Evaluation of a possible association of urban air toxics and asthma.

Abstract

The prevalence of asthma, measured either as the frequency of hospital admissions or number of deaths attributed to asthma, has increased over the last 15 to 20 years. Rapid increases in disease prevalence are more likely to be attributable to environmental than genetic factors. Inferring from past associations between air pollution and asthma, it is feasible that changes in the ambient environment could contribute to this increase in morbidity and mortality. Scientific evaluation of the links between air pollution and the exacerbation of asthma is incomplete, however. Currently, criteria pollutants [SOX, NOW, 03, CO, Pb, particulate matter (PM10)] and other risk factors (exposure to environmental tobacco smoke, volatile organic compounds, etc.) are constantly being evaluated as to their possible contributions to this situation. Data from these studies suggest that increases in respiratory disease are associated with exposures to ambient concentrations of particulate and gaseous pollutants. Similarly, exposure to environmental tobacco smoke, also a mixture of particulate and gaseous air toxics, has been associated with an increase in asthma among children. In addition, current associations of adverse health effects with existing pollution measurements are often noted at concentrations below those that produce effects in controlled animal and human exposures to each pollutant alone. These findings imply that adverse responses are augmented when persons are exposed to irritant mixtures of particles and gases and that current measurements of air pollution are, in part, indirect in that the concentrations of criteria pollutants are acting as surrogates of our exposure to a complex mixture. Other irritant air pollutants, including certain urban air toxics, are associated with asthma in occupational settings and may interact with criteria pollutants in ambient air to exacerbate asthma. An evaluation of dose-response information for urban air toxics and biological feasibility as possible contributors to asthma is therefore needed. However, this evaluation is compounded by a lack of information on the concentrations of these compounds in the ambient air and their effects on asthma morbidity and mortality. Through an initial review of the current toxicological literature, we propose a tentative list of 30 compounds that could have the highest impact on asthma and respiratory health. These compounds were selected based on their ability to induce or exacerbate asthma in occupational and nonoccupational settings, their allergic potential and ability to react with biological macromolecules, and lastly, their ability to irritate the respiratory passages. We recommend better documentation of exposure to these compounds through routine air sampling and evaluation of total exposure and further evaluation of biological mechanisms through laboratory and epidemiological studies directed specifically at the role these substances play in the induction and exacerbation of asthma. -Environ Health Perspect 1 03(Suppl 6): 253-271 (1995)

Epidemiologic evidence for asthma and exposure to air toxics: linkages between occupational, indoor, and community air pollution research.

“…ETS also contains other toxic air pollutants, including 29 air toxics of 49 major components (68), making it difficult to ascribe effects to any one pollutant. Serum IgE is higher in smokers than in nonsmokers (69)(70)(71)(72) and is possibly higher in ETSexposed subjects (72,73).…”

“…The research to date is too sparse to evaluate causality from indoor home VOCs, but there is even less information to evaluate the public health impact on respiratory health from outdoor VOCs, which include some of the same compounds found indoors. (68). For the Kanawha study compared with a Los Angeles ambient exposure study, for example, average toluene was 9.7 µg/m 3 versus 13 µg/m 3 , respectively, and for benzene, 3.2 µg/m 3 versus 3.5 µg/m 3 , respectively (153).…”

Molecular evidence of an interaction between prenatal environmental exposures and birth outcomes in a multiethnic population.

“…2003). ETS is a complex mixture of > 4,000 chemicals, including PAHs and carbon monoxide (Leikauf et al 1995). ETS measured by self-report or by biomarkers such as cotinine has been shown in many studies to adversely affect fetal growth as well as child growth and development (reviewed in Eskenazi et al 1995;Etzel 1997;National Research Council 1986).…”

Respiratory symptoms and peak expiratory flow in children with asthma in relation to volatile organic compounds in exhaled breath and ambient air

“…These studies may have been subject to unmeasured confounding by other indoor causal agents, including aeroallergens and environmental tobacco smoke, which can contain benzene among other air toxics (Leikauf et al, 1995). There is even less information to evaluate respiratory health effects from outdoor ambient VOCs, which include some of the same compounds from indoor sources.…”