D. Limitations of Animal Studies

children has been reported in any epidemiological studies (Samet et al. 1987). While

a few studies have suggested effects of gas cooking on pulmonary function and

respiratory symptoms, and acute respiratory illness in adults, potential confounders

like cigarette smoking and chronic respiratory diseases were not considered in these

studies (Samet et al. 1987). Inconsistent results have been reported in studies of the

relation between indoor nitrogen dioxide exposure and respiratory health effects in

children (Anto and Sunyer 1995).

Recent studies of ETS have also shown inconsistent relationships between passive smoking and wheezing and asthma (Samet et al. 1987). The inconsistency

between workplace and spousal studies of ETS and lung cancer has been noted

(LeVois and Layard 1994). In particular, they suggest that an estimate of ETS-lung

cancer risk from female spousal smoking studies is inappropriate because of bias

arising from spousal smoking study designs.

Studies regarding the assessment of hazards from biological contaminants are

also limited. For instance, in studies of house dust mites it has been difficult to

assess the relationship between the severity of asthma and exposure to dust mites,

as well as determining the prevalence of house dust-mite-related asthma (Samet

et al. 1988).

Although several studies suggest an increased frequency of respiratory symptoms

among adults and children in damp houses (and consequently exposed to mold

species), these studies have not considered the role of nonallergenic mechanisms

(Becher et al. 1996). Such mechanisms include inhalation exposure to airborne toxic

factors such as bacterial cell wall components and spores of toxin-producing molds

with mycotoxins.

There is controversy regarding the health effects from exposure to particulate

matter (Moolgavkar and Luebeck 1996). Issues of coherence, consistency, strength

of association, linearity of exposure–response relationships, specificity, temporality,

and biological plausibility have been raised. A lack of consistent association between

symptom data and measures of particulate matter air pollution has been noted

(Gamble and Lewis 1996). It has also been noted that individual-level study results

of particulate matter are not coherent with time-series ecologic study results of

hospital emissions (Gamble and Lewis 1996). These issues may also be pertinent

to particulate matter in indoor environments. As mentioned earlier, particulate matter

can exist in both outdoor and indoor environments, and many investigators realize

the importance of measuring the relationships between outdoor and indoor environments. In addition, the potential mechanisms of possible causality between low levels

of indoor air pollutants and toxicity have not been addressed. This includes potential

interactive mechanisms among indoor air pollutants.



VI. SUMMARY

Various health hazards have been attributed to indoor air pollutants. Primary

hazards of concern include cancer, irritative and respiratory effects, neurological

effects, and developmental and reproductive toxicity. Several approaches are available



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to identify potential hazards associated with indoor air pollutants. These approaches

constitute the hazard identification step of the risk assessment process.

Uncertainty is inherent in the hazard identification process, as a result of limitations of epidemiologic and animal studies, the nonspecificity of the symptomatology

of indoor air pollutants, and the problems of inadequate quantification of the concentration of indoor air pollutants. These limitations and uncertainties are evident

in much of the literature on indoor air pollutants. There is a need for more data

concerning the potential hazards of indoor air pollutants following long-term exposure to low concentrations. More mechanistic data and a better understanding of the

roles of various constituents of complex mixtures of indoor air pollutants would also

be useful.

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