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Clearing the Air: Asthma and Indoor Air Exposures (2000)

Chapter: 6 Indoor Chemical Exposures

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Suggested Citation:"6 Indoor Chemical Exposures." Institute of Medicine. 2000. Clearing the Air: Asthma and Indoor Air Exposures. Washington, DC: The National Academies Press. doi: 10.17226/9610.
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Suggested Citation:"6 Indoor Chemical Exposures." Institute of Medicine. 2000. Clearing the Air: Asthma and Indoor Air Exposures. Washington, DC: The National Academies Press. doi: 10.17226/9610.
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Suggested Citation:"6 Indoor Chemical Exposures." Institute of Medicine. 2000. Clearing the Air: Asthma and Indoor Air Exposures. Washington, DC: The National Academies Press. doi: 10.17226/9610.
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6 INDOOR CHEMlcALExpos a res ~ oncern in recent years regarding the potential health ef- fects of indoor air exposures, as well as the marked increase in the prevalence of asthma in industrialized countries, has prompted a burgeoning of scientific research on exposure to airborne agents and asthma. The committee was charged with the task of evaluating the strength of the scientific evidence concerning the possible asso- ciation between these agents and asthma prevalence and severity. The committee was also tasked with examining possible means of mitigating or preventing exposure to these agents. In this chap- ter the committee evaluates indoor exposure to chemical agents, addressing the following to the extent permitted by available re- search: 1. which factors influence exposures to the agent; 2. whether a relationship exists between the agent and asthma prevalence or severity, taking into account the strength of the sci- entific evidence and the appropriateness of the methods used to detect the relationship; 3. what type of relationship exists between the agent and asthma; 4. whether there are special considerations regarding the 223

224 CLEARING THE AIR agent (for example, subpopulations at risk and interactions with other exposures); 5. which strategies effectively mitigate or prevent exposure to the agent; 6. whether these strategies only reduce exposures, or decrease the occurrence or exacerbation of asthma; and 7. whether these strategies are reasonable for use by the tar- get populations. Each section begins by providing a definition of the agent and a summary of the factors that influence exposure. The evidence concerning the possible association between the agent and asthma is discussed, followed by the committee's conclusions regarding the health impacts. Where information is available, evidence re- garding possible means of mitigating or preventing exposure to the agent is addressed. Each section concludes with any commit- tee recommendations for general or specific areas in which addi- tional research is needed with respect to the agent. Because there are great differences in the amount and type of information avail- able on specific agents, the sections vary in their depth and focus. NITROGEN DIOXIDE Definition of Agent and Means of Exposure Nitrogen dioxide (NO2) is a common indoor and outdoor pol- lutant that is produced, along with other oxides of nitrogen, whenever high-temperature combustion occurs. NO2 is one of six "criteria" air pollutants for which National Ambient Air Quality Standards are set by the U.S. Environmental Protection Agency (EPA). The current standard is 50 parts per billion (ppb) averaged over one year. Much higher indoor concentrations are sometimes observed when indoor sources are present due to the limited di- lution often observed in confined spaces. Indoor sources include gas stoves and space heaters, kerosene space heaters, and poorly vented furnaces and fireplaces. In homes with indoor combus- tion sources, personal NO2 exposures are usually driven by in- door concentration in the home, even in urban areas with elevated outdoor levels.

INDOOR CHEMICAL EXPOSURES 225 In addition to nitrogen oxides, indoor combustion appliances may also emit CO, SO2, formaldehyde, volatile organic com- pounds (VOCs), and submicron particulate matter (PM). Some of these pollutants, including SO2 and PM, are known respiratory irritants. Most epidemiologic studies reviewed in this section have assessed NO2 exposure based on the presence or absence of gas appliances in the home, rather than on the basis of NO2 measure- ments. Few if any studies have simultaneously measured NO2 and associated co-pollutants such as PM. As a result, it is usually not possible to attribute health effects associated with gas appli- ance use to NO2 exposures per se. Factors Influencing Exposure Indoor exposure to NO2 resulting from the use of gas appli- ances is common. On average, about half of U.S. homes have gas stoves or ovens, and much higher percentages of gas appliances exist in some urban areas (Samet et al., 1987~. Considerable data exist on indoor NO2 exposures in U.S. homes and the factors that influence them (Goldstein et al., 1988; Leaderer et al., 1986; Quackenboss et al., 1986; Ryan et al., 1988; Spengler et al., 1983, 1994, 1996~. Indoor NO2 concentrations de- pend on the presence and emission strength of indoor sources, the ventilation rate of the home, and the penetration of outdoor NO2 (Drye et al., 1989; Spengler et al., 1996~. Important indoor sources include unvented cooking and heating appliances that burn gas or kerosene. The use of a gas range results in an increase of about 25 ppb in the background NO2 concentration in a home, with peaks as high as 200 to 400 ppb in the kitchen during cooking (Samet et al., 1987~. In a large study carried out in Albuquerque, New Mexico, the highest two-week average indoor NO2 concentrations were observed in homes with gas stoves that had continuous pilot lights and in homes where the stove or unvented gas or kerosene heaters were used for supplemental heating (Spengler et al., 1996~. In the same study, higher indoor NO2 concentrations were ob- served in gas cooking than in electric cooking homes, but this difference was much less pronounced in the summer when home ventilation rates were higher. Regardless of stove type, indoor

226 CLEARING THE AIR concentrations are generally higher in locations with high out- door concentrations, such as large urban areas, due to the infiltra- tion of outdoor air; however, indoor sources still explain most of the variance in personal exposures in urban areas. There is some evidence to suggest that homes with gas stoves in underprivi- leged, inner city communities may have uniquely high NO2 lev- els, possibly due to higher frequency and longer duration of cook- ing, small home volume, and use of stoves for supplemental winter heating (Goldstein et al., 1988~. Further research into this question is warranted. Data collected in multiple locations in homes with gas stoves show that strong NO2 concentration gradients exist, with kitchen levels higher than elsewhere (Matti et al., 1999~. Kitchen concen- trations during cooking may exceed long-term average concen- trations by an order of magnitude or more. These spatial and tem- poral characteristics imply differential exposures for different residents depending on time spent in the kitchen while cooking is taking place. Evidence Regarding Asthma Exacerbation and Development Numerous epidemiologic studies have examined whether respiratory health effects are associated with exposures to typical indoor NO2 concentrations. Most such studies have addressed respiratory symptoms and/or Jung function variables as the pri- mary outcomes, both of which include measures (i.e., wheeze or decline in FEF25 75) that are usually associated with the clinical diagnosis of asthma. However, few studies have focused on asthma as an outcome or on respiratory effects among asthmatic subjects specifically. This limits the utility of the existing litera- ture for assessing the impact of NO2 on the development or exac- erbation of asthma. Epidemiologic study designs have included cross-sectional surveys, case-control studies, longitudinal cohort studies, and time-series pane] studies assessing acute impacts. Exposures in most studies have been assigned based on answers to questions regarding the presence of gas stoves or other indoor combustion appliances. Some studies have included limited indoor or occa

INDOOR CHEMICAL EXPOSURES 227 signally personal NO2 measurements using passive diffusion samplers. As a group, epidemiologic studies have the advantage of studying realistic levels and patterns of NO2 exposures. How- ever, results can be difficult to interpret due to possible confound- ing. There have also been several clinical experiments involving brief controlled exposures of humans in environmental chambers. Such studies enable careful control of experimental conditions in- cluding exposure level and duration. They also make it more fea- sible to examine asthma-related respiratory outcomes other than symptoms and lung function, such as airway hyperresponsive- ness (AHR), pulmonary cells and cytokines obtained by bronchos- copy, and effects on allergen responsiveness. A limitation of the experimental chamber studies is that they usually employ NO2 concentrations much higher than those typically observed in the indoor environment. Also, the study populations have typically been small and, to some extent, unrepresentative of the more sen- sitive members of the general population. Very few epidemiologic studies have evaluated asthma diag- nosis as an outcome in relation to NO2 exposure, and results from these few studies have been mixed. A well-conducted case-con- tro! study found no association between the presence of a gas cooking appliance in the home and incident asthma (odds ratio [OR]=1.33; 95°/O confidence interval [CI] 0.68-2.58) among chil- dren 3-4 years old in Montreal (Infante-Rivard, 1993~. The main study analyzed 457 cases (children with a first diagnosis of asthma made by a pediatrician) and 457 controls (matched on age and census tract), and found significant associations between in- cident asthma and several factors other than gas appliances, in- cluding heavy maternal smoking, childhood atopy, and others. A subset of 140 subjects provided a 24-hour personal NO2 sample. In an unmatched analysis of this subset, there was a significant association with asthma for subjects in the highest category of NO2 exposure (>15 ppb); however, the small size of the exposed group and the post hoc nature of the analysis preclude any mean- ingfu] inferences regarding the causality of this association. Strachan and Carey (1995) analyzed environmental risk factors for severe wheezing among school children aged 11-16 years in Sheffield, England; 486 cases and 475 age- and school-matched

228 CLEARING THE AIR controls were analyzed, where cases were children whose parents reported 12 or more wheezing episodes in the past 12 months or an attack of wheezing that limited speech. Controls had no his- tory of asthma or wheezing at any age. Non-feather bedding and ownership of furry pets were both significantly associated with case status; however, the use of gas for cooking was not. In contrast, two large questionnaire-based cross-sectional sur- veys, one in Canada and the other in Australia, reported signifi- cant associations between asthma and gas stove use. The first study analyzed data from a nationwide survey of Canadian par- ents. It found a significant association between current, doctor- diagnosed asthma and gas cooking in the homes of children be- tween 5 and 8 years of age, controlling for age, race, sex, parental education, environmental tobacco smoke (ETS), and other factors (Dekker et al., 1991~. The adjusted odds ratio for gas cooking was 1.95 (95°/O CI 1.41-2.68) when 634 subjects with asthma were com- pared to 9,207 with neither asthma, chest symptoms, nor other respiratory diseases. However, the authors cautioned against over-interpretation given the small number of asthma cases ex- posed to gas cooking (N = 60 out of 634 total asthma cases). Asso- ciations were also reported with ETS, living in a damp home, and use of a humidifier. These factors, but not gas cooking, were also associated with reports of wheezing. A second, similar study in South Australia analyzed data from 14,124 families with a child aged 4.25 to 5 years of age (Volkmer et al., 1995~. Gas versus elec- tric stove use was associated with slightly increased prevalence of asthma (OR = 1.24, 95°/O CI 1.07-1.42) and wheezing in the pre- ceding 12 months (OR = 1.16, 95°/O CI 1.01-1.32~. The cross-sec- tional associations found in these two surveys suggest the possi- bility of small impacts of NO2 on asthma risk; however, prospective cohort studies would be needed to rigorously test this hypothesis. Respiratory symptoms that are associated with asthma, such as coughing, wheezing, and shortness of breath, have been stud- ied in relation to gas stove usage and/or NO2 measurements in a large number of cross-sectional surveys, longitudinal pane] stud- ies, and a more limited number of prospective cohort studies. Symptom outcomes have also been analyzed in one chamber ex- posure study.

INDOOR CHEMICAL EXPOSURES 229 Cross-sectional surveys assess association between symptoms and measures of exposure collected simultaneously by question- naires in general population samples, usually controlling for covariates with known or suspected effects on symptoms, such as ETS, home dampness, allergies, and so forth. Although results have been mixed, the accumulating evidence supports the exist- ence of small associations between respiratory symptoms and gas appliance use. At least ten survey studies have reported signifi- cant associations between symptoms and gas stove exposure in adults and/or children (Dodge, 1982; Garrett et al., 1998; larvis et al., 1996, 1998; ledrychowski et al., 1995; Koo et al., 1990; Melia et al., 1977; Viegi et al., 1991, 1992; Volkmer et al., 1995~. For example, in a survey of 1,159 men and women in England, larvis et al. (1996) detected significant associations for women only between symptoms in the past 12 months and the use of gas appliances, adjusting for covariates. The adjusted odds ratios were 2.07 (95°/O CI 1.41-3.05) for wheezing, 2.32 (95°/O CI 1.25-4.34) for waking with shortness of breath, and 2.60 (95°/O CI 1.20-5.65) for asthma attacks. Other cross-sectional survey studies have reported no as- sociations between respiratory symptoms and gas appliances (Braun-Fahriander et al., 1992; Dekker et al., 1991; Dijkstra et al., 1990; Hosein et al., 1989~. There are no obvious differences be- tween the two groups of studies that would explain the differ- ences in results. Several of the cross-sectional studies mentioned above have assessed exposure using actual NO2 measurements, as well as the more common questionnaire-based assessments of gas appliance usage (Brunekreef et al., 1990; Garrett et al., 1998~. Interestingly, such studies have generally found no analytical advantage to the actual NO2 measurements. This counterintuitive finding may have several explanations, including non-representativeness of NO2 measurement times or locations, and/or that NO2 per se is not the causal agent responsible for gas stove associations with symptoms. In a prospective cohort study, Neas et al. (1991) followed res- piratory symptoms over a 12-month period in 1,567 white chil- dren aged 7-11 living in six U.S. cities. Indoor home NO2 mea- surements were collected over two weeks in the winter and in the summer. Incident symptoms were analyzed in relation to mean

230 CLEARING THE AIR NO2 levels. A 15 ppb increase in average household NO2 concen- trations was associated with increased cumulative incidence of any of several lower respiratory symptoms (OR = 1.4,95% CI 1.1- 1.7~. The effect was larger for girls than boys. Two 1999 studies of asthmatic children, available only in abstract form when this re- port was completed, appear to generally support these findings (Kattan, 1999; Smith et al., 1999~. Longitudinal pane] studies and experimental chamber stud- ies assess the acute relationship between brief (episodic) NO2 ex- posures and respiratory symptoms. These studies have not pro- vided strong evidence for acute effects on symptoms at relevant indoor concentrations. Chamber studies involving one- to three- hour exposures to 50-1,500 ppb NO2 did not detect effects on res- piratory symptoms among normal or asthmatic subjects (Salome et al., 1996; Utell et al., 1991~. In a pane! study involving daily recording of symptoms and gas stove use among 164 asthmatic adults over the winter months in Denver, Colorado, Ostro et al. (1994) reported statistically significant associations between a va- riety of respiratory symptoms and stove use. However, interpre- tation of these results as a causal effect of gas stove emissions (e.g., NO2) is hampered by questions of biologic plausibility as well as concerns about potential reporting bias. One 1999 abstract suggests acute effects of NO2 on the severity of symptoms associ- ated with respiratory syncytial virus (RSV) infections (Chauhan et al., 1999), and an environmental chamber study concluded that NO2 exposure increases the susceptibility of airway epithelial cells to injury from respiratory viruses (Boscia et al., 1999~. Experimental chamber studies have noted increases in airway responsiveness to carbocho! or methacholine following brief, high-level (1,500 or 2,000 ppb) NO2 exposures in normal subjects (Frampton et al., 1991; Mohsenin, 1988; Utell et al., 1991) expo- sure levels that have not typically elicited direct effects on Jung function. Studies in asthmatics report enhanced airway responses to histamine or methacholine challenges at concentrations as low as 500-600 ppb, suggesting that the airways of asthmatics, already more responsive to nonspecific stimuli, are more sensitive to the enhancing effects of NO2 (Mohsenin, 1987; Salome et al., 1996~. While the mechanism for these effects remains uncertain, proinflammatory effects of NO2 (Blomberg et al., 1999) may be

INDOOR CHEMICAL EXPOSURES 231 involved. Although the relevance of these findings to typical in- door NO2 concentrations encountered by the general public re- mains unclear, they do raise concerns for persons, such as moth- ers and infants, who may spend large amounts of time in kitchens where gas stoves are being used, especially in conjunction with low rates of home ventilation. In addition to the enhancement of airway responses to non- specific stimuli, NO2 exposure at 400 ppb has been shown in ex- perimental chamber studies to enhance the lung response, mea- sured by a drop in forced expiratory volume in one second (FIVE ), to house dust mite aerosol inhalation by asthmatic adults (Rusznak et al., 1996; Tunnicliffe et al., 1994~. Devalia and col- leagues (1994) reported that exposure to a combination of SO2 and NO2 in concentrations that could be encountered in heavy traffic areas produced a statistically significant decrease in the concentration of allergen required to produce a 20% decrease in FIVE (PD20FEV~) of adult asthmatics challenged with Dermato- phagoides pteronyssinus dust mite allergen. Again, no direct effects of NO2 on Jung function decline were noted in these studies. Because of the importance of acute respiratory infections as triggers of asthma symptoms, an effect of NO2 exposure on in- creased risk of respiratory infections might represent an indirect mechanism linking NO2 with asthma exacerbations. In the late 1970s, Melia and colleagues reported an increased risk of respira- tory infections among children living in homes with gas stoves in a large British cross-sectional survey (Melia et al., 1977, 1985~. However, other studies have not confirmed this finding (Samet et al., 1993; Ware et al., 1984~. In a prospective cohort study of in- fants, no association was found between NO2 exposure or stove type and the incidence rate or duration of respiratory infections (Samet et al., 1993~. Samet and colleagues (1987) extensively re- viewed the historical literature on NO2 and respiratory infections, concluding that "the findings on NO2 exposure and respiratory illnesses indicate that the magnitude of the NO2 effect at concen- trations encountered in most U.S. homes is likely to be small." Although there is insufficient new evidence to alter this conclu- sion, it is worth noting that a 1999 longitudinal pane] study re- ported enhanced severity of RSV infections in association with high indoor NO2 concentrations (Chauhan et al., 1999~.

232 CLEARING THE AIR Inconsistent associations between gas appliance use or NO2 concentrations and declines in Jung function have been reported in epidemiologic studies (Brunekreef et al., 1990; Dijkstra et al., 1990; Dodge, 1982; Fischer et al., 1985; Garrett et al., 1998; Hack- ney et al., 1992; Hasselblad et al., 1981; Hosein et al., 1989; larvis et al., 1996, 1998; ledrychowski et al., 1995; Kattan, 1999; Speizer et al., 1980; Viegi et al., 1991; Ware et al., 1984), with significant associations reported in less than half of the studies. Where present, the nature of the lung function associations has not been consistent across studies, and the possibility of confounding ex . . fists In some cases. As noted earlier, little evidence of acute Jung function impacts of brief exposure to high concentrations of NO2 has been observed in experimental chamber studies (Frampton et al., 1991; Hackney et al., 1992; Mohsenin, 1987, 1988; Salome et al., 1996; Tunnicliffe et al., 1994; Utell et al., 1991), except for four-hour exposures to very high concentrations (i.e., 2,000 ppb) (Blomberg et al., 1999~. The committee concludes that Jung function is not markedly af- fected either acutely or chronically by NO2 at typical indoor con- centrations. Conclusions: Asthma Exacerbation and Development · There is sufficient evidence of an association between brief high-level exposures to NO2 and increased airway responses to both nonspecific chemical irritants and inhaled allergens among asthmatic subjects. These effects have been observed in human chamber studies at concentrations (400-700 ppb) that may occur only in poorly ventilated kitchens with gas appliances in use. · There is limited or suggestive evidence of an association between the use of gas appliances and increased risk of respira- tory symptoms, increased risk of respiratory infections, and to a lesser extent, decreased lung function. Data supporting this con- clusion derive from epidemiologic studies. · There is limited or suggestive evidence of no association between brief NO2 exposures and acutely decreased Jung func- tion. This evidence comes from chamber studies of human sub- jects. · There is inadequate or insufficient evidence to determine

INDOOR CHEMICAL EXPOSURES 233 whether or not an association exists between emissions from gas appliances and asthma development. However, the association observed between the use of gas appliances and the diagnosis of childhood asthma in two, large cross-sectional population sur- veys indicates that this topic should be examined more carefully in future research. As noted above, few studies have simulta- neously measured NO2 and associated co-pollutants and it is thus usually not possible to attribute health effects associated with gas appliance usage to NO2 or other combustion by-product expo sures per se. Evidence and Conclusions: Exposure Mitigation and Prevention Indoor NO2 mitigation has received relatively little attention in the published literature. Samet (1990) notes that general con- tro! options for pollutants emitted by indoor combustion appli- ances include source modification (removal, substitution, or emis- sion reduction), ventilation (exhaust or dilution), or pollutant removal (filtration or reactivity). Source modification is usually the most effective approach. For example, that study recom- mended that "unvented combustion space heaters should not be used, particularly in cold climates where they may be on for pro- longed periods." On the other hand, while removal of gas stoves would in theory represent an effective exposure reduction strat- egy, it may not be practical or economically feasible in most cases. Continuous pilot lights add between 10 and 20 ppb of NO2 to background indoor levels and should be turned off or eliminated (Samet, 1990~. Kitchen ventilation has the potential to be effective in reducing the impact of gas appliance emissions. However, ex- haust hoods should be vented outdoors and must be used consis- tently while the appliance is on to be effective. Evidence suggests that only a small fraction of kitchens with gas stoves achieve these objectives (Fuhibrigge and Weiss, 1997~. For NO2, pollutant re- moval via air cleaning is not a feasible approach. The committee did not identify any studies that addressed whether lowering in- door NO2 levels had an effect on asthma outcomes.

234 CLEARING THE AIR Research Needs Future research into the relationship between indoor NO2 and asthma should target population subgroups that are likely to be most exposed. These include women and infants, especially those at the lower end of the socioeconomic spectrum, who may spend more time in kitchens during cooking. Further research is needed on the distributions of peak and mean personal exposures, on the relationship between exposure and asthma, and on the exacerba- tion of asthma among those with preexisting asthma. Research is also needed into the development of practical, economical venti- lation methods for kitchens. PESTICIDES Definition of the Agent and Means of Exposure "Pesticide" is a general term for an agent used to kill an unde- sirable organism. Among the categories of agents covered by this umbrella term are fungicides, herbicides, insecticides, and roden- ticides. Residential pesticides represent a broad class of chemicals and applications aimed at controlling flies, ants, moths, cockroaches, fleas, ticks, infectious organisms, fungi, plants and other un- wanted species in and around the residential environment. Pesti- cides that have been measured in residential indoor air include chiordane, heptachior, aldrin, dieldrin, diazinon, propoxur, dichiorvos, naphthalene, p-dichiorobenzene, pentachiorophenol, chiorpyrifos, malathion, and carbary! (Baker and Wilkinson, 1990). Factors Influencing Exposure For members of the general population, the home represents the principal setting for pesticide exposures. It has been reported that approximately 90°/O of U.S. homes use pesticides, and ~84% use them inside the house (Baker and Wilkinson, 1990; U.S. EPA, 1979~. Eskenazi and colleagues (1999) note that younger children may have higher exposure than others in a contaminated envi

INDOOR CHEMICAL EXPOSURES 235 ronment because of the greater amount of time spent indoors and closer contact with contaminated surfaces. They also identify farmworkers and their families as a vulnerable population through agents that penetrate or are tracked indoors. Children who live in poverty may be at particular risk of exposure through greater use of legal and illegal pesticides in urban environments (Landrigan et al., 1999~. In addition to diet and dermal absorption, inhalation of air- borne pesticides, either in vapor form or adsorbed on particles, is an important route of exposure in the residential setting. Surveys of residential air concentrations of a range of pesticides were sum- marized by Baker and Wilkinson (1990, Table 2-11~. ChIorpyrifos, which is currently one of the most commonly used residential pesticides, ranged in concentration from 2 to 37 ,ug/m3 in a sur- vey of U.S. homes published in 1983 (U.S. EPA, 1983~. Evidence Regarding Asthma Exacerbation and Development Although there is a great deal of interest in the possibility of an association between pesticide exposure and asthma, relatively little research has been done on the topic to date. There is evi- dence suggesting that high-level exposures to some pesticides may elicit, via irritative mechanisms, persistent asthma. This consists primary of anecdotal and case reports. A case report (Deschamps et al., 1994) gives an account of a 26-year-old male who developed persistent asthma after work- ing in a closed room that was heavily treated with the organo- phosphate insecticide dichiorvos. Occupational exposure to the fungicides metam sodium (Cone et al., 1994), captafo] (Royce et al., 1993), tetrachIoroisophthalonitrile (chIorthalonil) (Honda et al., 1992), and tributy] tin oxide (Shelton et al., 1992) have also been associated with new asthma onset in case reports. Etze! (1995) cites additional examples. Exposure to pyrethrins or pyre- throids insecticides commonly used in over-the-counter flea and insect sprays and powders may cause allergic rhinitis (O'Malley, 1997~. Individuals who are allergic to ragweed may also exhibit an allergic reaction to pyrethrins (Wax and Hoffman, 1994~. Although it is not known whether and how these findings

236 CLEARING THE AIR are relevant to the general population, they do raise concern about the possibility of asthmogenic effects of prolonged low- leve! exposures. There is little relevant epidemiologic information in the lit- erature. Senthilselvan and colleagues (1992) surveyed 1,939 male farmers in Saskatchewan on work, respiratory health, and expo- sure to chemicals. The prevalence of self-reported asthma was sig- nificantly associated with the use of carbamite insecticides. Other studies in agricultural and rural settings list pesticides along with numerous other exposures (animal, arthropod, and insect aller- gens; endotoxins; molds; plant proteins; pollen) potentially asso- ciated with asthma or other respiratory health outcomes (ATS, 1998). The response noted in many of these reports appears to be similar to the reactive airways dysfunction syndrome (RADS), which is an asthma-like response that occurs in some people when exposed, even briefly, to a single high concentration of irritative chemicals, usually in the occupational setting. Whether a similar response may occur in a subset of the general population follow- ing lower-level but repeated exposures to irritating chemicals in- cluding pesticides is not known. This is an area that deserves fur- ther study. Although some pesticides may affect the immune system, there is currently a lack of information on whether pesticide ex- posures can have an impact on the allergic asthma response. It has also been suggested that dysregulation of parasympathetic and sympathetic autonomic control of the airways through pesti- cide exposure may provide a mechanism (Eskenazi et al., 1999~. Chan-Yeung and Lam (1986) note that acute asthma has been de- scribed in farm workers who use organophosphate insecticides, which act as an anticholinesterase and probably precipitate air- flow obstruction on a pharmacologic basis without the require- ment of an underlying predisposition to asthma. Conclusions: Asthma Exacerbation and Development · There is inadequate or insufficient evidence to determine whether or not an association exists between pesticide exposures at the levels typically encountered in nonoccupational or residen

INDOOR CHEMICAL EXPOSURES 237 tial settings and the development or exacerbation of asthma. As noted in Chapter 5, proper use of some pesticides as part of an exposure control program may yield benefits for asthmatics through elimination or reduction of sources of allergen. Evidence and Conclusions: Exposure Mitigation and Prevention There is considerable potential for reducing indoor residen- tial exposures to pesticides. The methods of integrated pest management (IPM), which emphasize habitat modification in conjunction with minimal and selective use of pesticides, should be useful in this regard. Although strategies exist that may be effective in reducing indoor pesticide concentrations, it is not known whether reducing these concentrations has any significant impact on the risk of asthma development or exacerbation. Research Needs The most immediate need for research in this area is for infor- mation on whether prolonged exposures to low to moderate con- centrations of airborne pesticides can elicit an irritative asthma response in susceptible individuals. Animal models may be help- fu] in this regard. Koren and O'Neill (1998) report that a presently unpublished study on a microbial biopesticide used against cock- roaches suggests it can induce asthma in mice. It has been sug- gested that Flinders Sensitive Line rats, which exhibit increased responses to an agent similar to commonly used organophosphate pesticides, may be useful in the study of asthma outcomes. VOLATILE ORGANIC COMPOUNDS Definition of Agent and Means of Exposure Volatile organic compounds are any of a large number of or- ganic molecules that exist either as free vapors or adsorbed onto particles in air. More than 300 VOCs have been measured in in- door air (Wallace, 1987~. Table 6-1 lists some of the more common VOCs and their sources.

238 TABLE 6-1 Common VOCs and Their Sources CLEARING THE AIR Chemical Major Sources of Exposure 1,1 ,1 -Trichloroethane Aliphatic hydrocarbons (octane, decane, undecane) Aromatic hydrocarbons (toluene, xylenes, ethyl-benzene, tri methyl benzene) Benzene Carbon tetrachloride Methylene chloride ~Dichlorobenzene Terpenes (limonene, oc-pinene) Tetrachloroethylene Trichloroethylene Wearing or storing dry-cleaned clothes; aerosol sprays; fabric protectors Paints, adhesives, gasoline, combustion sources Paints, adhesives, gasoline, combustion sources Smoking, auto exhaust, passive smoking, driving, pumping gas Industrial-strength cleaners Paint stripping, solvent usage Room deodorizers, moth cakes Scented deodorizers, polishes, fabrics, fabric softeners, cigarettes, food, beverages Wearing or storing dry-cleaned clothes; visiting dry cleaners Unknown (cosmetics, electronic parts) SOURCE: Adapted from Samet. Indoor Air Pollution: A Health Perspective. pp. 253. 1991, The Johns Hopkins University Press. Factors Influencing Exposure Most available data suggest that personal exposures to VOCs are dominated by indoor exposures, even for persons living in urban areas near major outdoor VOC sources such as the petro- chemical industry (Wallace, 1991; Wallace et al., 1987~. Numerous VOC sources exist indoors, including cigarette smoking, combus- tion appliances, solvents, printed materials, photocopying ma- chines, chlorinated water, dry-cleaned clothes, pesticides, silicone caulk, floor adhesive, particleboard, moth crystals, floor wax, wood stain, paint, furniture polish, floor finish, carpet shampoo, room deodorizer, and viny] flooring and tiles (Gold, 1992; Samet, 1990; Wallace, 1991~. Cleaning agents used in homes either may be a direct source of VOC emissions or may release VOCs through

INDOOR CHEMICAL EXPOSURES 239 chemical decomposition of the surface being washed (Wolkoff et al., 1998~. Indoor VOC concentrations and time spent indoors are the two main factors influencing personal exposures to VOCs. Fac- tors that modify indoor concentrations, including emission rates from sources and removal rates due to building ventilation, thus have a strong impact on personal exposures. Depending on the type of building material and the VOC, temperature and relative humidity may influence emission rates (Wolkoff, 1998~. Activity patterns, personal habits, and hobbies also help determine expo- sure. Many VOCs can adsorb onto clothing and interior surfaces, which can then serve as reemission sources. Table 6-2 shows average and maximum concentrations of 18 VOCs observed in a U.S. study of 24-hour and 12-hour personal exposures and in a German study of two-week average indoor concentrations. Average values ranged from 2 to 84 ,ug/m3, with most concentrations falling below 10-15 ,ug/m3. Wallace and col- leagues (1987) reported data on simultaneous personal and out- door VOC measurements in randomly selected groups of sub- jects living in two urban areas of New Jersey, in a moderately sized city in North Carolina, and in a small town in North Da- kota. Personal exposures were consistently higher than simulta- neous outdoor measurements in all three populations, presum- ably due to the dominant influence of indoor exposures. While outdoor concentrations increased with degree of urbanization across the three locations, personal exposures showed much less interlocution variability. In contrast to combustion pollutants such as NO2 and par- ticulate matter, many VOCs tend to be source specific (Wallace et al., 1987~. For example, the major source of chloroform in indoor air is hot water that has undergone chlorination. The principal sources of benzene in indoor air are smoking and gasoline vapors from attached garages. Tetrachioroethylene (PERC) is a VOC as- sociated with dry cleaning; personal exposures are driven by time spent in laundromats and proximity to clothes that have been dry cleaned. p-DichIorobenzene is a principal ingredient in both moth crystals and room deodorizers, two materials whose presence in- doors is strongly predictive of variations in human exposure. Be- cause human exposures to many VOCs are associated with spe

240 CLEARING THE AIR TABLE 6-2 Concentrations of VOCs (,ug/m3) in Indoor Air in Germany Comparecl to Personal Exposures in the Unitecl States Arithmetic Mean Maximum Compound West United West United States Germany States Chlorinated ChloroformNM3 NM 1,1,1-Trichloroethane9522608,300 Trichloroethylene116120350 Tetrachloroethylene1416810250 p-Dichlorobenzene14251,2601,600 Aromatic Benzene101690510 Styrene234176 Ethylbenzene109160380 o-Xylene7945750 m + p-Xylene2326NM300 Toluene84NM1,710NM Aliphatic Octane5492122 Nonane1012140177 Decane156240161 Undecane108120385 Dodecane647272 Terpenes oc-Pinene104120208 Limonene28433202,530 NOTE: NM = not measured. SOURCE: Adapted from Samet. IndoorAir Pollution: A Health Perspective. p. 259. O 1991 The Johns Hopkins University Press. cific indoor source materials, exposure mitigation can be directed at reducing contact with specific sources. Evidence Regarding Asthma Exacerbation and Development A series of studies examined associations between asthma or asthma-related symptoms and indoor environmental factors in

INDOOR CHEMICAL EXPOSURES 241 eluding VOCs in Uppsala, Sweden. Norback and colleagues (1995) reported results from a small case-control study nested within a stratified population-based survey of adults 20-45 years old in this community: 47 cases with doctor-diagnosed asthma or asthma symptoms in the past year were compared with 41 sub- jects lacking both a diagnosis and symptoms. The symptom noc- turnal shortness of breath was associated with the presence of carpets and indoor VOC, formaldehyde, and CO2 concentrations. Significant VOC odds ratios ranged from 4.9 (95°/O CI 1.1-22.8) for toluene to 9.9 (95°/O CI 1.7-58.8) for total VOCs. The authors also reported associations between AHR and limonene (a terpene). Variability in peak flow rates was related to two other terpenes, oc-pinene and b-carene. A subsequent analysis of data from the same underlying population survey reported a marginally sig- nificant cross-sectional association (OR = 1.5, 95°/O CI 1.0-2.4) be- tween asthma prevalence and the presence of newly painted inte- rior surfaces in the home (Wieslander et al., 1997~. Blood eosinophi] concentrations were also elevated in subjects from re- cently painted dwellings. In a separate cross-sectional survey of 627 school children age 13-14 years, associations were observed between current asthma and school VOC concentrations in a lo- gistic regression analysis that controlled for atopy, food allergies, and day care histories (Smoke et al., 1997~. Many other environ- mental factors besides VOCs were associated with asthma, includ- ing school size, the presence of open shelves in classrooms, lower room temperature, higher relative humidity, and formaldehyde concentrations. This makes it difficult to attribute the association to VOCs alone. The VOC association was not robust to different VOC measurement methods; only passive, but not active, VOC monitoring data were associated with asthma. A mouse bioassay performed by Wolkoff and colleagues (1999) found that a mixture of (+~-oc-pinene and ozone at concentrations close to their no-ef- fect levels (NOELs) produced reaction products including form- aldehyde and induced strong airway irritation. The authors de- termined that after accounting for sensitivity differences between mice and humans, the measured concentrations of formaldehyde and ozone in the reaction mixture were "not unrealistic for in door settings." While these studies suggest a variety of associations between

242 CLEARING THE AIR indoor factors and measures of asthma status, because of the mul- tiple correlations observed among exposure factors, it is not possible to clearly implicate VOCs as the causative agents. The possibility of residual confounding also clouds any causal inter- pretation. Despite these limitations, the studies reviewed here have generated several intriguing hypotheses regarding the pos- sible influences of VOCs and other indoor environmental factors on asthma. Small, acute impacts of high-level VOC exposures on de- creased lung function and increased nasal inflammation have been suggested in controlled human chamber studies (Harving et al., 1991; Koren et al., 1992~. Harving and colleagues (1991) re- ported a significant 9°/0 pre-post exposure drop in FEVER among 11 asthmatics with bronchial reactivity who were exposed for 85 minutes to 25-mg/m3 of a VOC mixture. However, this FEVER de- cline was not statistically different from the decline observed af- ter sham exposure. Koren and colleagues (1992) exposed 16 adults without asthma or allergy to a 25 mg/m3 VOC mixture for four hours. Significant increases in inflammatory cells (neutrophils) were observed in nasal washings performed immediately and 18 hours after exposure, adjusting for changes observed following sham exposure. The relevance of these high-exposure findings to the hundredfold lower concentrations observed in indoor resi- dential settings in uncertain. Conclusions: Asthma Exacerbation and Development There is inadequate or insufficient evidence to determine whether or not an association exists between indoor residential VOC exposures and the development or the exacerbation of asthma, although elevated indoor concentrations of VOC mix- tures are suspected to play a role in the constellation of symptoms known as sick building syndrome (e.g., headaches, fatigue, eye and upper respiratory irritation). Evidence and Conclusions: Exposure Mitigation and Prevention Although there is not clear evidence for a role of VOC expo

INDOOR CHEMICAL EXPOSURES 243 sures in asthma, it is deemed prudent to limit indoor exposures where practical. Approaches include indoor source removal or control (e.g., eliminating or reducing indoor smoking, air fresh- eners, moth crystals, use of solvent-based paints and solvent stor- age), source avoidance (e.g., altering activity patterns and habits to minimize exposures), and increased ventilation (e.g., increas- ing the overall home air exchange rate, installing ventilation fans in spaces containing sources). Research Needs With the advent of small, unobtrusive passive diffusion moni- tors capable of measuring microgram quantities of VOCs in 48- hour samples, it should be possible to incorporate personal VOC exposure assessment into future epidemiologic studies address- ing environmental factors and asthma, yielding an expanded data base on which to judge the possible role of VOCs in asthma de- velopment and exacerbation. Prospective cohort studies that characterize time-averaged personal VOC exposures of study subjects using passive badges and then follow subjects to assess the development and/or exac- erbation of asthma could generate information that would allow a more confident assessment of any potential risk. FORMALDEHYDE Definition of the Agent and Means of Exposure Although formaldehyde is a member of the VOC family, it is usually discussed separately from other VOCs because of the large body of scientific literature that specifically addresses form- aldehyde exposures and human health. A colorless but character- istically pungent-smelling gas, formaldehyde is the simplest of the aldehydes, with the chemical formula HCHO. Formaldehyde is a component of many building materials, consumer products, and combustion gases. Potential indoor sources include urea- formaldehyde foam insulation (UFFI); glues used in plywood and pressed-board products; paper products including tissues, tow

244 CLEARING THE AIR els, and bags; cosmetics and detergents; and emissions from gas stoves and tobacco smoking. Because of its polar structure, formaldehyde is highly soluble in water and thus is rapidly absorbed in the mucous membranes of the upper respiratory system. Because formaldehyde is highly reactive, it exerts its irritant effects primarily at or near the site of deposition. Factors Influencing Exposure Formaldehyde pollution i s present both outdoors and in- doors. Outdoor sources include motor vehicle exhaust, especially when oxygenates are used as fuel additives. Indoor concentra- tions are determined by the presence, number, and age of sources and by the degree of ventilation with fresh air. Formaldehyde off- gassing by materials decays over time, with the highest emission rates occurring when materials are new. Thus, formaldehyde con- centrations will typically be highest in newly constructed or reno- vated interior spaces or in those containing new furniture and/or carpets, to the extent that these materials contain formaldehyde resins. Because mobile homes often contain a high percentage of such materials, as well as being relatively airtight, such structures will often contain higher formaldehyde concentrations than other types of residences. Indoor residential formaldehyde concentrations in large num- bers of conventional and mobile homes have been reported from several studies (Dally et al., 1981; Hanrahan et al., 1984; Ritchie and Lehnen, 1985; Sexton et al., 1986; Stock and Mendez, 1985) and were summarized by Marbury and Kreiger (1991~. In moni- toring surveys carried out in response to physician or resident requests, formaldehyde concentrations ranged from 0.01 to 5.62 parts per million (ppm), with mean concentrations falling below 0.50 ppm (Dally et al., 1981; Ritchie and Lehnen, 1985~. In other studies, where populations were chosen either at random or by convenience, lower levels ranging from 0.01 to 0.80 ppm were observed, with means falling below 0.20. According to an EPA review (U.S. EPA, 1987), average concentrations in mobile homes (0.2 to 0.5 ppm) usually exceed those in conventional homes (0.03 to 0.09 ppm).

INDOOR CHEMICAL EXPOSURES Evidence Regarding Asthma Exacerbation and Development 245 Several excellent reviews of formaldehyde exposures and health have been published (Marbury and Krieger, 1991; Samet, 1990~. The known health effects of formaldehyde at high expo- sure levels include nasal cancers in laboratory animals (Kerns et al., 1983) and irritation of the mucous membranes of the eyes, nose, and throat in humans. The influence of formaldehyde on asthma is much less clear, except for relatively rare cases of occu- pational asthma among workers exposed to high-level formalde- hyde concentrations (Hendrick and Lane, 1977~. With respect to occupational asthma, it remains unclear to what extent formalde- hyde acts through immunologic mechanisms involving specific sensitization as opposed to irritant mechanisms (Nordman et al., 1985~. Although several surveys have reported high rates of upper- respiratory symptoms among residents of mobile homes and/or homes containing UFFI (Breysse, 1980; Dally et al., 1981; Norsted et al., 1985; Sardinas et al., 1979), interpretation is often difficult due to potential selection bias, the lack of adequate control groups, or the absence of exposure data (Marbury and Krieger, 1991~. One large population-based study compared symptom rates between 1,396 residents of UFFI-containing homes and 1,395 residents of non-UFFI homes (Thun et al., 1982~. Reports of wheezing were unusually low overall but were more frequent in residents of UFFI-containing homes (0.6 versus 0.1%~. No air- borne formaldehyde measurements were carried out however. Broder and colleagues (1988) reported elevated rates of a wide range of symptoms, including wheezing among 1,726 residents of UFFI-containing homes compared with 720 subjects from non- UFFI homes. Measured formaldehyde levels did not predict symptoms in a consistent way, suggesting the possible influence of other air contaminants besides, or in addition to, formaldehyde. Several more recent population-based surveys suggest pos- sible associations between indoor formaldehyde levels, along with many other indoor factors, and measures of asthma preva- lence and/or symptoms in children and adults based on studies in the city of Uppsala, Sweden (Norback et al., 1995; Smoke et al.,

246 CLEARING THE AIR 1997; Wieslander et al., 1997) (see earlier discussion of VOCs). None of these studies were able to isolate formaldehyde specifi- cally as the causative agent in the reported associations. How- ever, they do demonstrate the strong associations that may be found between a variety of measures of indoor air quality and health outcomes related to asthma. Conclusions: Asthma Exacerbation and Development · There is limited or suggestive evidence of an association between formaldehyde exposure and wheezing and other respi- ratory symptoms. · There is inadequate or insufficient evidence to determine whether or not an association exists between formaldehyde expo- sure and asthma development. Evidence and Conclusions: Exposure Mitigation and Prevention Options for indoor formaldehyde mitigation include source control, air cleaning, and dilution (Samet, 1990~. As is generally the case, source control is the option of first choice since it has the greatest potential for significant exposure reductions. The use of UFFI was banned in 1982 by the Consumer Products Safety Com- mission, eliminating this important source of indoor formalde- hyde (Ashford et al., 1983~. Interestingly, studies in which UFFI has been removed from houses have not demonstrated substan- tial decreases in formaldehyde levels. Of the remaining indoor sources, particleboard and hardwood plywood are the most sig- nificant. While removing these products from interior spaces would in theory represent an effective strategy for further expo- sure reduction, the resulting asthma risk reductions, if any, are considered unlikely to justify the costs associated with substitute materials. An additional consideration is the age of the material, since formaldehyde emission rates from these products diminish rapidly in the first year after they are manufactured (Samet, 1990~. In-situ control of emissions can be achieved through the applica- tion of sealant coatings or coverings over the formaldehyde-con- taining materials, although VOC emissions from liquid coatings

INDOOR CHEMICAL EXPOSURES 247 are likely to result. Other approaches to source reduction that have demonstrated effectiveness include ammonia fumigation and indoor temperature and humidity reduction. Conclusions Regarding Means of Source Mitigation or Prevention Although strategies exist that may be effective in reducing indoor formaldehyde concentrations, there is inadequate or in- sufficient evidence to determine whether or not an association exists between the implementation of these strategies and a de- crease in asthma development or exacerbation. Research Needs No specific research is recommended. FRAGRANCES Definition of Agent and Means of Exposure Fragrances are constituents of many personal (perfume, co- logne, soap, shampoo, hairspray, shaving cream, deodorant, hand lotion, nail color and enamel) and household (detergent, fabric softener, dishwashing liquid, dishwasher detergent, air freshener) products. A 1991 survey identified several classes of polar VOCs in emissions from such products, including alcohols, esters, and aldehydes (Wallace et al., 1991~. It is estimated that more than 3,000 chemicals are used in fragrance manufacture and that syn- thetic organic chemicals constitute the vast maioritv of the con- stituent raw materials (Fisher, 1998~. Evidence Regarding Asthma Exacerbation and Development I J There is limited and largely anecdotal epidemiologic evidence suggesting that exposure to fragrances may induce asthma-like symptoms in some sensitive individuals and that some patients with asthma are sensitive to strong scents. A small number of con

248 CLEARING THE AIR trolled clinical challenge studies have been carried out, with some but not all of these demonstrating respiratory effects following fragrance exposure in sensitive population groups. A study by Shim and Williams (1986) examined the effect of cologne and a saline placebo challenge on the expiratory volume of four patients with sensitivity to cologne. The researchers found an ~20-60% decline from baseline in FIVE during the 10-minute cologne exposure. Occlusion of the nostrils prevented the decline in one of the subjects. Kumar and colleagues (1995) studied the effect of exposure to commercial perfume-scented strips on 29 asthmatic adults and 13 nonasthmatic controls. They reported that perfume inhalation challenges produced significant declines in FEVER in asthmatic patients compared to control subjects, with greater declines noted among the more severely asthmatic sub- jects and among atopic (versus nonatopic) asthma subjects. A study by Miliqvist and Lowhagen (1998) examined 10 asthmatic patients who complained of sensitivity to strong scents. The pa- tients were challenged with methacholine, perfume (with and without a nose clip to block smell perception), and a placebo. They found no changes in Jung function after the perfume provocation, although all of the patients were very sensitive to provocation with methacholine. Miliqvist and colleagues (1999) conducted a single-blinded, placebo-controlled randomized study of perfume exposure, us- ing face masks or nose clips to block smell perception. They found that a group of 11 patients with a history of hyperreactivity to scents exhibited asthma-like symptoms that increased over the 30-minute exposure period when provoked. An earlier study by Miliqvist and Lowhagen (1996) found that breathing through a carbon filter had no protective effect for nine patients with respi- ratory symptoms (but without immunogIobulin E [IgE] mediated allergy) subjected to perfume provocation, suggesting that the symptoms were not transmitted via the olfactory nerve. Mecha- nisms were also examined in an animal study by Hilton and col- leagues (1996~. They concluded that the fragrances eugeno! and isoeugeno] did not cause sensitization of the respiratory tract of mice or guinea pigs. Anderson and Anderson (1998) found that one-hour exposure to emissions of five commercial colognes or

INDOOR CHEMICAL EXPOSURES 249 toilet water elicited pulmonary irritation and decreases in expira- tory airflow velocity in male Swiss-Webster mice. A clinic-based occupational study (Ross et al., 1998) found that workers in the perfume industry were among the groups with the highest incidence rates of occupational asthma in 1997. However, the specific workplace exposures that might account for the observation were not identified. Conclusions: Asthma Exacerbation and Development It is difficult to draw conclusions concerning a possible direct role of chemical fragrances in eliciting respiratory symptoms be- cause many studies fad] to control for the possible influence of odor perception. The studies that do account for this factor pro- vide limited or suggestive evidence of an association between ex- posure to certain fragrances and the manifestation of respiratory symptoms in asthmatics sensitive to such exposures. The com- mittee did not identify any carefully controlled studies that ad- dress the relationship between fragrance exposure and the devel- opment of asthma. In summary: · There is limited or suggestive evidence of an association between exposure to certain fragrances and the manifestation of respiratory symptoms in asthmatics sensitive to such exposures. · There is inadequate or insufficient evidence to determine whether or not an association exists between exposure to fra- grances and asthma development. Evidence and Conclusions: Exposure Mitigation and Prevention There is no scientific literature on the effectiveness of fra- grance exposure prevention measures for sensitive asthmatics. However, avoidance is clearly the most straightforward means of addressing problematic exposures for sensitive individuals.

250 CLEARING THE AIR Research Needs Future research on fragrance exposures has to carefully con- tro! for confounding factors such as odor perception and to focus on objective measures of respiratory health. Additional research elucidating the mechanism or mechanisms underlying adverse respiratory reactions to nonacute exposure to fragrances or their component chemicals would also be helpful. PLASTICIZERS Definition of Agent and Means of Exposure Chemicals that soften or enhance the flexibility of resins are called "plasticizers." These chemicals, which are also VOCs, are used primarily to process polyvinyl chloride (PVC) resin into use- ful forms. Plasticizer residues may be found in household items such as sheet viny] flooring, wall coverings, viny] upholstery, and shower curtains. Evidence Regarding Asthma Exacerbation and Development There is a small literature addressing the possible connection between plasticizer exposure and asthma. Di(2-ethy~hexyI) phthalate (DEHP), a plasticizer widely used in building materi- als, has been implicated in airway inflammation, and it has been suggested that residential exposure to DEHP may have a role in asthma pathogenesis (0ie et al., 1997) and bronchial obstruction (die et al., 1999~. Doelman and colleagues (1990) report that mono(2-ethy~hexyI) phthalate (MEHP), a breakdown product of DEHP, induces bronchial hyperreactivity in rats. Anderson and Anderson (1999) found that one-hour exposure to emissions of six brands of waterproof crib mattress covers, five of which were manufactured with PVC cores, induced asthma-like symptoms in male Swiss-Webster mice. There are also reports of asthma exacerbation and develop- ment related to occupational exposures to plasticizers (Cipolla et al., 1999) and plastics manufacturing (Kogevinas et al., 1999), al

INDOOR CHEMICAL EXPOSURES 251 though their relevance to nonoccupational environments is open to question. Conclusions: Asthma Exacerbation and Development and Research Needs While the reports described above have attracted some inter- est in the research and building trades communities, there is in- adequate or insufficient evidence to determine whether or not an association exists between nonoccupational exposure to plasticiz- ers and the development or exacerbation of asthma. Research characterizing residential exposure to such compounds and evaluating asthma outcomes while controlling for known con- founders would help resolve the question of their influence. OTHER CHEMICAL EXPOSURES IN THE INDOOR ENVIRONMENT Some outdoor air pollutants potentially associated with asthma penetrate the indoor environment and therefore present opportunities for indoor exposure. The following section ad- dresses three of these pollutants: ozone, non-biologic particulate matter with sources other than tobacco smoke, and sulfur diox- ide. Since the committee's mandate was to address indoor air pol- Jutants, the discussion of these is less detailed than others in the chapter and no conclusions are drawn concerning indoor expo- sures and asthma outcomes. Ozone Ozone (03) iS a natural part of the atmosphere that is also a by-product of the chemical reactions that create smog. Outdoor ozone penetrates dwellings only partially, depending on ventila- tion rate and reactions with indoor surfaces. In buildings without indoor sources, average ratios of indoor to outdoor (i/o) concen- trations are typically around 0.5, although i/o ratios as low as 0.1 are observed in tightly sealed homes with air conditioners . The ~ Chapter 10 discusses the relationship of ventilation and air cleaning to pollut- ant exposures associated with asthma and asthma symptoms.

252 CLEARING THE AIR primary indoor residential source of ozone is an appliance called an ionizer or ozone generator, which is sold as an air freshening or air cleaning device. The EPA report Ozone Generators That Are Sold as Air Cleaners (U.S. EPA, 1999) details potential health prob- lems from ozone exposure associated with the use of these de- vices. Xerographic copying machines found in offices, schools, and some other indoor environments also produce ozone. Time-series epidemiologic studies have demonstrated signifi- cant associations between daily asthma hospitalizations and/or emergency room visits and daily outdoor ozone concentrations (U.S. EPA, 1996~. Although outdoor ozone concentrations usually exceed indoor levels, it is likely that relevant exposures in these studies occurred predominantly indoors. Other studies indicate that higher ozone levels cause coughing and shortness of breath in asthmatics and nonasthmatics, and exacerbation of symptoms in asthmatics (Bielory and Deener, 1998~. Peden and colleagues' (19951 stub of 11 asthmatics who were allergic to dust mites ~ , ~ (Dermatophagoidesfarinae) found that ozone exposure had both a priming effect on allergen-induced responses and an intrinsic in- flammatory action in the nasal airways. A mixture of (+~-oc-pinene and ozone yielded reaction products including formaldehyde and induced strong airway irritation in male mice (Wolkoff et al., 1999~. The authors determined that after accounting for sensitiv- ity differences between mice and humans, the measured concen- trations of formaldehyde and ozone in the reaction mixture were "not unrealistic for indoor settings." There are no data suggesting that ozone exposure is associated with the development of asthma. Chapter 10 contains an extended discussion of the impact of ventilation on the indoor concentrations of gaseous pollutants. As noted in that chapter, ozone is also removed from indoor air at a significant rate by deposition on or reaction with indoor sur- faces. Rates of removal depend on the intensity of indoor air mo- tion and other factors. Particulates {Nonbiologic Particles} "Particulate matter" (PM) is the name given to solid and liq- uid particles suspended in the air. Aside from outdoor infiltrate,

INDOOR CHEMICAL EXPOSURES 253 the primary indoor sources of nonbiologic PM in indoor environ- ments are combustion sources and tobacco smoke (which is ad- dressed separately and in greater detail in Chapter 7~. Unvented or poorly vented coal stoves and wood-burning stoves and fire- places where present may be significant sources of indoor PM. For spaces without significant sources, indoors is a protective en- vironment. Studies consistently report an association between exposure to high outdoor levels of air pollutants, including PM, and ad- verse respiratory health effects (Koren, 1995~. Evidence suggests that for fine particles (i.e., those with aerodynamic diameters less than 2.5 rim), outdoor PM often penetrates readily indoors. The literature specifically addressing asthma suggests an association between PM exposure and asthma exacerbation (e.g., Pope and Dockery, 1992; Roemer et al., 1993; Sheppard et al., 1999~. Ostro and colleagues (1998) list three classes of possible mechanisms for this: 1. reflex bronchoconstriction via nonspecific irritant effects; 2. direct toxicity to the airway epithelium and resident im- mune cells, augmenting preexisting inflammation and airway hyperresponsiveness; and 3. induction of an inflammatory immune response, either be- cause the particles themselves are allergenic or by permitting ac- cess of other allergens to the underlying tissues. Aside from studies of the health effects of environmental to- bacco smoke, where PM is part of a more complex exposure, data have not shown an association between PM and asthma develop- ment. Ongoing research is addressing this topic, including stud- ies using animal models. Limiting or eliminating sources is clearly the most straight- forward means of addressing indoor PM exposures. Chapter 10 includes a discussion of the use of high-efficiency particulate air (HEPA) filters in lowering concentrations of indoor particulates. Sulfur Dioxide Sulfur dioxide (SO2) is one of a family of gases called sulfur

254 CLEARING THE AIR oxides (SOx) formed when fuel containing sulfur primarily coal and of] is burned. Outdoor levels of SO2 have diminished sig- nificantly since the 1960s in the United States due to the elimina- tion of high-sulfur coal and of! as primary fuels for power genera- tion and heating. Indoor sources include fossil fuel appliances and furnaces. However, these are not significant in most indoor envi- ronments, where outdoor infiltrate is the primary source. Sensitive asthmatics breathing at elevated ventilation rates (during exercise, for example) experience bronchoconstriction and other airway responses in reaction to brief exposure to SO2. These effects, which are relatively transitory, exhibit a dose-re- sponse relationship. Sulfur dioxide may both have a direct irri- tant effect and, possibly in combination with other air pollutants, potentiate the effect of antigens (Bielory and Deener, 1998~. Expo- sure to a combination of SO2 and NO2 in concentrations that could be encountered in heavy-traffic areas produced a statistically sig- nificant decrease in the concentration of dust mite allergen re- quired to produce a 20% decrease in FEVER of adult asthmatics (Devalia et al., 1994~. There is no established mechanism for the effects of SO2 on airways, although candidate mechanisms have been proposed (Peden, 1997~. The committee did not identify any studies addressing indoor exposures to SO2 and asthma develop- ment. The exposure mitigation and prevention strategies discussed above for indoor sources of NO2 are also relevant for SO2. REFERENCES Anderson RC, Anderson JH. 1998. Acute toxic effects of fragrance products. Archives of Environmental Health 53~2~:138-146. Anderson RC, Anderson JH. 1999. Respiratory toxicity in mice exposed to mattress covers. Archives of Environmental Health 54~3~:202-209. Ashford NA, Ryan CW, Caldart CC. 1983. Law and science policy in federal regulation of formaldehyde. Science 222~4626~:894-900. ATS (American Thoracic Society).1998. Respiratory health hazards in agriculture. Official Conference Report. American Journal of Respiratory and Critical Care Medicine 158~5 Pt 2~:S1-S76. Baker SR and Wilkinson CF Eds.1990. The Effects of Pesticides on Human Health. Princeton, NJ: Princeton Scientific Publishing Co. Bielory L, Deener A. 1998. Seasonal variation in the effects of major indoor and outdoor environmental variables on asthma. Journal of Asthma 35~1~:7-48.

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Since about 1980, asthma prevalence and asthma-related hospitalizations and deaths have increased substantially, especially among children. Of particular concern is the high mortality rate among African Americans with asthma.

Recent studies have suggested that indoor exposures--to dust mites, cockroaches, mold, pet dander, tobacco smoke, and other biological and chemical pollutants--may influence the disease course of asthma. To ensure an appropriate response, public health and education officials have sought a science-based assessment of asthma and its relationship to indoor air exposures.

Clearing the Air meets this need. This book examines how indoor pollutants contribute to asthma-- its causation, prevalence, triggering, and severity. The committee discusses asthma among the general population and in sensitive subpopulations including children, low-income individuals, and urban residents. Based on the most current findings, the book also evaluates the scientific basis for mitigating the effects of indoor air pollutants implicated in asthma. The committee identifies priorities for public health policy, public education outreach, preventive intervention, and further research.

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