Early-Life Exposure to Air Pollution and Childhood Asthma Cumulative Incidence in the ECHO CREW Consortium.

Importance: Exposure to outdoor air pollution contributes to childhood asthma development, but many studies lack the geographic, racial and ethnic, and socioeconomic diversity to evaluate susceptibility by individual-level and community-level contextual factors. Objective: To examine early life exposure to fine particulate matter (PM2.5) and nitrogen oxide (NO2) air pollution and asthma risk by early and middle childhood, and whether individual and community-level characteristics modify associations between air pollution exposure and asthma. Design, Setting, and Participants: This cohort study included children enrolled in cohorts participating in the Children's Respiratory and Environmental Workgroup consortium. The birth cohorts were located throughout the US, recruited between 1987 and 2007, and followed up through age 11 years. The survival analysis was adjusted for mother's education, parental asthma, smoking during pregnancy, child's race and ethnicity, sex, neighborhood characteristics, and cohort. Statistical analysis was performed from February 2022 to December 2023. Exposure: Early-life exposures to PM2.5 and NO2 according to participants' birth address. Main Outcomes and Measures: Caregiver report of physician-diagnosed asthma through early (age 4 years) and middle (age 11 years) childhood. Results: Among 5279 children included, 1659 (31.4%) were Black, 835 (15.8%) were Hispanic, 2555 (48.4%) where White, and 229 (4.3%) were other race or ethnicity; 2721 (51.5%) were male and 2596 (49.2%) were female; 1305 children (24.7%) had asthma by 11 years of age and 954 (18.1%) had asthma by 4 years of age. Mean values of pollutants over the first 3 years of life were associated with asthma incidence. A 1 IQR increase in NO2 (6.1 µg/m3) was associated with increased asthma incidence among children younger than 5 years (HR, 1.25 [95% CI, 1.03-1.52]) and children younger than 11 years (HR, 1.22 [95% CI, 1.04-1.44]). A 1 IQR increase in PM2.5 (3.4 µg/m3) was associated with increased asthma incidence among children younger than 5 years (HR, 1.31 [95% CI, 1.04-1.66]) and children younger than 11 years (OR, 1.23 [95% CI, 1.01-1.50]). Associations of PM2.5 or NO2 with asthma were increased when mothers had less than a high school diploma, among Black children, in communities with fewer child opportunities, and in census tracts with higher percentage Black population and population density; for example, there was a significantly higher association between PM2.5 and asthma incidence by younger than 5 years of age in Black children (HR, 1.60 [95% CI, 1.15-2.22]) compared with White children (HR, 1.17 [95% CI, 0.90-1.52]). Conclusions and Relevance: In this cohort study, early life air pollution was associated with increased asthma incidence by early and middle childhood, with higher risk among minoritized families living in urban communities characterized by fewer opportunities and resources and multiple environmental coexposures. Reducing asthma risk in the US requires air pollution regulation and reduction combined with greater environmental, educational, and health equity at the community level.

Personal exposure to ultrafine particles in multiple microenvironments among adolescents.

BACKGROUND: Experimental studies suggest ultrafine particles (UFPs), the smallest size fraction of particulate matter, may be more toxic than larger particles, however personal sampling studies in children are lacking. OBJECTIVE: The objective of this analysis was to examine individual, housing, and neighborhood characteristics associated with personal UFP concentrations as well as the differences in exposures that occur within varying microenvironments. METHODS: We measured weekly personal UFP concentrations and GPS coordinates in 117 adolescents ages 13-17 to describe exposures across multiple microenvironments. Individual, home, and neighborhood characteristics were collected by caregiver completed questionnaires. RESULTS: Participants regularly exposed to secondhand tobacco smoke had significantly higher indoor concentrations of UFPs compared to participants who were not. We observed that the 'home' microenvironment dominated the relative contribution of overall UFP concentrations and sampling time, however, relative proportion of integrated UFP exposure were higher in 'other' environments. IMPACT STATEMENT: In this study, we employed a novel panel study design, involving real-time measurement of UFP exposure within the multiple microenvironments of adolescents. We found a combination of personal sampling and detailed activity patterns should be used in future studies to accurately describe exposure-behavior relationships.

Lung function and secondhand smoke exposure among children with cystic fibrosis: A Bayesian meta-analysis.

BACKGROUND: Secondhand smoke exposure, an important environmental health factor in cystic fibrosis (CF), remains uniquely challenging to children with CF as they strive to maintain pulmonary function during early stages of growth and throughout adolescence. Despite various epidemiologic studies among CF populations, little has been done to coalesce estimates of the association between secondhand smoke exposure and lung function decline. METHODS: A systematic review was performed using PRISMA guidelines. A Bayesian random-effects model was employed to estimate the association between secondhand smoke exposure and change in lung function (measured as FEV1% predicted). RESULTS: Quantitative synthesis of study estimates indicated that second-hand smoke exposure corresponded to a significant drop in FEV1 (estimated decrease: -5.11% predicted; 95% CI: -7.20, -3.47). The estimate of between-study heterogeneity was 1.32% predicted (95% CI: 0.05, 4.26). There was moderate heterogeneity between the 6 analyzed studies that met review criteria (degree of heterogeneity: I2=61.9% [95% CI: 7.3-84.4%] and p = 0.022 from the frequentist method.) CONCLUSIONS: Our results quantify the impact at the pediatric population level and corroborate the assertion that secondhand smoke exposure negatively affects pulmonary function in children with CF. Findings highlight challenges and opportunities for future environmental health interventions in pediatric CF care.

Childhood Asthma Incidence, Early and Persistent Wheeze, and Neighborhood Socioeconomic Factors in the ECHO/CREW Consortium.

Importance: In the United States, Black and Hispanic children have higher rates of asthma and asthma-related morbidity compared with White children and disproportionately reside in communities with economic deprivation. Objective: To determine the extent to which neighborhood-level socioeconomic indicators explain racial and ethnic disparities in childhood wheezing and asthma. Design, Setting, and Participants: The study population comprised children in birth cohorts located throughout the United States that are part of the Children's Respiratory and Environmental Workgroup consortium. Cox proportional hazard models were used to estimate hazard ratios (HRs) of asthma incidence, and logistic regression was used to estimate odds ratios of early and persistent wheeze prevalence accounting for mother's education, parental asthma, smoking during pregnancy, child's race and ethnicity, sex, and region and decade of birth. Exposures: Neighborhood-level socioeconomic indicators defined by US census tracts calculated as z scores for multiple tract-level variables relative to the US average linked to participants' birth record address and decade of birth. The parent or caregiver reported the child's race and ethnicity. Main Outcomes and Measures: Prevalence of early and persistent childhood wheeze and asthma incidence. Results: Of 5809 children, 46% reported wheezing before age 2 years, and 26% reported persistent wheeze through age 11 years. Asthma prevalence by age 11 years varied by cohort, with an overall median prevalence of 25%. Black children (HR, 1.47; 95% CI, 1.26-1.73) and Hispanic children (HR, 1.29; 95% CI, 1.09-1.53) were at significantly increased risk for asthma incidence compared with White children, with onset occurring earlier in childhood. Children born in tracts with a greater proportion of low-income households, population density, and poverty had increased asthma incidence. Results for early and persistent wheeze were similar. In effect modification analysis, census variables did not significantly modify the association between race and ethnicity and risk for asthma incidence; Black and Hispanic children remained at higher risk for asthma compared with White children across census tracts socioeconomic levels. Conclusions and Relevance: Adjusting for individual-level characteristics, we observed neighborhood socioeconomic disparities in childhood wheeze and asthma. Black and Hispanic children had more asthma in neighborhoods of all income levels. Neighborhood- and individual-level characteristics and their root causes should be considered as sources of respiratory health inequities.

NAT1 genetic variation increases asthma risk in children with secondhand smoke exposure.

OBJECTIVE: We previously reported that children exposed to secondhand smoke (SHS) that carried variants in the NAT1 gene had over two-fold higher hair cotinine levels. Our objective was to determine if NAT1 polymorphisms confer increased risk for developing asthma in children exposed to SHS. METHODS: White participants in the Cincinnati Childhood Allergy and Air Pollution Study (n = 359) were genotyped for 10 NAT1 variants. Smoke exposure was defined by hair cotinine and parental report. Asthma was objectively assessed by spirometry and methacholine challenge. Findings were replicated in the Genomic Control Cohort (n = 638). RESULTS: Significant associations between 5 NAT1 variants and asthma were observed in the CCAAPS exposed group compared to none in the unexposed group. There was a significant interaction between NAT1 rs13253389 and rs4921581 with smoke exposure (p = 0.02, p = 0.01) and hair cotinine level (p = 0.048, p = 0.042). Children wildtype for rs4921581 had increasing asthma risk with increasing hair cotinine level, whereas those carrying the NAT1 minor allele had an increased risk of asthma regardless of cotinine level. In the GCC, 13 NAT1 variants were associated with asthma in the smoke-exposed group, compared to 0 in the unexposed group, demonstrating gene-level replication. CONCLUSIONS: Variation in the NAT1 gene modifies asthma risk in children exposed to secondhand-smoke. To our knowledge, this is the first report of a gene-environment interaction between NAT1 variants, smoke exposure, cotinine levels, and pediatric asthma. NAT1 genotype may have clinical utility as a biomarker of increased asthma risk in children exposed to smoke.

Childhood exposure to Libby amphibole asbestos and respiratory health in young adults.

OBJECTIVES: Vermiculite ore containing Libby amphibole asbestos (LAA) was mined in Libby, MT, from the 1920s-1990. Recreational and residential areas in Libby were contaminated with LAA. This objective of this study was to characterize childhood exposure to LAA and investigate its association with respiratory health during young adulthood. METHODS: Young adults who resided in Libby prior to age 18 completed a health and activity questionnaire, pulmonary function testing, chest x-ray and HRCT scan. LAA exposure was estimated based on participant report of engaging in activities with potential LAA exposure. Quantitative LAA estimates for activities were derived from sampling data and literature reports. RESULTS: A total of 312 participants (mean age 25.1 years) were enrolled and reported respiratory symptoms in the past 12 months including pleuritic chest pain (23%), regular cough (17%), shortness of breath (18%), and wheezing or whistling in the chest (18%). Cumulative LAA exposure was significantly associated with shortness of breath (aOR = 1.12, 95% CI 1.01-1.25 per doubling of exposure). Engaging in recreational activities near Rainy Creek Road (near the former mine site) and the number of instances heating vermiculite ore to make it expand or pop were also significantly associated with respiratory symptoms. LAA exposure was not associated with pulmonary function or pleural or interstitial changes on either chest x-ray or HRCT. CONCLUSIONS: Pleural or interstitial changes on x-ray or HRCT were not observed among this cohort of young adults. However, childhood exposure to LAA was significantly associated with respiratory symptoms during young adulthood. Pleuritic chest pain, in particular, has been identified as an early symptom associated with LAA exposure and therefore warrants continued follow-up given findings of progressive disease in other LAA exposed populations.

Parental Snoring and Environmental Pollutants, but Not Aeroallergen Sensitization, Are Associated with Childhood Snoring in a Birth Cohort.

The objective of this study was to determine whether atopy and other clinical and environmental variables predict the risk of childhood habitual snoring (HS) in a birth cohort born to atopic parents. Participants completed clinical evaluations and questionnaires at ages 1-4 and age 7. HS was defined as snoring ≥3 nights/week. Traffic-related air pollution (TRAP) exposure was estimated using land-use regression. The association between early (≤age 4) and current (age 7) allergic disease, environmental exposures, and snoring at age 7 was examined using adjusted logistic regression. Of the 609 children analyzed the prevalence of HS at age 7 was 21%. Early tobacco smoke exposure [environmental tobacco smoke (ETS)] [odds ratio (OR) 1.79, 95% CI (confidence interval) 1.12-2.84], rhinitis (OR 1.74, 95% CI 1.06-2.92), wheezing (OR 1.63, 95% CI 1.05-2.53), maternal HS (OR 2.08, 95% CI 1.36-3.18), and paternal HS (OR 1.83, 95% CI 1.14-3.00) were significantly associated with HS at age 7. Current TRAP (OR 1.93, 95% CI 1.13-3.26), respiratory infections (OR 1.16, 95% 1.03-1.35), maternal HS (OR 2.86, 95% CI 1.69-4.84), and paternal HS (OR 3.01, 95% CI 1.82-5.09) were significantly associated with HS at age 7. To our knowledge, this is the largest birth cohort examining longitudinal predictors of snoring in children born to atopic parents. Parental HS was the only variable consistently associated with childhood HS from ages 1 to 7. Early rhinitis, early ETS exposure, and concurrent traffic pollution exposure increased the risk of HS at age 7, while aeroallergen sensitization did not. Children with these characteristics should be considered for screening of sleep disorders.

Ten-eleven translocation 1 (TET1) methylation is associated with childhood asthma and traffic-related air pollution.

BACKGROUND: Asthma is a complex disorder influenced by genetics and the environment. Recent findings have linked abnormal DNA methylation in T cells with asthma; however, the potential dysregulation of methylation in airway epithelial cells is unknown. Studies of mouse models of asthma have observed greater levels of 5-hydroxymethylcytosine (5-hmC) and ten-eleven translocation 1 (TET1) expression in lungs. TET proteins are known to catalyze methylation through modification of 5-methylcytosine to 5-hmC. OBJECTIVE: We sought to examine the association of TET1 methylation with asthma and traffic-related air pollution (TRAP). METHODS: TET1 methylation levels from DNA derived from nasal airway epithelial cells collected from 12 African American children with physician-diagnosed asthma and their nonasthmatic siblings were measured by using Illumina 450K arrays. Regions of interest were verified by means of locus-specific pyrosequencing in 35 sibling pairs and replicated in an independent population (n = 186). Exposure to TRAP in participants' early life and at current home addresses was estimated by using a land-use regression model. Methylation studies in saliva, PBMCs, and human bronchial epithelial cells were done to support our findings. RESULTS: Loss of methylation at a single CpG site in the TET1 promoter (cg23602092) and increased global 5-hmC levels were significantly associated with asthma. In contrast, TRAP exposure at participants' current homes significantly increased methylation at the same site. Patterns were consistent across tissue sample types. 5-Aza-2'-deoxycytidine and diesel exhaust particle exposure in human bronchial epithelial cells was associated with altered TET1 methylation and expression and global 5-hmC levels. CONCLUSIONS: Our findings suggest a possible role of TET1 methylation in asthmatic patients and response to TRAP.

Secondhand smoke and traffic exhaust confer opposing risks for asthma in normal and overweight children.

OBJECTIVE: Exposure to ultrafine particles (UFP) in secondhand smoke (SHS) and traffic-related air pollution (TRAP) may elicit chronic inflammation. It was hypothesized that the association between these exposures would be potentiated in overweight versus normal-weight children. METHODS: Average lifetime exposure to TRAP and SHS and objective, physician-diagnosed asthma were determined for 575 children at age 7. Overweight was defined as having a body mass index (BMI) >85th percentile for age and gender. The association between TRAP and SHS exposure and asthma was examined by logistic regression stratified by BMI. RESULTS: A total of 131 children were overweight; the prevalence of asthma was 24.4% and 14.2% among overweight and normal-weight children, respectively. Exposure to SHS was significantly associated with asthma among overweight (adjusted odds ratio [adjOR] = 3.0; 95% confidence interval [CI] = 1.2, 7.4) but not normal-weight children (adjOR = 1.1; 95% CI = 0.4, 2.7). In contrast, TRAP was significantly associated with asthma among normal-weight (adjOR = 1.8; 95% CI = 1.0, 3.4) but not overweight children (adjOR = 0.7; 95% CI = 0.4, 2.7). CONCLUSIONS: The association between SHS and TRAP exposure and asthma is modified by children's weight. Children's time-activity patterns, including time spent indoors or outdoors, may vary by weight and play an important role in these UFP exposures.

Traffic-related air pollution and asthma hospital readmission in children: a longitudinal cohort study.

OBJECTIVE: To examine the association between exposure to traffic-related air pollution (TRAP) and hospital readmission for asthma or bronchodilator-responsive wheezing. STUDY DESIGN: A population-based cohort of 758 children aged 1-16 years admitted for asthma or bronchodilator-responsive wheezing was assessed for asthma readmission within 12 months. TRAP exposure was estimated with a land use regression model using the home address at index admission, with TRAP dichotomized at the sample median (0.37 µg/m3). Covariates included allergen-specific IgE, tobacco smoke exposure, and social factors obtained at enrollment. Associations between TRAP exposure and readmission were assessed using logistic regression and Cox proportional hazards models. RESULTS: The study cohort was 58% African American and 32% white; 19% of the patients were readmitted within 12 months of the original admission. Higher TRAP exposure was associated with a higher readmission rate (21% vs. 16%; P = .05); this association was not significant after adjusting for covariates (aOR, 1.4; 95% CI, 0.9-2.2). Race modified the observed association; white children with high TRAP exposure had 3-fold higher odds of asthma readmission (OR, 3.0; 95% CI, 1.1-8.1), compared with white children with low TRAP exposure. In African American children, TRAP exposure was not associated with increased readmission (OR, 1.1; 95% CI, 0.6-1.8). In children with high TRAP exposure, TRAP exposure was associated with decreased time to readmission in white children (hazard ratio, 3.2; 95% CI, 1.5-6.7) compared with African American children (hazard ratio, 1.0; 95% CI, 0.7-1.4). African American children had a higher readmission rate overall. CONCLUSION: TRAP exposure is associated with increased odds of hospital readmission in white children, but not in African American children.

Role of financial and social hardships in asthma racial disparities.

BACKGROUND AND OBJECTIVES: Health care reform offers a new opportunity to address child health disparities. This study sought to characterize racial differences in pediatric asthma readmissions with a focus on the potential explanatory role of hardships that might be addressed in future patient care models. METHODS: We enrolled 774 children, aged 1 to 16 years, admitted for asthma or bronchodilator-responsive wheezing in a population-based prospective observational cohort. The outcome was time to readmission. Child race, socioeconomic status (measured by lower income and caregiver educational attainment), and hardship (caregivers looking for work, having no one to borrow money from, not owning a car or home, and being single/never married) were recorded. Analyses used Cox proportional hazards. RESULTS: The cohort was 57% African American, 33% white, and 10% multiracial/other; 19% were readmitted within 12 months. After adjustment for asthma severity classification, African Americans were twice as likely to be readmitted as whites (hazard ratio: 1.98; 95% confidence interval: 1.42 to 2.77). Compared with whites, African American caregivers were significantly more likely to report lower income and educational attainment, difficulty finding work, having no one to borrow money from, not owning a car or home, and being single/never married (all P ≤ .01). Hardships explained 41% of the observed racial disparity in readmission; jointly, socioeconomic status and hardship explained 49%. CONCLUSIONS: African American children were twice as likely to be readmitted as white children; hardships explained >40% of this disparity. Additional factors (eg, pollution, tobacco exposure, housing quality) may explain residual disparities. Targeted interventions could help achieve greater child health equity.

Chronic traffic pollution exposure is associated with eosinophilic, but not neutrophilic inflammation in older adult asthmatics.

OBJECTIVE: Airway inflammatory patterns in older asthmatics are poorly understood despite high asthma-related morbidity and mortality. In this study, we sought to define the relationship between exposure to traffic pollutants, biomarkers in induced sputum, and asthma control in older adults. METHODS: Induced sputum was collected from 35 non-smoking adults ≥65 years with a physician's diagnosis of asthma and reversibility with a bronchodilator or a positive methacholine challenge. Patients completed the Asthma Control Questionnaire (ACQ), and Elemental Carbon Attributable to Traffic (ECAT), a surrogate for chronic diesel particulate exposure, was determined. Equal numbers of subjects with high (≥0.39 µg/m(3)) versus low (<0.39 µg/m(3)) ECAT were included. Differential cell counts were performed on induced sputum, and myeloperoxidase (MPO) and eosinophil peroxidase (EPO) were measured in supernatants. Regression analyses were used to evaluate the relationship between sputum findings, ACQ scores, and ECAT. RESULTS: After adjustment for potential confounders, subjects with poorly controlled asthma based on ACQ ≥ 1.5 (n = 7) had significantly higher sputum eosinophils (median = 4.4%) than those with ACQ < 1.5 (n = 28; eosinophils = 2.6%; ß = 10.1 [95% CI = 0.1-21.0]; p = 0.05). Subjects with ACQ ≥ 1.5 also had significantly higher sputum neutrophils (84.2% versus 65.2%; ß = 7.1 [0.2-14.6]; p = 0.05). Poorly controlled asthma was associated with higher sputum EPO (ß = 2.4 [0.2-4.5], p = 0.04), but not MPO (p = 0.9). High ECAT was associated with higher eosinophils (ß = 10.1 [1.8-18.4], p = 0.02) but not higher neutrophils (p = 0.6). CONCLUSIONS: Poorly controlled asthma in older adults is associated with eosinophilic and neutrophilic inflammation. Chronic residential traffic pollution exposure may be associated with eosinophilic, but not neutrophilic inflammation in older asthmatics.

Unraveling the relationship between aeroallergen sensitization, gender, second-hand smoke exposure, and impaired lung function.

BACKGROUND: Contradictory findings on the differential effects of second-hand smoke (SHS) on lung function in girls and boys may result from masked relationships between host and environmental factors. Allergic sensitization may augment the relationship between SHS and decreased lung function, although its role in relation to the inconsistent gender differences in children has not been elucidated. HYPOTHESIS: We hypothesize that there will be differences between boys and girls related to early-life allergic sensitization and exposure to SHS on pulmonary function later in childhood. METHODS: Participants in this study (n = 486) were drawn from the Cincinnati Childhood Allergy and Air Pollution (CCAAPS) birth cohort study consisting of 46% girls. Allergic sensitization was assessed by skin prick test (SPT) to 15 aeroallergens at ages 2, 4, and 7, while pulmonary function and asthma diagnosis occurred at age 7. SHS exposure was measured by hair cotinine at ages 2 and/or 4. Gender differences of SHS exposure on pulmonary function among children with positive SPTs at ages 2, 4, and 7 as well as first- and higher-order interactions were examined by multiple linear regression. Interactions significant in the multivariate models were also examined via stratification. Comparisons within and between stratified groups were assessed by examining the slope of the parameter estimates/beta coefficients and associated p-values and confidence intervals. RESULTS: Increased cotinine levels were significantly associated with decreases in FEV(1) (-0.03 l, p < 0.05), peak expiratory flow (-0.07 l/s, p < 0.05), and FEF (25-75%) (-0.06 l/s, p < 0.01). The interaction between cotinine and sensitization at age 2 was borderline significant (p = 0.10) in the FEF(25-75%) model and showed an exposure response effect according to the number of positive SPTs at age 2; zero (-0.06 l/s, p < 0.01), one (-0.09 l/s, p < 0.05), or two or more positive SPTs (-0.30 l/s, p < 0.01). Despite increased polysensitization among boys, the association between cotinine and FEF(25-75%) among girls, with two or more positive SPTs at age 2, showed the greatest deficits in FEF(25-75%) (-0.34 l/s vs. -0.05 l/s and -0.06 l/s for non-sensitized girls and boys, respectively. Girls with two or more positive SPTs showed a twofold greater decrease in FEF(25-5%) (-0.34 l/s; 95% CI: -0.55, -0.13) compared to boys with the same degree of allergic sensitization (-0.18 l/s; 95% CI: -0.41, 0.06), although this difference was not statistically significant. CONCLUSIONS: Reductions in lung function were observed among children exposed to SHS, and the number of aeroallergen-positive SPTs at age 2 modifies this relationship. Girls experiencing early childhood allergic sensitization and high SHS exposure are at greater risk of decreased lung function later in childhood compared to non-sensitized girls and boys and demonstrate greater deficits compared to boys with similar degrees of sensitization.

Erionite in road gravel associated with interstitial and pleural changes--an occupational hazard in western United States.

OBJECTIVE: To determine the rate of chest radiographic abnormalities among residents of North Dakota potentially exposed to road gravel containing the fibrous mineral erionite. METHODS: Participants (n = 34) completed a questionnaire, chest radiograph, and high resolution computed tomography scan to assess the rate of interstitial and pleural changes consistent with fibrous mineral exposure. RESULTS: Interstitial, pleural, or both changes typically associated with asbestos exposure were observed by high resolution computed tomography in seven (21%) individuals. The primary exposure pathway for six of these was from gravel pits, road maintenance, or both. Three participants (8.8%) demonstrated bilateral localized pleural changes with calcification; two of these also had accompanying interstitial changes. All three reported extensive work in gravel pits, road maintenance, or both. CONCLUSIONS: These results indicate that occupational exposure to erionite contained within road gravel in the United States represents a potential health hazard. CLINICAL SIGNIFICANCE: This study identifies chest radiographic changes among residents of North Dakota occupationally exposed to road gravel containing erionite. Public health officials and physicians in affected areas should be aware of the potential health effects of erionite exposure. Precautionary measures should be taken to limit occupational exposure to gravel containing erionite.

Exposure to traffic exhaust and night cough during early childhood: the CCAAPS birth cohort.

Though studies have investigated the association between air pollution and respiratory health outcomes in children, few have focused on night cough. The study objective was to simultaneously evaluate family factors (i.e., race, gender, maternal and paternal asthma, and breastfeeding), health (allergen sensitization and wheezing symptoms), home factors (dog, cat, mold, endotoxin, and dust mite), and other environmental exposures (traffic exhaust and second-hand tobacco smoke) for associations with recurrent dry night cough (RNC) during early childhood. A structural equation model with repeat measures was developed assessing RNC at ages one, two, and three. The prevalence of RNC was relatively large and similar at ages, one, two, and three at 21.6%, 17.3%, and 21.1%, respectively. Children exposed to the highest tertile of traffic exhaust had an estimated 45% increase in risk of RNC compared with children less exposed (adjusted OR 1.45, 95% CI: 1.09, 1.94). Also, wheezing was associated with a 76% higher risk of RNC (adjusted OR 1.76, 95% CI: 1.36, 2.26). A protective trend for breastfeeding was found with a 27% reduction in risk associated with breastfeeding (adjusted OR 0.73, 95% CI: 0.53, 1.01). No other factors were significant. These results suggest that traffic exhaust exposure may be a risk factor for night cough in young children.

Mold exposure during infancy as a predictor of potential asthma development.

BACKGROUND: Exposure to mold has been associated with exacerbation of asthma symptoms in children. OBJECTIVE: To report how the presence of visible mold and exposure to (1-3)-beta-D-glucan in infancy affects the risk of asthma at the age of 3 years as defined by an Asthma Predictive Index (API). METHODS: Visible mold was evaluated by means of home inspection. (1-3)-beta-D-glucan levels were measured in settled dust. Children were considered to be at high risk for asthma at later ages if they reported recurrent wheezing at the age of 3 years and met at least 1 of 3 major or 2 of 3 minor API criteria. RESULTS: Children aged 3 years with high visible mold in the home during infancy were 7 times more likely to have a positive API than were those with no visible mold (adjusted odds ratio [aOR], 7.1; 95% confidence interval [CI], 2.2-12.6). In contrast, at low (1-3)-beta-D-glucan levels (< 22 microg/g), children were at increased risk of a positive API (aOR, 3.4; 95% CI, 0.5-23.5), whereas those with high (1-3)-beta-D-glucan levels (> 133 microg/g) were at decreased risk (aOR, 0.6; 95% CI, 0.2-1.6). Of the other covariates, mother's smoking was the strongest significant risk factor for the future development of asthma based on a positive API (aOR, 4.4; 95% CI, 1.7-11.6). CONCLUSIONS: The presence of high visible mold and mother's smoking during infancy were the strongest risk factors for a positive API at the age of 3 years, suggesting an increased risk of asthma. High (1-3)-beta-D-glucan exposure seems to have an opposite effect on API than does visible mold.

Associations between multiple environmental exposures and Glutathione S-Transferase P1 on persistent wheezing in a birth cohort.

OBJECTIVE: To determine the impact of environmental exposures (diesel exhaust particle [DEP], environmental tobacco smoke [ETS], and mold) that may contribute to oxidative stress on persistent wheezing in the Cincinnati Childhood Allergy and Air Pollution Study (CCAAPS) birth cohort and to determine how the impact of these exposures is modified by the GST-P1 Ile105Val polymorphism. STUDY DESIGN: A land-use regression model was used to derive an estimate of each child's DEP exposure. ETS exposure was determined by questionnaire data. Each child's home was evaluated for visible mold by a trained professional. Children in the CCAAPS cohort were genotyped for the GST-P1 polymorphism (n = 570). Persistent wheezing was defined as wheezing at both 12 and 24 months. RESULTS: High DEP exposure conferred increased risk for wheezing phenotypes but only among the Val(105) allele carriers. Infants with multiple exposures were significantly more likely to persistently wheeze despite their genotype. CONCLUSION: There is evidence for an environmental effect of DEP among carriers of the GST-P1 Val(105) allele in the development of persistent wheezing in children. The protective effect of the GST-P1 Ile(105) genotype may be overwhelmed by multiple environmental exposures that converge on oxidative stress pathways.

Environmental risk factors of rhinitis in early infancy.

Previous studies of allergic rhinitis in children have not documented the environmental risk factors for infants at age one. We examined the relationship of environmental tobacco smoke (ETS) and visible mold exposures on the development of allergic rhinitis, rhinitis and upper respiratory infection (URI) in a birth cohort where at least one parent was skin prick test (SPT) positive. ETS exposure and upper respiratory symptoms were obtained by questionnaires. Visible mold was classified as none, low or high during home visit. Infants had a SPT at age one. After adjustment for potential confounders, exposure to >20 cigarettes per day was associated with an increased risk of developing allergic rhinitis at age one [odds ratio (OR)=2.7; 95% CI 1.04-6.8] and rhinitis symptoms during the first year (OR=1.9; 95% CI 1.1-3.2). Infants with low (OR=1.5; 95% CI 1.1-2.3) or high (OR=5.1; 95% CI 2.2-12.1) levels of visible mold in their homes were more likely to have more frequent URI during the first year. Older siblings were protective for development of both rhinitis symptoms and allergic rhinitis. This study suggests that ETS exposure, rather than visible mold, is associated with rhinitis and allergic rhinitis in infants. The analysis also suggests that mold may be a stronger risk factor for URI that ETS.