ISSN:0272-4332    

DOI:10.1111/j.1539-6924.1990.tb01011.x

出版商:Blackwell Publishing Ltd    

年代:1990

数据来源: WILEY

ISSN:0272-4332    

DOI:10.1111/j.1539-6924.1990.tb01012.x

出版商:Blackwell Publishing Ltd    

年代:1990

数据来源: WILEY

ISSN:0272-4332    

DOI:10.1111/j.1539-6924.1990.tb01013.x

出版商:Blackwell Publishing Ltd    

年代:1990

数据来源: WILEY

ISSN:0272-4332    

DOI:10.1111/j.1539-6924.1990.tb01014.x

出版商:Blackwell Publishing Ltd    

年代:1990

数据来源: WILEY

ISSN:0272-4332    

DOI:10.1111/j.1539-6924.1990.tb01015.x

出版商:Blackwell Publishing Ltd    

年代:1990

数据来源: WILEY

摘要:

The combustion of tobacco indoors results in the emission of a wide range of air contaminants that are associated with a variety of acute and chronic health and comfort effects. Exposures to environmental tobacco smoke (ETS) are assessed for epidemiologic studies and risk assessment and risk management applications. An individual's or population's exposure to ETS can be assessed by direct methods, which employ personal air monitoring and biomarkers, and indirect methods, which utilize various degrees of microenvironmental measurements of spaces, models, and questionnaires in combination with time–activity information. The major issues related to assessing exposures to ETS are summarized and discussed, including the physical–chemical nature of ETS air contaminants, use of proxy air contaminants to represent ETS, use of biomarkers, models for estimating ETS concentrations indoors, and the application of questionnai

ISSN:0272-4332    

DOI:10.1111/j.1539-6924.1990.tb01016.x

出版商:Blackwell Publishing Ltd    

年代:1990

数据来源: WILEY

摘要:

Risk assessment methodologies have been successfully applied to control societal risk from outdoor air pollutants. They are now being applied to indoor air pollutants such as environmental tobacco smoke (ETS) and radon. Nonsmokers' exposures to ETS have been assessed based on dosimetry of nicotine, its metabolite, continine, and on exposure to the particulate phase of ETS. Lung cancer responses have been based on both the epidemiology of active and of passive smoking. Nine risk assessments of nonsmokers' lung cancer risk from exposure to ETS have been performed. Some have estimated risks for lifelong nonsmokers only; others have included ex‐smokers; still others have estimated total deaths from all causes. To facilitate interstudy comparison, in some cases lung cancers had to be interpolated from a total, or the authors' original estimate had to be adjusted to include ex‐smokers. Further, all estimates were adjusted to 1988. Excluding one study whose estimate differs from the mean of the others by two orders of magnitude, the remaining risk assessments are in remarkable agreement. The mean estimate is approximately 5000 ± 2400 nonsmokers' lung cancer deaths (LCDSs) per year. This is a 25% greater risk to nonsmokers than is indoor radon, and is about 57 times greater than the combined estimated cancer risk from all the hazardous outdoor air pollutants currently regulated by the Environmental Protection Agency: airborne radionuclides, asbestos, arsenic, benzene, coke oven emissions, and vinyl chlo

ISSN:0272-4332    

DOI:10.1111/j.1539-6924.1990.tb01017.x

出版商:Blackwell Publishing Ltd    

年代:1990

数据来源: WILEY

摘要:

Demonstration of a dose‐response relationship for environmental tobacco smoke (ETS) is an important indication of causality. Central to the analysis and interpretation of dose‐response relations as described in epidemiological studies is the relationship between dose and exposure. It must be recognized that in studies of ETS we have only surrogate measures of dose, and these surrogate measures (based on exposure) are imperfect. The question‐based measures of ETS exposure generally have not been standardized, may have limited validity and reliability, and cannot comprehensively describe total ETS exposure, exposure to individual ETS components, nor doses of biologically relevant agents at target sites. Nevertheless, useful data have been yielded in epidemiologic studies linking ETS exposure to increased respiratory infection and symptoms, reduced lung growth in children, and increased lung cancer in nonsmoking adults. The more consistent exposure‐response data for studies on acute health in children may reflect the greater difficulty in measuring exposure in studies of chronic health in adults.SUMMARYFor children, adverse effects have been causally associated with exposure to ETS. The epidemiological evidence and the supporting toxicological data link ETS to increased lower respiratory illness, increased respiratory symptoms, and reduced lung growth. Exposure‐response relationships have been described for these effect; errors in exposure estimates would tend to lessen rather than to exaggerate these relationships. By contrast, in adults, the evidence for adverse cardiopulmonary effects of ETS exposures, other than lung cancer, it's presently less conclusive. Misclassification of exposure may be more severe for adults than for children, and the resulting bias toward the null may obscure effects of respiratory symptoms and lung function. Research on adults is hindered by the difficulty of estimating exposures received in diverse environments over a lengthy period. Continued controversy related to the effects of ETS exposure in the workplace and in public locations provides a rationale for further research. However, more valid methods for assessing the exposures of adults to ETS are needed for such

ISSN:0272-4332    

DOI:10.1111/j.1539-6924.1990.tb01018.x

出版商:Blackwell Publishing Ltd    

年代:1990

数据来源: WILEY

摘要:

A number of air pollutants are being found in low concentrations in indoor and outdoor air. Several studies have measured these concentrations for a large number of compounds in hundreds of residences. The concentrations range over several orders of magnitude over time and space. The log‐normal distributions that are found make it possible to assess the impact on the health of populations, especially for genotoxic effects for which a threshold concentration is not expected to exist. Spreadsheets can be constructed which incorporate the unit risk of a substance for cancer, the distribution of concentrations of the substance in the population, and the size of the population into an assessment of the expected excess cases of cancer that can be attributed to the population exposure to such a toxicant. This approach allows for the evaluation of population risk for different substances as found in different environments, and for the evaluation of the relative efficacy of different strategies for population risk reductio

ISSN:0272-4332    

DOI:10.1111/j.1539-6924.1990.tb01019.x

出版商:Blackwell Publishing Ltd    

年代:1990

数据来源: WILEY

摘要:

The major sources of human exposure to about a dozen volatile organic chemicals (VOCs) have recently been identified.1For nearly every chemical, the major sources of exposure are completely different from the major sources of emissions. This finding implies that current environmental regulations and control strategies are misdirected. Important sources of exposure are typically not regulated in any way, whereas unimportant sources are heavily regulated. Vast sums of money are spent on problems involving little risk (e.g., hazardous waste sites), whereas few resources are expended on problems involving higher risk (e.g., indoor air pollution). The following paper summarizes recent findings regarding major sources of exposure to several VOCs. Benzene is selected as a case study. Brief discussions of tetrachloroethylene and paradichlorobenzene are also included.

ISSN:0272-4332    

DOI:10.1111/j.1539-6924.1990.tb01020.x

出版商:Blackwell Publishing Ltd    

年代:1990

数据来源: WILEY