay products, Rn-d, are well known as among the most powerful carcinogenic agents to which human beeings are exposed as members of the general public (e.g. indoor exposure), as a consequence of occupation (e.g. uranium miner) or as part of... [Pg.503]

Chameaud, J., Masse, R. and Lafuma, J., Influence of Radon Daughter Exposure at low Doses on Occurrence of Lung Cancer in Rats, in Radiation Protection Dosimetry Indoor Exposure to Natural Radiation and Associated Risk Assessment, (Clemente, G., F. et al, eds) pp.385-388, Nuclear Technology Publishing, Anacapri (1983). [Pg.513]

Before standards for indoor exposure to radon can be formally established, work is necessary to determine whether remedies are feasible and what is likely to be involved. Meanwhile, the Royal Commission on Environmental Pollution (RCEP) in the UK has considered standards for indoor exposure to radon decay products (RCEP, 1984). For existing dwellings, the RCEP has recommended an action level of 25 mSv in a year and that priority should be given to devising effective remedial measures. An effective dose equivalent of 25 mSv per year is taken to correspond to an average radon concentration of about 900 Bq m 3 or an average radon decay-product concentration of about 120 mWL, with the assumption of an equilibrium factor of 0.5 and an occupancy factor of 0.83. [Pg.536]

Chronic Obstructive Lung Disease (COLD) and Cor pulmonale COLD is known to be an outcome of chronic air pollution exposure. Although tobacco smoke is known to be the major risk factor, studies in India and Nepal have found that non-smoking women who regularly cook on biomass stoves exhibit a higher prevalence of COLD than would be expected, or which appears in women who use them less frequently. Indeed, due to indoor exposure, nearly 15% of non-smoking women in Nepal (20 years and older) had chronic bronchitis a very high rate for nonsmokers (ESCAP, 1995). [Pg.240]

H ASHRAE standards can be filled in instead, fh ASHRAE indoor exposure guideline (24-hr average)... [Pg.369]

Humans can be exposed to POPs through diet, occupational exposures (for example, farmworkers may be exposed to POPs through pesticides), industrial accidents and the environment (including indoor exposure). Exposure to POPs, either acute or chronic, can be associated with a wide range of adverse health effects, including illness and death (L. Ritter et al., 1995). Laboratory animal studies and wildlife studies have associated POPs with endocrine disruption, reproductive and immune dysfunction, neurobehavioral disorders and cancer. More recently, some POPs have also been connected to reduced immunity in infants and children and a concomitant increase in infections. Other studies have linked POPS concentrations in humans with developmental abnormalities, neurobehavioral impairment and cancer and tumor induction or promotion.4... [Pg.18]

Another subject of recent interest has been the question of indoor-outdoor oxidant concentrations. Available measurements and models suggest that indoor exposures may be substantially reduced by appropriate choices of ventilation sterns, air filters, and interior surface materials. The cost-benefit relationships coming from these studies may well have a great impact on future devious based on atmospheric concentrations of oxidant pollutants. [Pg.678]

Haddad S, Tardif GC, Tardif R (2006) Development of physiologically based toxicokinetic models for improving the human indoor exposure assessment to water contaminants trichloroethylene and trihalomethanes. J Toxicol Environ Health A 69(23) 2095-2136... [Pg.134]

Camarasa and Serra-Baldrich [94] reported allergic contact dermatitis after repeated contact with TPP-treated plastics. Meeker and Stapleton [95] indicated endocrine disruptive properties for TPP and TDCiPP, through a negative correlation with semen quality and thyroid hormone levels, respectively. Kanazawa et al. [71] associated mucosal symptoms of the sick building syndrome with high indoor exposure to TBP. These symptoms include irritation to the eyes, nose, and throat symptoms such as flushing, and mucosal symptoms such as irritation to the eyes, nose, and throat the latter symptoms were strongly associated with TBP levels in air and dust. [Pg.256]

Kanazawa A, Saito I, Araki A, Takeda M, Ma M, Saijo Y, Kishi R (2010) Association between indoor exposure to semi-volatile organic compounds and building-related symptoms among the occupants of residential dwellings. Indoor Air 20 72-84... [Pg.292]

WallaeeL. 1992. Recent field studies of personal and indoor exposures to environmental pollutants. Ann New York Acad Sci 641 7-16. [Pg.196]

Time of wetness (TOW), considered as the time during which the corrosion process occurs, is an important parameter to study the atmospheric corrosion of metals. According to ISO-9223 standard, TOW is approximately the time when relative humidity exceeds 80% and temperature is higher than 0°C. No upper limit for temperature is established. In tropical climates, when temperature reaches values over 25°C, evaporation of water plays an important role and the possibility to establish an upper limit respecting temperature should be analyzed. The concept of TOW assumes the presence on the metallic surface of a water layer however, there are recent reports about the formation of water microdrops during the initial periods of atmospheric corrosion, showing that the idea of the presence of thin uniform water layers is not completely in agreement with the real situation in some cases (particularly indoor exposures). [Pg.61]

The calculation of Time of Wetness established in ISO 9223 should be revised based on new results obtained in outdoor and indoor conditions in tropical humid marine climate. Some proposals are made to improve the estimation of TOW, taking into account changes in its nature depending on outdoor or indoor exposure, linear relationship between time and TOW, the effect of rain, and the role of contaminants and air temperature. [Pg.62]

The concept of TOW assumes the presence on the metallic surface of a water layer however, there are recent reports about the formation of water microdrops during the initial periods of atmospheric corrosion, showing that the idea of the presence of thin uniform water layers is not completely in agreement with the real situation in some cases (particularly indoor exposures). [Pg.142]

Fig. 6.16 Carbonation depth of latex-modified mortars after 10-year outdoor and indoor exposure (Soroushian and TIili [91]). Fig. 6.16 Carbonation depth of latex-modified mortars after 10-year outdoor and indoor exposure (Soroushian and TIili [91]).
Hoek, G., B. Brunekreef, and P. Hofschreuder, Indoor Exposure to Airborne Particles and Nitrogen Dioxide during an Air Pollution Episode, JAPCA, 39, 1348-1349 (1989). [Pg.866]

Koutrakis, P., M. Brauer, S. L. K. Briggs, and B. P. Leaderer, Indoor Exposures to Fine Aerosols and Acid Gases, Environ. Health Perspect., 95, 23-28 (1991). [Pg.867]

Bioavailability from Environmental Media. Diazinon can be absorbed following inhalation, dermal, or oral exposures. Absorption through the skin is of major concern for exposures of farmers, farm workers, commercial applicators, or homeowners related to the use of diazinon as an insecticide or nematocide (Davis et al. 1983). Absorption via inhalation is a major concern particularly with respect to indoor exposures to diazinon within 2 days postapplication of the compound as a pest control agent in commercial buildings and homes (Currie et al. 1990 Jackson and Lewis 1981 Lenhart and Kawamoto 1994 Williams et al. 1987). Additional information on the concentrations of diazinon in indoor air and in groundwater from domestic wells, particularly from environments near hazardous waste sites, is needed to determine the bioavailability of diazinon in these media. [Pg.158]


See other pages where Indoor exposure is mentioned: [Pg.429]    [Pg.437]    [Pg.439]    [Pg.441]    [Pg.514]    [Pg.256]    [Pg.259]    [Pg.221]    [Pg.359]    [Pg.155]   
See also in sourсe #XX -- [ Pg.422 ]

See also in sourсe #XX -- [ Pg.2530 ]




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