The NSLAH was the first study to examine the role of residential mouse allergen exposures in relation to asthma in nationally representative sample of U.S. households. We found that elevated levels of mouse allergen significantly increased the likelihood of having asthma-related symptoms among atopic individuals. In contrast, we found no association in nonatopic individuals. The association remained consistent after adjusting for potential confounders. Therefore, our findings suggest that mouse allergen exposure in the home is an important risk factor for allergic asthma and contributes independently to asthma morbidity among allergic individuals.
In allergic asthma, allergens play a key role in triggering and exacerbating asthma symptoms (Langley et al. 2003
; Nelson 2000
). Because people spend most of their time indoors, especially at home, allergen exposures in the home environment are of great importance in relation to asthma (Leech et al. 2002
). Although mouse allergen is a well-recognized and widely studied allergen in occupational settings (Bush and Stave 2003
; Phipatanakul 2002
), it has only recently identified as a household allergen that may influence asthma morbidity in domestic settings. To date, most research has focused on inner-city homes in which mouse allergen has been found to be ubiquitous (Chew et al. 2003
; Matsui et al. 2005
; Phipatanakul et al. 2000a
). The results from the NSLAH, however, suggest that the presence of mouse allergen in U.S. homes is surprisingly common even outside inner-city environments. Although exposure levels tend to be higher in low-income, urban neighborhoods (Matsui et al. 2004
; Simons et al. 2007
), our findings demonstrate that elevated levels are not restricted to those environments. However, restricting the analysis to low-income, urban homes in the NSLAH, the prevalence and distributions of mouse allergen compared well with previous findings from inner-city populations. For example, in the NCICAS and NSLAH, 95% of low-income urban homes had detectable mouse allergen levels in at least one room. Detectable levels of mouse allergen in kitchens were also comparable (83% in the NSLAH; 87% in the NCICAS). However, the prevalence of elevated mouse allergen levels (> 1.6 μg/g) in kitchens was higher in the NCICAS than in the NSLAH (50% in the NCICAS; 33% in the NSLAH) (Cohn et al. 2004
; Phipatanakul et al. 2000a
). On the other hand, some studies in low-income urban populations have observed lower mouse allergen levels than those found in the NCICAS (Chew et al. 2006
In the NSLAH, elevated mouse allergen levels were associated with asthma-related outcomes. After adjusting for potential confounders, including the presence of other indoor allergens, endotoxin, or dust weight, elevated levels of mouse allergen (> 1.6 μg/g) in the home increased the odds of having asthma symptoms in the past year approximately 2-fold. However, the observed association was modified by atopic status; we found the association in atopic but not in nonatopic individuals. Because elevated mouse allergen levels have been associated with several other environmental exposures, particularly exposures that relate to poor housing conditions (Simons et al. 2007
), we cannot exclude the possibility that additional factors may have contributed to current asthma symptoms. Indeed, we have previously shown that Alternaria
and endotoxin exposures contribute to asthma morbidity in this population (Salo et al. 2006
; Thorne et al. 2005
). However, our results suggest an independent association between asthma symptoms and mouse allergen levels because the observed association did not change appreciably after adjusting for potential confounders.
Although degree of atopy has been associated with mouse sensitivity and elevated mouse allergen levels among asthmatic inner-city children (Phipatanakul et al. 2000b
), atopy per se was not associated with mouse allergen levels in the NSLAH. This may reflect differences in population characteristics: The NCICAS included only asthmatic children, whereas the NSLAH sample represented the general population. Studies have shown that the prevalence and degree of atopy tend to be higher among asthmatic inner-city children than among the general U.S. population (Arbes et al. 2005
; Crain et al. 2002
; Eggleston et al. 1998
; Stevenson et al. 2001
). Because we were not able to ascertain the specificity or degree of atopy in the NSLAH, atopy reflects subjects’ allergic status in general, not specific sensitization to mouse allergen. Although atopy is often confirmed by clinical measures (serum IgE, skin prick tests), the diagnosis of clinically relevant allergy also depends on symptom history. The presence of allergen-specific antibodies or a positive skin test response to a specific allergen does not necessarily mean that a patient has clinically significant symptoms when exposed to an allergen (Pastorello et al. 1995
). However, questionnaire-based data may underestimate the prevalence of atopy because questionnaires are unlikely sensitive enough to detect all individuals who are atopic (Lakwijk et al. 1998
). We acknowledge that the lack of objective information on study subjects’ atopic status is a limitation, but findings from the NCICAS suggest that mouse allergen concentrations > 1.6 μg/g are associated with increased risk for IgE-mediated mouse sensitization.
Because the literature-derived cutoff point that we used to dichotomize the exposure variable is somewhat arbitrary, we further characterized the relationship between current asthma and mouse allergen levels by conducting additional statistical analyses, including modeling the exposure as continuous variable and using complementary modeling techniques. Our modeling results remained rather consistent regardless of the methods used. Most of the site-specific analyses supported the concept that the prevalence of current asthma increased with increasing mouse allergen concentrations, but the trend was less clear for bedroom bed and living room upholstery dusts. Although a recent study has suggested that the shape of the dose–response relationship between mouse allergen levels and allergen-specific sensitization may not be linear, particularly at higher mouse allergen levels (Matsui et al. 2007
), it is unlikely that the nonlinear shape of the smooth curves is associated with this phenomenon. In fact, mouse allergen levels in bedroom bed and living room upholstery dusts were lower than in the other sites. Furthermore, these two sites had more missing observations than did floor dust samples, which may have influenced the modeling accuracy.
Wheezing was not significantly associated with elevated mouse allergen levels in the total study population. Although wheezing is a common symptom of asthma, a variety of respiratory disorders that lead to airway narrowing or obstruction can be associated with wheezing (Gong 1990
). Because most of those who reported recent wheezing did not report asthma symptoms, we hypothesized that diseases other than asthma (e.g., COPD) might have contributed to wheezing. However, COPD is a slowly progressive disease and rarely occurs in individuals < 40 years of age (Halbert et al. 2003
; Stang et al. 2000
). When we restricted our analysis to a younger subpopulation (< 40 years of age), wheezing was strongly associated with elevated mouse allergen levels among atopic individuals. Consistent with reported asthma symptoms, we saw the strongest effects with elevated MUP levels in bedroom floor and living room dusts. We recognize that the wheezing-related results should be interpreted with some caution because we were not able to ascertain and differentiate whether wheezing resulted from asthma, COPD, or other respiratory disorders.
We acknowledge that our study has limitations. Because of the cross-sectional nature of the study, temporal relationships may be difficult to determine. Therefore, we focused mainly on asthma-related outcomes in the recent past. We lacked detailed sensitization data (e.g., skin prick test, specific IgE) but assessed atopy on self-reported physician-diagnosed allergies. Although airborne allergen concentrations are considered more relevant measures of personal exposure, large-scale epidemiologic studies traditionally use measurement of allergen concentration in reservoir dust as a surrogate measure of exposure, largely because of practical and financial reasons. In this study, we assessed mouse allergen levels in dust across multiple household sites, in order to characterize the exposure in detail. The NSLAH conducted sampling in each geographic region throughout seasons to mitigate any possible seasonal bias. Although the cutoff point that we used to dichotomize the exposure for modeling is somewhat arbitrary, findings from the NCICAS study have shown that mouse allergen concentrations above this threshold have been associated with an increased risk for IgE-mediated mouse sensitization (Phipatanakul et al. 2000b
). Moreover, Matsui et al. (2005)
have demonstrated that even with lower allergen concentrations in dust, mouse allergen is detectable in the vast majority of air samples; in their study, 90% of the participants with > 0.5 μg/g of mouse allergen in settled dust samples had detectable levels of airborne mouse allergen in their home.
The major strength of the study is its national representativeness. Vojta et al. (2002)
showed that the demographic characteristics of the weighted survey sample did not differ appreciably from characteristics of other national surveys, including the 1995 and 1997 American Housing Survey and the 1998 and 1999 Current Population Survey. Furthermore, asthma prevalence rates compared well with other national estimates (Centers for Disease Control and Prevention 2006
). The NSLAH was the first study to evaluate the importance of residential mouse allergen exposures among the general U.S. population.
In summary, this study suggests that mouse allergen is an important household allergen in U.S. homes. We found that higher mouse allergen levels significantly increased the likelihood of having atopic wheeze and/or asthma symptoms among allergic individuals. Our study extends prior research findings from inner-city populations to the general population. Further research, however, is required to develop and evaluate environmental control measures that cost-effectively reduce and sustain low mouse allergen levels in problem homes. To date, very little information on interventions targeting reductions in residential mouse allergen levels is available (Phipatanakul et al. 2004
). We encourage future studies to determine clinically relevant exposure levels for mouse allergen and to provide information on clinical benefits of effective interventions.