Childhood asthma and indoor allergens in Native Americans in New York
© Surdu et al; licensee BioMed Central Ltd. 2006
Received: 17 February 2006
Accepted: 21 July 2006
Published: 21 July 2006
The objective of this study was to assess the correlation between childhood asthma and potential risk factors, especially exposure to indoor allergens, in a Native American population.
A case-control study of St. Regis Mohawk tribe children ages 2–14 years, 25 diagnosed with asthma and 25 controls was conducted. Exposure was assessed based on a personal interview and measurement of mite and cat allergens (Der p 1, Fel d 1) in indoor dust.
A non-significant increased risk of childhood asthma was associated with self-reported family history of asthma, childhood environmental tobacco smoke exposure, and air pollution. There was a significant protective effect of breastfeeding against current asthma in children less than 14 years (5.2 fold lower risk). About 80% of dust mite and 15% of cat allergen samples were above the threshold values for sensitization of 2 and 1 μg/g, respectively. The association between current asthma and exposure to dust mite and cat allergens was positive but not statistically significant.
This research identified several potential indoor and outdoor risk factors for asthma in Mohawks homes, of which avoidance may reduce or delay the development of asthma in susceptible individuals.
Asthma is one of the most common chronic illnesses in the general population and is the most common chronic illness in children, with about 7.5 million children under age 18 in the United States having asthma in 2001 . Asthma prevalence has been increasing to epidemic levels, especially in areas with high urbanization. Over 300 million people worldwide are affected by asthma, with a high negative impact on quality of life, productivity and health care costs . Children aged 0 to 4 years show the largest increase in prevalence and incur greater health care use, while adolescents have the highest mortality. Peak asthma prevalence was 7.5% of the population in 1995. Lower socioeconomic status has been found to be related to increased rates of asthma morbidity and mortality, with asthma rates being consistently reported to be very high in minority populations and in people living in poverty [3, 4]. This difference is reflected in the number of emergency room visits, hospitalizations and death, and is thought to reflect differences in risk factors of exposure and asthma control with socioeconomic status.
The risks for developing asthma are still uncertain, but depend on a complex interaction of hereditary and environmental factors. Risk factors that have been identified include: genetic predisposition (family history of atopy or asthma); perinatal factors (low birth weight, prematurity); allergen exposures (sensitization and exposure to cockroaches, house dust mites, rodents, furry animals and molds); infections (respiratory infections, especially those caused by respiratory syncytial virus); environmental air pollution; tobacco smoke; diet and obesity [5–13].
Some kinds of early life exposures, such as having older siblings, attending daycare, exposure to animals and being breastfed, have been reported to be protective, perhaps secondary to microbial factors and immunity [14–16]. People who have a diet rich in fruits and vegetables have a lower risk of respiratory disease, perhaps due to the antioxidant nutrients these foods contain [17, 18].
House dust mites constitute an important indoor allergen (Der p 1). Exposure to dust mite allergens is a known risk factor for sensitization and is a trigger for asthma attacks . Dust mites are ubiquitous in most humid and warm areas. Although 13 species of house dust mites have been identified, only three are common in homes: Dermatophagoides farinae, Dermatophagoides pteronyssinus, and Euroglyphus maynei. Most mite infestations in the United States are caused by D farinae or D pteronyssinus . Dust mite exposure can trigger asthma exacerbations as well as contribute to the development of asthma . The suggested threshold for sensitization to Der p1 is 2 μg/g house dust, with the threshold for exacerbation of symptoms being 10 μg/g .
Cats are currently the most popular pet present in the United States homes, with over 25% of all households having cats. The major cat allergen is Fel d 1, which causes IgE responses in >90% of people allergic to cats. Early exposure to pet dander may either be protective or result in sensitivity . There is evidence that the effect of exposure to pets may be different in different relative risk groups, based on parental allergy. Cat allergen is present as small particles that can aerosolize and persist in the environment for months .
Reducing exposure to indoor allergens, especially in genetically susceptible children, can reduce the development of allergic sensitization to house dust mites and cat allergens, and this may prevent childhood asthma and decrease the frequency and severity of asthma attacks [23, 24].
The main objectives of this study were to evaluate the sources of indoor air pollution in the Mohawk community that may contribute to asthma in households at Akwesasne, to measure the levels of exposure to house dust mites and cat allergens, and to assess the correlation between potential risk factors and the childhood asthma.
A case-control study was done on a population of 50 Mohawk children aged 2–14 years with and without asthma. The number of subjects was limited by the available funds allocated for this Pilot Study by the granting agency (EPA Region II). Sample analyses were completed as in-kind contribution by one of the authors (Dr. Montoya) so as to minimize lab expenses and maximize field expenditures. Of particular significance was the need to employ members of the Akwesasne community to conduct the field work, which constituted a large portion of the budget. Using the medical records at the St. Regis Mohawk Health Service, children 14 years of age and younger who were diagnosed with asthma were identified. Starting with those 14 years of age they were approached to participate in the study until a total of 25 asthmatic children had been recruited. Control subjects were also identified through the medical records of the St. Regis Mohawk Health Service based on lack of respiratory disease, and were selected by matching year of age and gender to the cases. Only one child per household was eligible to participate in the study, the oldest child being selected first. Informed consent was obtained from all participating children's parent or guardian. This study was approved by the University at Albany's Internal Review Board (human subjects assurance number FWA00001970, our protocol #99267).
The exposure information was collected through a personal interview and dust and air samples in the 50 Akwesasne households. The personal interview was conducted by a trained Mohawk interviewer and was given to both the child and a parent or caregiver. The questionnaire included information relevant to asthma risk factors, including: socioeconomic status (age, gender, marital status, educational level, employment status), family history of asthma, environmental tobacco smoke, the use of indoor combustion devices, the presence of biological contaminants, usage of pesticides, the presence of formaldehyde sources, pollution control methods, number of hours spent outdoors, smoking during pregnancy, birth weight and premature birth, breast-feeding history, and day-care attendance during the first two years of life. The last section of the interview asked about respiratory symptoms or signs known to be associated with indoor air pollution.
At the same home visit where the interview was obtained, dust and air sampling was performed. In each house two dust samples were collected, one from the living room (floor, rugs) and the other from the bedroom (floor, carpets, mattress, bedding), using a domestic vacuum equipped with a dust trap (The Boss Mighty Mite, Eureka, model 3670A, Bloomington, IN, USA). The air samples were collected using a filter cassette connected to a personal sampler (pump) running at 4.0 liters per minute. Since background concentration of airborne allergens are generally very low and they are usually detectable only during disturbances which cause the release of settled allergens, the filter was placed on the investigator collecting the dust sample at his/her breathing level while the dust sampling was performed. For allergen quantification of the mite and cat allergens indoor level (Der p 1, Fel d 1) in the dust and air samples, a two-site monoclonal enzyme-linked immunosorbent assay (ELISA) was used.
Data analyses were performed using SAS and Microsoft Excel. Sample data collected were assumed to be from a normally distributed population. As such, the means of the sample data were compared by Student's t-test. Allergen concentration data was transformed to a logarithmic scale with the assumption of normal distribution. The results were reported as geometric means and 90% Confidence Intervals for the means. Between group comparisons were conducted using log-transformed data. Proportions were compared by the Mantel-Haenszel Chi-Square test. Statistical significance was accepted at the 5% level.
Characteristics of the study population.
Prevalence and risks associated with asthma status for selected hereditary and environmental factors in the Mohawk population.
Asthma cases with factor
Family history of asthma
Smoking in the home in the last 12 months
Smoking in the home during the child's lifetime
Garage attached to the home
Burn-barrel within 5-minute walk from the home
Pet(s) in the house
Moist walls, ceilings, carpets, furniture
Mold in the house
Cockroaches, ants, other insects in the house
Smoking during pregnancy
Born before due date
Breast feed infant
Attended day-care during the first two years of life
Concentration of major mite and cat allergens in living room and bedroom dust samples collected from Akwesasne households.
No. samples analyzed
No. samples with detectable levels
Allergen concentration (μg/g dust)
Cat allergen (Fel d 1)
Mite allergen (Der p1)
Concentration of major mite and cat allergens in dust samples collected from Akwesasne households by site and case/control group.
Living room samples concentration (μg/g dust)
Bedroom samples concentration (μg/g dust)
No. of samples
No. of samples
Cat allergen (Fel d 1)
Mite allergen (Der p 1)
Dust mite and cat allergen levels were not found to be statistically different in the group of subjects with asthma as compared to the subjects without asthma, neither in the living room dust samples nor in the bedroom dust samples.
Prevalence of house dust mite and cat allergen exposure by current asthma status in the Mohawk study population.
Population Attributable Risk (PAR)
Fel d 1
≥ 8 μg/g dust
≥ 1 μg/g dust
Der p 1
≥ 10 μg/g dust
≥ 2 μg/g dust
The results of the present study are consistent with the evidence that premature children are at an increased risk of asthma, the risk being increased two-fold for the subjects born prematurely [5, 6]. Previous studies have suggested that the development of protective immune responses to microbes early in life may reduce the likelihood of the development of allergies, and as a result the development of asthma , which would be in accordance to our findings related to daycare attendance as protective factors for current asthma.
Different studies indicate that asthma morbidity among Native Americans/Alaskan Natives is very common and may be higher than other racial/ethnic groups [25, 29–34]. According to the 2001 California Health Interview Survey , Native Americans were more likely to have been diagnosed with asthma than any other racial/ethnic group. Approximately 25.5% of Native American children and 20% of Native American adults have been diagnosed with asthma in their lifetime, compared to 21% of African American children and 16% of African American adults, 14% Caucasian children and adults, 11.7% Asian children and 9.2% Asian adults, and 10% of Hispanic children and 7% of Hispanic adults.
According to the New York State Department of Health , the three year average (2000–2002) asthma discharge from hospitalization rates per 10,000 population for children under 14 years of age living in the Akwesasne area was 21.4, which is much higher than in the adjacent Franklin County rate of 13.3 and higher than the New York State rate (excluding NYC) of 18.1. The U.S. Census 2000 Demographic Profile showed that the total population in the New York portion of Akwesasne was 2,558 inhabitants, of which 96.5% are Native American. The population age distribution indicated that 762 inhabitants were between 0–14 years old. This indicates the difficulties of performing this type of study on such a small population.
The major limitation of our report is the size of the population studied. Because the population available for investigation was small, few of the results were statistically significant, although most of the results were in the direction expected from previous studies. We found an increased risk of current asthma in children associated with a self-reported family history of asthma, current and lifetime childhood environmental tobacco smoke (ETS) exposure, and air pollution (garage attached to the house, a burn-barrel within 5-min walk from the house), but none of these results were statistically significant. This problem is difficult to avoid when one studies a small population. Since attention to quantitative estimates of house allergen exposure in relation with asthma in children has received relatively little attention, we believe our results to be useful in spite of this problem. This is particularly true for Native American children in rural communities.
The Institute of Medicine  concluded that there is sufficient evidence to associate environmental tobacco smoke exposure with the development and exacerbation of asthma. Maternal smoking during pregnancy increased the occurrence of physician-diagnosed asthma during childhood in our study population, a finding which is consistent with the literature suggesting that the exposure to tobacco compromises the development of the fetal lungs and as a result, an increased risk of developing asthma [9, 37].
Perinatal factors, including gestational age and birth weight, influence the development of atopy in early life, increase the risk of developing lower respiratory tract infections, and play a possible role in the development of asthma in later life [5, 6]. Human milk contains numerous components protecting the infant against infections, including factors that provide specific immunity, nonspecific protective factors that inhibit the binding of bacterial pathogens and their toxins, and lipids that may disrupt enveloped viruses . Breast milk contains cytokines and growth factors that may play an important role in modulating the development of asthma by preventing sensitization to environmental allergens, enhancing infant lung development and reducing susceptibility to respiratory infections [38, 39]. The role of breastfeeding as a protective factor against asthma and atopic diseases, however, continues to be controversial, with some studies showing a negative effect of breastfeeding [40, 41], and others showing a protective association [16, 42, 43]. There are, however, differences among various studies in relation to breastfeeding definition, study populations and age of the child when the association is assessed. Immunoprotection conferred by human milk may vary in relation with the mother's atopic constitution, infections, immune status, and diet. Our results support a strong protective effect of breastfeeding against current asthma in children under 14 years of age.
The levels of dust allergens measured in the Akwesasne households ranged from non-detectable to values exceeding the sensitizing or asthma symptoms triggering threshold concentrations. The threshold values for allergen exposure most widely accepted are as follows: 2 μg or more of Group 1 mite allergens per gram of dust (Der p 1, Der f 1) as a risk factor for development of IgE antibody and asthma, and a higher level of 10 μg Group 1 mite allergens per gram of dust as a risk factor for an acute attack of asthma; 1 μg or more of cat allergen (Fel d 1) per gram of dust as a risk factor for sensitization to cats, and a higher level of 8 μg cat allergen per gram of dust as a risk factor for asthma symptoms in most cat allergic patients [21, 28].
Dust mite allergen levels reported by other studies conducted around the world are characterized by high variability, dependent mostly upon humidity levels, from less than 2 μg/g of dust in very cold or dry climates (e.g., Stockholm, Arizona) to mean levels in the range of 2–15 μg/g in countries with climates more suited to mite reproduction (costal areas of Europe and USA). In some regions of Australia, Singapore and South America where the climate is suited for mite growth throughout most of the year, the mean allergen levels range between 10–40 μg/g . The dust mite allergen levels found in the Akwesasne area ranged between 0.05–11.15 μg/g, and approximately 80% of the households had levels less than 2 μg/g. The Akwesasne Reservation is situated on the 45th parallel of latitude with fairly moderate climate that puts our results in line with the findings published in the literature.
Pets are one of the most common indoor allergens along with dust mites, cockroaches and molds. In many countries, over 50% of homes have cats and/or dogs . In our study population, 48% of the Mohawk households had pets in the house, and 22% of the study subjects reported having one or more cats in the home. The mean value of cat allergen measured in dust samples ranged between 0.02–12.64 μg/g, and about 18% of the households had levels over 1 μg/g that is the suggested threshold for sensitization. The cat allergen results showed a higher mean value in the dust samples collected from the living room as compared to the bedroom, which is in concordance with the results of other studies of cat allergen distribution, possibly due to the fact that pets are not allowed in bedrooms.
It is difficult to compare the dust mite and cat allergen levels between studies due to different study populations and dust sampling settings and methods (e.g., vacuum cleaner used, filter size, time and area sampling). Furthermore, the dust mite and cat allergen concentrations vary greatly by indoor humidity and consequently by climate, season, building floor, ventilation rates, dampness, floor type, occupant density, and many other factors indirectly associated with humidity.
The dust mite mean levels in our study were higher in the samples collected from households of children with current asthma, and this was also true for the cat allergen measured in bedroom samples. The mite allergen mean value was about two times higher in asthmatic children than controls, but the difference was not statistically significant due to the small baseline sample size. There was a slight increase in the risk of asthma in children living in homes with cat allergen concentrations over the sensitizing value of 1 μg/g (OR = 1.06; PAR = 1.8%) and a three-fold increase in risk of asthma for children exposed to 8 μg/g or more (OR = 3.45; PAR = 9.3%). Thirteen percent of children with current asthma had cat allergen exposure over 8 μg/g as compared to only 4.2% of non-asthmatic children.
The results reported by other case-control studies showed either a small positive or negative association between allergen exposure and current asthma in children. A case-control study conducted on 126 children, 1–15 years of age, found a small positive association of Fel d 1 over 8 μg/g and current asthma (OR = 1.4; PAR = 13%) , similar to those showed by another study conducted on 97 children, 12–14 years of age, for exposure over 10 μg/g (OR = 1.4, 1.6; PAR = 17%, 21%) [46, 47]. Another case-control study conducted on 57 children, 3–15 years of age, found a negative association between cat allergen exposure over 10 μg/g and current asthma , as well as in the previously mentioned study on children 12–14 years of age exposed to levels over 2 μg/g. The risk of current asthma in relation to dust mite allergen exposure could not be calculated due to the fact that all control subjects were free of sensitizing or triggering exposure. All of these studies, including ours, are limited by the fact that the number of analyzed samples was small.
Asthma has been considered rare among Native Americans, but in the last 20 years asthma prevalence is increasing, especially in children. Mohawk children are at risk of exposure to a number of perinatal and environmental factors which may be causally related to the increasing rates of asthma in this population. While most results did not show statistically significant differences due to the unavoidably small sample size, Mohawk households of children with current asthma had higher mean values of cat allergen (Fel d 1) and dust mite allergen (Der p 1) as compared to homes of children without the disease. The risk of current asthma was increased 3.5 fold for children exposed to cat allergen in dust above the triggering threshold level. All of the children without asthma had dust mite allergen concentrations under the sensitizing threshold, while over two-thirds of children with current asthma were above this concentration. Breast feeding was found to be a significant protective factor against asthma. These observations indicate that asthma is not only a problem for inner city minority populations, but also is an important public health issue in rural Native American communities. Further study of indoor and outdoor risk factors which trigger asthma attacks and study of means to reduce or delay the development of asthma in susceptible individuals in this population are needed.
Supported by the Radiation and Indoor Air Branch of the US Environmental Protection Agency, Region 2, grant #X992926-01-0 to LM, and the Fogarty International Center, National Institutes of Health, grant # TW00636 to DOC. We thank the St. Regis Mohawk Health Service and the Akwesasne Mohawk community for their cooperation and participation in this research.
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