To examine the association of social and environmental factors with levels of second hand smoke (SHS) exposure, as measured by salivary cotinine, in young inner city children with asthma.
We used data drawn from a home-based behavioral intervention for young high risk children with persistent asthma post emergency department (ED) treatment (N=198). SHS exposure was measured by salivary cotinine and caregiver report. Caregiver demographic and psychological functioning, household smoking behavior and asthma morbidity were compared with child cotinine concentrations. Chi-square and ANOVA tests and multivariate regression models were used to determine the association between cotinine concentrations with household smoking behavior and asthma morbidity.
Over half (53%) of the children had cotinine levels compatible with SHS exposure and mean cotinine concentrations were high at 2.42 ng/ml (SD 3.2). The caregiver was the predominant smoker in the home (57%) and (63%) reported a total home smoking ban. Preschool age children, and those with caregivers reporting depressive symptoms and high stress had higher cotinine concentrations than their counterparts. Among children living in a home with a total home smoking ban, younger children had significantly higher mean cotinine concentration than older children (Cotinine: 3–5 year olds, 2.24 ng/ml (SD 3.5); 6–10 year olds, 0.63 ng/ml (SD 1.0); p <0.05). In multivariate models, the factors most strongly associated with high child cotinine concentrations were increased number of household smokers (β = 0.24) and younger child age (3–5 years) (β = 0.23; P <0.001, R2 = 0.35).
Over half of young inner-city children with asthma were exposed to second hand smoke and caregivers are the predominant household smoker. Younger children and children with depressed and stressed caregivers are at significant risk of smoke exposures, even when a household smoking ban is reported. Further advocacy for these high-risk children is needed to help caregivers quit and to mitigate smoke exposure.
asthma; children; cotinine; second hand smoke
Asthma can be exacerbated by environmental factors including airborne particulate matter (PM) and environmental tobacco smoke (ETS). We report on a study designed to characterize PM levels and the effectiveness of filters on pollutant exposures of children with asthma. 126 households with an asthmatic child in Detroit, Michigan, were recruited and randomized into control or treatment groups. Both groups received asthma education; the latter also received a free-standing high efficiency air filter placed in the child’s bedroom. Information regarding the home, emission sources, and occupant activities was obtained using surveys administered to the child's caregiver and a household inspection. Over a one-week period, we measured PM, carbon dioxide (CO2), environmental tobacco smoke (ETS) tracers, and air exchange rates (AERs). Filters were installed at midweek. Before filter installation, PM concentrations averaged 28 µg m−3, number concentrations averaged 70,777 and 1,471 L−1 in 0.3–1.0 and 1–5 µm size ranges, respectively, and the median CO2 concentration was 1,018 ppm. ETS tracers were detected in 23 of 38 homes where smoking was unrestricted and occupants included smokers and, when detected, PM concentrations were elevated by an average of 15 µg m−3. Filter use reduced PM concentrations by an average of 69 to 80%. Simulation models representing location conditions show that filter air flow, room volume and AERs are the key parameters affecting PM removal, however, filters can achieve substantial removal in even "worst" case applications. While PM levels in homes with asthmatic children can be high, levels can be dramatically reduced using filters.
indoor environment; free-standing HEPA air filters; asthmatic children; particulate matter; exposures
Home dampness and the presence of mold and allergens have been associated with asthma morbidity. We examined changes in asthma morbidity in children as a result of home remediation aimed at moisture sources.
In this prospective, randomized controlled trial, symptomatic, asthmatic children (n = 62), 2–17 years of age, living in a home with indoor mold, received an asthma intervention including an action plan, education, and individualized problem solving. The remediation group also received household repairs, including reduction of water infiltration, removal of water-damaged building materials, and heating/ventilation/air-conditioning alterations. The control group received only home cleaning information. We measured children’s total and allergen-specific serum immuno-globulin E, peripheral blood eosinophil counts, and urinary cotinine. Environmental dust samples were analyzed for dust mite, cockroach, rodent urinary protein, endotoxin, and fungi. The follow-up period was 1 year.
Children in both groups showed improvement in asthma symptomatic days during the preremediation portion of the study. The remediation group had a significant decrease in symptom days (p = 0.003, as randomized; p = 0.004, intent to treat) after remodeling, whereas these parameters in the control group did not significantly change. In the postremediation period, the remediation group had a lower rate of exacerbations compared with control asthmatics (as treated: 1 of 29 vs. 11 of 33, respectively, p = 0. 003; intent to treat: 28.1% and 10.0%, respectively, p = 0.11).
Construction remediation aimed at the root cause of moisture sources and combined with a medical/behavioral intervention significantly reduces symptom days and health care use for asthmatic children who live in homes with a documented mold problem.
asthma; children; damp housing; home remediation; indoor mold
The effect of indoor nitrogen dioxide concentrations on asthma morbidity among inner-city preschool children is uncertain.
Our goal was to estimate the effect of indoor NO2 concentrations on asthma morbidity in an inner-city population while adjusting for other indoor pollutants.
We recruited 150 children (2–6 years of age) with physician-diagnosed asthma from inner-city Baltimore, Maryland. Indoor air was monitored over a 72-hr period in the children’s bedrooms at baseline and 3 and 6 months. At each visit, the child’s caregiver completed a questionnaire assessing asthma symptoms over the previous 2 weeks and recent health care utilization.
Children were 58% male, 91% African American, and 42% from households with annual income < $25,000; 63% had persistent asthma symptoms. The mean (± SD) in-home NO2 concentration was 30.0 ± 33.7 (range, 2.9–394.0) ppb. The presence of a gas stove and the use of a space heater or oven/stove for heat were independently associated with higher NO2 concentrations. Each 20-ppb increase in NO2 exposure was associated significantly with an increase in the number of days with limited speech [incidence rate ratio (IRR) = 1.15; 95% confidence interval (CI), 1.05–1.25], cough (IRR = 1.10; 95% CI, 1.02–1.18), and nocturnal symptoms (IRR = 1.09; 95% CI, 1.02–1.16), after adjustment for potential confounders. NO2 concentrations were not associated with increased health care utilization.
Higher indoor NO2 concentrations were associated with increased asthma symptoms in preschool inner-city children. Interventions aimed at lowering NO2 concentrations in inner-city homes may reduce asthma morbidity in this vulnerable population.
asthma; indoor pollutants; inner city; nitrogen dioxide; preschool
To explore the relationship between environmental tobacco smoke (ETS) exposure and behavior among inner-city children with significant asthma.
We analyzed baseline data for 200 children 4 to 10 years old who were enrolled in an asthma program. Environmental tobacco smoke exposure was measured by the child’s salivary cotinine level. Caregivers completed the 28-item Behavior Problem Index (BPI). Positive responses were summed for a total BPI score, and children with scores >14 were considered to have significant behavior problems. We conducted Student t tests and multivariate regression analyses to determine the association of children’s cotinine levels with BPI scores.
Overall, 56% of children were male, 65% were black, and 72% had Medicaid. Mean cotinine level was 1.47 ng/mL. Overall, 30% of children had total BPI scores >14. Children with cotinine values >1.47 ng/mL had significantly higher scores compared with children with lower cotinine values on total BPI (12.5 vs 10.2), as well as externalizing (9.0 vs 7.2), antisocial (2.3 vs 1.7), and immature (2.1 vs 1.6) subscales. In a multivariate model, log cotinine remained independently associated with externalizing (P = .04), headstrong (P = .04), and antisocial behavior (P = .04).
Cotinine levels are independently associated with problem behaviors among this sample of urban children with asthma.
behavior; childhood asthma; environmental smoke exposure; inner-city
The purpose of this article is to review indoor air pollution factors that can modify asthma severity, particularly in inner-city environments. While there is a large literature linking ambient air pollution and asthma morbidity, less is known about the impact of indoor air pollution on asthma. Concentrating on the indoor environments is particularly important for children, since they can spend as much as 90% of their time indoors. This review focuses on studies conducted by the Johns Hopkins Center for Childhood Asthma in the Urban Environment as well as other relevant epidemiologic studies. Analysis of exposure outcome relationships in the published literature demonstrates the importance of evaluating indoor home environmental air pollution sources as risk factors for asthma morbidity. Important indoor air pollution determinants of asthma morbidity in urban environments include particulate matter (particularly the coarse fraction), nitrogen dioxide, and airborne mouse allergen exposure. Avoidance of harmful environmental exposures is a key component of national and international guideline recommendations for management of asthma. This literature suggests that modifying the indoor environment to reduce particulate matter, NO2, and mouse allergen may be an important asthma management strategy. More research documenting effectiveness of interventions to reduce those exposures and improve asthma outcomes is needed.
particulate matter; air pollution; pediatric; urban; bronchial hyperreactivity
Objectives: To examine (1) whether dust and surfaces in households of smokers are contaminated with environmental tobacco smoke (ETS); (2) whether smoking parents can protect their infants by smoking outside and away from the infant; and (3) whether contaminated dust, surfaces, and air contribute to ETS exposure in infants.
Design: Quasi-experiment comparing three types of households with infants: (1) non-smokers who believe they have protected their children from ETS; (2) smokers who believe they have protected their children from ETS; (3) smokers who expose their children to ETS.
Setting: Homes of smokers and non-smokers.
Participants: Smoking and non-smoking mothers and their infants ⩽ 1 year.
Main outcome measures: ETS contamination as measured by nicotine in household dust, indoor air, and household surfaces. ETS exposure as measured by cotinine levels in infant urine.
Results: ETS contamination and ETS exposure were 5–7 times higher in households of smokers trying to protect their infants by smoking outdoors than in households of non-smokers. ETS contamination and exposure were 3–8 times higher in households of smokers who exposed their infants to ETS by smoking indoors than in households of smokers trying to protect their children by smoking outdoors.
Conclusions: Dust and surfaces in homes of smokers are contaminated with ETS. Infants of smokers are at risk of ETS exposure in their homes through dust, surfaces, and air. Smoking outside the home and away from the infant reduces but does not completely protect a smoker's home from ETS contamination and a smoker's infant from ETS exposure.
Asthma is a common complex disease responsible for considerable morbidity and mortality, particularly in urban minority populations. The Mechanistic Indicators of Childhood Asthma study was designed to pilot an integrative approach in children's health research. The study incorporates exposure metrics, internal dose measures, and clinical indicators to decipher the biological complexity inherent in diseases such as asthma and cardiovascular disease with etiology related to gene-environment interactions.
205 non-asthmatic and asthmatic children, (9-12 years of age) from Detroit, Michigan were recruited. The study includes environmental measures (indoor and outdoor air, vacuum dust), biomarkers of exposure (cotinine, metals, total and allergen specific Immunoglobulin E, polycyclic aromatic hydrocarbons, volatile organic carbon metabolites) and clinical indicators of health outcome (immunological, cardiovascular and respiratory). In addition, blood gene expression and candidate SNP analyses were conducted.
Based on an integrative design, the MICA study provides an opportunity to evaluate complex relationships between environmental factors, physiological biomarkers, genetic susceptibility and health outcomes.
IRB Number 05-EPA-2637: The human subjects' research protocol was reviewed by the Institutional Review Board (IRB) of the University of North Carolina; the IRB of Westat, Inc., the IRB of the Henry Ford Health System; and EPA's Human Subjects' Research Review Official.
Environmental tobacco smoke (ETS) causes increased morbidity among children with asthma, however pediatricians do not consistently screen and counsel families of asthmatic children regarding ETS. An index score based on parent report of exposure could help providers efficiently screen for ETS.
1) To develop an index measure of ETS based on parent self-report of smoking behaviors; 2) To determine whether the index score is associated with children’s present and future cotinine levels.
Data were drawn from a community intervention for inner-city children with persistent asthma (n=226, response rate 72%). Measures of child salivary cotinine and parent self-reported ETS-related behaviors were obtained at baseline and 7–9 months later. To develop the index score, we used a 15-fold cross-validation method on 70% of our data that considered combinations of smoke exposure variables, controlling for demographics. We chose the most parsimonious model that minimized the mean square predictive error. The resulting index score included primary caregiver smoking and home smoking ban status. We validated our model on the remaining 30% of data. ANOVA and multivariate analyses were used to determine the association of the index score with children’s cotinine levels.
54% of asthmatic children lived with ≥1 smoker and 51% of caregivers reported a complete home smoking ban. The children’s mean baseline cotinine was 1.55ng/ml (range 0.0–21.3). Children’s baseline and follow-up cotinine levels increased as scores on the index measure increased. In a linear regression, the index score was significantly and positively associated with children’s cotinine measurements at baseline (p<.001, model R2=.37) and 7–9 months later (p<.001, R2=.38).
An index measure with combined information regarding primary caregiver smoking and household smoking restrictions helps to identify asthmatic children with the greatest exposure to ETS, and can predict children who will have elevated cotinine levels 7–9 months later.
Environmental tobacco smoke; asthma; children; primary care; screening
Study objective: The aim of this study was to compare the two biomarkers of exposure to environmental tobacco smoke (ETS); urine cotinine and hair nicotine, using questionnaires as the standard.
Design: A cross sectional study of children consecutively admitted to hospital for lower respiratory illnesses during the period of the study.
Settings: Three regional hospitals in the larger Wellington area, New Zealand.
Participants: Children aged 3–27 months and admitted to the above hospitals during August 1997 to October 1998. A total of 322 children provided 297 hair samples and 158 urine samples.
Main results: Hair nicotine levels were better able to discriminate the groups of children according to their household's smoking habits at home (no smokers, smoke only outside the home, smoke inside the house) than urine cotinine (Kruskall-Wallis; χ2=142.14, and χ2=49.5, respectively (p<0.0001)). Furthermore, hair nicotine levels were more strongly correlated with number of smokers in the house, and the number of cigarettes smoked by parents and other members of the child's households. Hair nicotine was better related to the questionnaire variables of smoking in a multivariate regression model (r2=0.55) than urine cotinine (r2=0.31).
Conclusions: In this group of young children, hair nicotine was a more precise biomarker of exposure to ETS than urine cotinine levels, using questionnaire reports as the reference. Both biomarkers indicate that smoking outside the house limits ETS exposure of children but does not eliminate it.
Although outdoor particulate matter (PM) has been linked to mortality and asthma morbidity, the impact of indoor PM on asthma has not been well established.
This study was designed to investigate the effect of in-home PM on asthma morbidity.
For a cohort of 150 asthmatic children (2–6 years of age) from Baltimore, Maryland, a technician deployed environmental monitoring equipment in the children’s bedrooms for 3-day intervals at baseline and at 3 and 6 months. Caregivers completed questionnaires and daily diaries during air sampling. Longitudinal data analyses included regression models with generalized estimating equations.
Children were primarily African Americans (91%) from lower socioeconomic backgrounds and spent most of their time in the home. Mean (± SD) indoor PM2.5–10 (PM with aerodynamic diameter 2.5–10 μm) and PM2.5 (aerodynamic diameter < 2.5 μm) concentrations were 17.4 ± 21.0 and 40.3 ± 35.4 μg/m3. In adjusted models, 10-μg/m3 increases in indoor PM2.5–10 and PM2.5 were associated with increased incidences of asthma symptoms: 6% [95% confidence interval (CI), 1 to 12%] and 3% (95% CI, –1 to 7%), respectively; symptoms causing children to slow down: 8% (95% CI, 2 to 14%) and 4% (95% CI, 0 to 9%), respectively; nocturnal symptoms: 8% (95% CI, 1 to 14%) and 6% (95% CI, 1 to 10%), respectively; wheezing that limited speech: 11% (95% CI, 3 to 19%) and 7% (95% CI, 0 to 14%), respectively; and use of rescue medication: 6% (95% CI, 1 to 10%) and 4% (95% CI, 1 to 8%), respectively. Increases of 10 μg/m3 in indoor and ambient PM2.5 were associated with 7% (95% CI, 2 to 11%) and 26% (95% CI, 1 to 52%) increases in exercise-related symptoms, respectively.
Among preschool asthmatic children in Baltimore, increases in in-home PM2.5–10 and PM2.5 were associated with respiratory symptoms and rescue medication use. Increases in in-home and ambient PM2.5 were associated with exercise-related symptoms. Although reducing PM outdoors may decrease asthma morbidity, reducing PM indoors, especially in homes of inner-city children, may lead to improved asthma health.
air pollution; asthma; indoor; particulate matter; pediatric; urban
Childhood asthma is a growing public health concern in low-income urban communities. Indoor exposure to asthma triggers has emerged as an important cause of asthma exacerbations. We describe indoor environmental conditions related to asthma triggers among a low-income urban population in Seattle/King County, Washington, as well as caregiver knowledge and resources related to control of these triggers.
Data are obtained from in-person, structured, closed-end interviews with the caretakers of children aged 4–12 years with persistent asthma living in households with incomes less than 200% of poverty. Additional information is collected during a home inspection. The children and their caregivers are participants in the ongoing Seattle-King County Healthy Homes Project, a randomized controlled trial of an intervention to empower low-income families to reduce exposure to indoor asthma triggers. We report findings on the conditions of the homes prior to this intervention among the first 112 enrolled households.
A smoker was present in 37.5% of homes. Mold was visible in 26.8% of homes, water damage was present in 18.6% of homes, and damp conditions occurred in 64.8% of households, while 39.6% of caregivers were aware that excessive moisture can increase exposures to allergens. Dust-trapping reservoirs were common; 76.8% of children's bedrooms had carpeting. Cockroach infestation in the past 3 months was reported by 23.4% of caregivers, while 57.1% were unaware of the association of roaches and asthma. Only 19.8% of the children had allergy-control mattress covers.
Many low-income urban children with asthma in King County live in indoor environments that place them at substantial risk of ongoing exposure to asthma triggers. Substandard housing and lack of resources often underlie these exposures. Initiatives involving health educators, outreach workers, medical providers, health care insurers, housing agencies, and elected officials are needed to reduce these exposures.
Asthma; Child; Indoor Air Pollution; Indoor Environment; Knowledge/Behaviors; Low-Income Populations
Environmental tobacco smoke (ETS) exposure is associated with poor asthma outcomes in children. However, little is known about natural changes in ETS exposure over time in children with asthma and how these changes may affect health-care utilization. This article documents the relationship between changes in ETS exposure and childhood asthma morbidity among children enrolled in a clinical trial of supervised asthma therapy.
Data for this analysis come from a large randomized clinical trial of supervised asthma therapy in which 290 children with persistent asthma were randomized to receive either usual care or supervised asthma therapy. No smoking cessation counseling or ETS exposure education was provided to caregivers; however, children were given 20 min of asthma education, which incorporated discussion of the avoidance of asthma triggers, including ETS. Asthma morbidity and ETS exposure data were collected from caregivers via telephone interviews at baseline and at the 1-year follow-up.
At baseline, 28% of caregivers reported ETS exposure in the home and 19% reported exposure outside of the primary household only. Among children whose ETS exposure decreased from baseline, fewer hospitalizations (p = 0.034) and emergency department (ED) visits (p ≤ 0.001) were reported in the 12 months prior to the second interview compared to the 12 months prior to the first interview. Additionally, these children were 48% less likely (p = 0.042) to experience an episode of poor asthma control (EPAC).
This is the first study to demonstrate an association between ETS exposure reduction and fewer EPACs, respiratory-related ED visits, and hospitalizations. These findings emphasize the importance of ETS exposure reduction as a mechanism to improve asthma control and morbidity. Potential policy implications include supporting ETS reductions and smoking cessation interventions for parents and caregivers of children with asthma. Research to identify the most cost-effective strategy is warranted.
Clinicaltrials.gov Identifier: NCT00110383
asthma; children; environmental tobacco smoke; tobacco smoke pollution
smoking is a major cause of respiratory morbidity in children. However,
few studies give accurate estimates of the health effects of passive
smoking in children with asthma using an objective measure of exposure.
The effects of passive smoking using salivary cotinine levels to
measure exposure were investigated.
METHODS—A sample of
438 children aged 2-12 years with asthma who had a parent who smoked
were recruited in Tayside and Fife, Scotland. Health service contacts
for asthma, assessed from GP case records, were used as a proxy for morbidity.
U-shaped relationship was found between the salivary cotinine level and
health service contacts for asthma: compared with low cotinine levels
those with moderate cotinine levels had a reduced contact rate
(relative rate (RR) = 0.91, 95% confidence interval (CI) 0.80 to
1.05), whereas high cotinine levels were associated with an increased
rate of contact (RR = 1.19, 95% CI 1.05 to 1.37). In contrast, a
strong association was seen with the amount the parent reported smoking
in front of the child: the higher the level the fewer visits were made
for asthma (RR for everyday exposure = 0.66, 95% CI 0.56 to 0.77).
This effect was not seen for non-respiratory visits. Demographic
factors, age of child, and number of children in the family all had a
powerful effect on the number of visits for asthma. The parents'
perception of asthma severity was associated with visit frequency
independent of actual severity (derived from drug treatment).
of parental smoking in the home are associated with a reduction in
health care contacts for asthma. This could be due to a lack of
awareness of asthma symptoms among heavy smokers or a reluctance to
visit the GP. Children with asthma who have parents who smoke heavily
may not be receiving adequate management.
To identify factors associated with motivation to quit smoking among parents of urban children with asthma.
We analyzed data from parents who smoke and had a child enrolled in the School-Based Asthma Therapy trial. We assessed asthma symptoms, children's cotinine, and parent smoking behaviors. Motivation to quit smoking was assessed by a 10-point continuous measure (1=not at all motivated; 10=very motivated).
209 parents smoked (39% of sample), and children's mean cotinine was 2.48 ng/ml. Motivation to quit was on average 6.9, and 47% of parents scored ≥8 on the scale. Parents who believed their child's asthma was not under good control, and parents who strongly agreed their child's asthma symptoms would decrease if they stopped smoking had higher motivation to quit compared to their counterparts (p <.05). In a multivariate analysis, parents who believed their child's asthma was not under control had more than twice the odds of reporting high motivation to quit.
Parents' perception of the risks of smoking to their child with asthma is associated with motivation to quit.
Raising awareness about the effect of smoking and quitting on children's asthma might increase motivation to quit among parents.
Asthma; parents; children; smoking cessation; motivation; environmental tobacco smoke
Evidence for environmental causes of asthma is limited, especially among African Americans. To look for systematic differences in early life domestic exposures between inner-city preschool children with and without asthma, we performed a study of home indoor air pollutants and allergens.
Children 2–6 years of age were enrolled in a cohort study in East Baltimore, Maryland. From the child’s bedroom, air was monitored for 3 days for particulate matter ≤ 2.5 and ≤ 10 μm in aerodynamic diameter (PM2.5, PM10), nitrogen dioxide, and ozone. Median baseline values were compared for children with (n = 150) and without (n = 150) asthma. Housing characteristics related to indoor air pollution were assessed by caregiver report and home inspection. In addition, indoor allergen levels were measured in settled dust.
Children were 58% male, 91% African American, and 88% with public health insurance. Housing characteristics related to pollutant exposure and bedroom air pollutant concentrations did not differ significantly between asthmatic and control subjects [median: PM2.5, 28.7 vs. 28.5 μg/m3; PM10, 43.6 vs. 41.4 μg/m3; NO2, 21.6 vs. 20.9 ppb; O3, 1.4 vs. 1.8 ppb; all p > 0.05]. Settled dust allergen levels (cat, dust mite, cockroach, dog, and mouse) were also similar in bedrooms of asthmatic and control children.
Exposures to common home indoor pollutants and allergens are similar for inner-city preschool children with and without asthma. Although these exposures may exacerbate existing asthma, this study does not support a causative role of these factors for risk of developing childhood asthma.
African American; air pollution; allergens; asthma; particulate matter; pediatric; urban
Community Action Against Asthma (CAAA) is a community-based participatory research (CBPR) project that assesses the effects of outdoor and indoor air quality on exacerbation of asthma in children, and tests household- and neighborhood-level interventions to reduce exposure to environmental asthma triggers. Representatives of community-based organizations, academia, an integrated health system, and the local health department work in partnership on CAAA's Steering Committee (SC) to design and implement the project.
To conduct a process evaluation of the CAAA community–academic partnership.
In-depth interviews containing open-ended questions were conducted with SC members. Analysis included established methods for qualitative data, including focused coding and constant comparison methods.
Community setting in Detroit, Michigan.
Twenty-three members of the CAAA SC.
Common themes identified by SC members relating to the partnership's ability to achieve project goals and the successes and challenges facing the partnership itself.
Identified partnership accomplishments included: successful implementation of a complex project, identification of children with previously undiagnosed asthma, and diverse participation and community influence in SC decisions. Challenges included ensuring all partners' influence in decision-making, the need to adjust to “a different way of doing things” in CBPR, constraints and costs of doing CBPR felt by all partners, ongoing need for communication and maintaining trust, and balancing the needs of science and the community through intervention.
CBPR can enhance and facilitate basic research, but care must be given to trust issues, governance issues, organizational culture, and costs of participation for all organizations involved.
community-based participatory research; asthma; partnership; process evaluation
Low socioeconomic status (SES) has been linked to higher morbidity in patients with chronic diseases, but may be particularly relevant to asthma, as asthmatics of lower SES may have higher exposures to indoor (e.g., cockroaches, tobacco smoke) and outdoor (e.g., urban pollution) allergens, thus increasing risk for exacerbations.
This study assessed associations between adult SES (measured according to educational level) and asthma morbidity, including asthma control; asthma-related emergency health service use; asthma self-efficacy, and asthma-related quality of life, in a Canadian cohort of 781 adult asthmatics. All patients underwent a sociodemographic and medical history interview and pulmonary function testing on the day of their asthma clinic visit, and completed a battery of questionnaires (Asthma Control Questionnaire, Asthma Quality of Life Questionnaire, and Asthma Self-Efficacy Scale). General Linear Models assessed associations between SES and each morbidity measure.
Lower SES was associated with worse asthma control (F = 11.63, p < .001), greater emergency health service use (F = 5.09, p = .024), and worse asthma self-efficacy (F = 12.04, p < .01), independent of covariates. Logistic regression analyses revealed that patients with <12 years of education were 55% more likely to report an asthma-related emergency health service visit in the last year (OR = 1.55, 95%CI = 1.05-2.27). Lower SES was not related to worse asthma-related quality of life.
Results suggest that lower SES (measured according to education level), is associated with several indices of worse asthma morbidity, particularly worse asthma control, in adult asthmatics independent of disease severity. Results are consistent with previous studies linking lower SES to worse asthma in children, and add asthma to the list of chronic diseases affected by individual-level SES.
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.
Characterizing factors which determine susceptibility to air pollution is an important step in understanding the distribution of risk in a population and is critical for setting appropriate policies. We evaluate general and specific measures of community health as modifiers of risk for asthma and congestive heart failure following an episode of acute exposure to wildfire smoke.
A population-based study of emergency department visits and daily concentrations of fine particulate matter during a wildfire in North Carolina was performed. Determinants of community health defined by County Health Rankings were evaluated as modifiers of the relative risk. A total of 40 mostly rural counties were included in the study. These rankings measure factors influencing health: health behaviors, access and quality of clinical care, social and economic factors, and physical environment, as well as, the outcomes of health: premature mortality and morbidity. Pollutant concentrations were obtained from a mathematically modeled smoke forecasting system. Estimates of relative risk for emergency department visits were based on Poisson mixed effects regression models applied to daily visit counts.
For asthma, the strongest association was observed at lag day 0 with excess relative risk of 66%(28,117). For congestive heart failure the excess relative risk was 42%(5,93). The largest difference in risk was observed after stratifying on the basis of Socio-Economic Factors. Difference in risk between bottom and top ranked counties by Socio-Economic Factors was 85% and 124% for asthma and congestive heart failure respectively.
The results indicate that Socio-Economic Factors should be considered as modifying risk factors in air pollution studies and be evaluated in the assessment of air pollution impacts.
Disparities and susceptibility; Air pollution; Climate change; Asthma; Congestive heart failure; Wildfires
This study was undertaken to determine whether exposure to
various indoor pollutants is associated with a higher prevalence of
respiratory symptoms, a diagnosis of asthma, or more variable peak flow
rates. Four hundred and twenty six children aged 8-11 years in four
junior schools at three locations recorded respiratory symptoms and
diagnosis of asthma using the ISAAC questionnaire. Daily peak flow
measurements were taken during two six-week periods (winter and
summer). Symptoms in children with and without asthma were not related
to gas fires, cookers, smokers, or pets in the home. However, the
variability of lung function, expressed as the coefficient of
variation, in all children was increased with a household smoker.
Environmental tobacco smoke increases airways variability in children
with and without asthma. Its effects were not apparent from a
questionnaire completed by parents, and the coefficient of variation of
serially measured peak flows was a more sensitive indicator of lung function.
Asthma disproportionately affects inner-city, minority children in the U.S. Outdoor pollutant concentrations, including particulate matter (PM), are higher in inner-cities and contribute to childhood asthma morbidity. Although children spend the majority of time indoors, indoor PM exposures have been less extensively characterized. There is a public health imperative to characterize indoor sources of PM within this vulnerable population to enable effective intervention strategies. In the present study, we sought to identify determinants of indoor PM in homes of Baltimore inner-city pre-school children.
Children ages 2-6 (n=300) who were predominantly African-American (90%) and from lower socioeconomic backgrounds were enrolled. Integrated PM2.5 and PM10 air sampling was conducted over a 3-day period in the children’s bedrooms and at a central monitoring site while caregivers completed daily activity diaries. Homes of pre-school children in inner-city Baltimore had indoor PM concentrations that were twice as high as simultaneous outdoor concentrations. The mean indoor PM2.5 and PM10 concentrations were 39.5±34.5 μg/m3 and 56.2±44.8 μg/m3, compared to the simultaneously measured ambient PM2.5 and PM10 (15.6±6.9 and 21.8±9.53 μg/m3, respectively). Common modifiable household activities, especially smoking and sweeping, contributed significantly to higher indoor PM, as did ambient PM concentrations. Open windows were associated with significantly lower indoor PM. Further investigation of the health effects of indoor PM exposure is warranted, as are studies to evaluate the efficacy of PM reduction strategies on asthma health of inner-city children.
Particulate matter; Air pollution; Asthma; Pediatric; Urban
Smoke-free air laws have been implemented in many Kentucky communities to protect the public from the harmful effects of secondhand smoke exposure. The impact of different strengths of smoke-free air laws on indoor air quality was assessed.
Indoor air quality in hospitality venues was assessed in seven communities before and after comprehensive smoke-free air laws and in two communities only after partial smoke-free air laws. One community was measured three times: before any smoke-free air law, after the initial partial law, and after the law was strengthened to cover all workplaces and public places with few exemptions. Real-time measurements of particulate matters with 2.5 μm aerodynamic diameter or smaller (PM2.5) were obtained.
When comprehensive smoke-free air laws were implemented, indoor PM2.5 concentrations decreased significantly from 161 to 20 μg/m3. In one community that implemented a comprehensive smoke-free law after initially passing a partial law, indoor PM2.5 concentrations were 304 μg/m3 before the law, 338 μg/m3 after the partial law, and 9 μg/m3 after the comprehensive law.
The study clearly demonstrated that partial smoke-free air laws do not improve indoor air quality. A significant linear trend indicated that PM2.5 levels in the establishments decreased with fewer numbers of burning cigarettes. Only comprehensive smoke-free air laws are effective in reducing indoor air pollution from secondhand tobacco smoke.
The Syracuse AUDIT (Assessment of Urban Dwellings for Indoor Toxics) project is a birth cohort study of wheezing in the first year of life in a low-income urban setting. Such studies are important because of the documented serious risks to children's health and the lack of attention and published work on asthma development and intervention in communities of this size. We studied 103 infants of mothers with asthma, living predominantly in inner-city households. Our study combines measurements of a large panel of indoor environmental agents, in-home infant assessments, and review of all prenatal and postnatal medical records through the first year of life. We found multiple environmental pollution sources and potential health risks in study homes including high infant exposure to tobacco smoke. The prevalence of maternal smoking during pregnancy was 54%; postnatal environmental tobacco smoke (ETS) exposure was nearly 90%. The majority (73%) of homes showed signs of dampness. Participants' lives were complicated by poverty, unemployment and single-parenthood. Thirty-three percent of fathers were not involved with their children, and 62% of subjects moved at least once during the study period. These socioeconomic issues had an impact on project implementation and led to modification of study eligibility criteria. Extensive outreach, follow up, and relationship-building were required in order to recruit and retain families and resulted in considerable work overload for study staff. Our experiences implementing the project will inform further studies on this and other similar populations. Future reports on this cohort will address the role of multiple environmental variables and their effects on wheezing outcome during the first year of life.
Birth cohort; Childhood exposure; Indoor pollution; Maternal asthma; Study design; Tobacco smoke exposure; Wheeze
We conducted this study to compare environmental exposures in suburban homes of children with asthma to exposures in inner city homes of children with asthma, to better understand important differences of indoor pollutant exposure that might contribute to increased asthma morbidity in the inner city. Indoor PM10, PM2.5, NO2, O3, and airborne and dust allergen levels were measured in the homes of 120 children with asthma, 100 living in inner city Baltimore and 20 living in the surrounding counties. Home conditions and health outcome measures were also compared. The inner city and suburban homes differed in ways that might affect airborne environmental exposures. The inner city homes had more cigarette smoking (67% vs. 5%, p < .001), signs of disrepair (77% vs. 5%, p < .001), and cockroach (64% vs. 0%, p < .001) and mouse (80% vs. 5%, p < .001) infestation. The inner city homes had higher geometric mean (GM) levels (p < .001) of PM10 (47 vs. 18 μg/m3), PM2.5 (34 vs. 8.7 μg/m3), NO2 [19 ppb vs. below detection (BD)], and O3 (1.9 vs. .015 ppb) than suburban homes. The inner city homes had lower GM bedroom dust allergen levels of dust mite (.29 vs. 1.2 μg/g, p = .022), dog (.38 vs. 5.5 μg/g, p < .001) and cat (.75 vs. 2.4 μg/g, p = .039), but higher levels of mouse (3.2 vs. .013 μg/g, p < .001) and cockroach (4.5 vs. .42 U/g, p < .001). The inner city homes also had higher GM airborne mouse allergen levels (.055 vs. .016 ng/m3, p = .002). Compared with the homes of suburban children with asthma, the homes of inner city Baltimore children with asthma had higher levels of airborne pollutants and home characteristics that predispose to greater asthma morbidity.
Indoor air; Inner city asthma; Particulate matter; Air pollution; Allergens