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The importance of domestic Alternaria exposure to allergic disease in urban communities is underrecognized relative to cockroach, dust mite, and mouse exposures. Concentrations of Alternaria are higher in outdoor than in indoor air; however, dampness, leaks, and resident behaviors can influence fungal penetrance and secondary growth indoors. Moreover, given the amount of time children spend indoors, domestic exposure may contribute more than outdoor exposure to asthma morbidity. Byproducts from fossil fuel combustion are common in urban air and are the most well-established anthropogenic environmental adjuvants of allergic sensitization. Black carbon and elemental carbon (EC), indicators of combustion exposure, vary across cities such as New York (NYC) because of vehicle and residential heating sources. Among NYC children, we previously demonstrated an interaction between exposure to combustion byproducts and cockroach allergen on cockroach sensitization and an association between black carbon measured inside homes and fractional exhaled nitric oxide (Feno), a marker of airway inflammation. Therefore, combustion byproducts might enhance the effect of fungal exposure on allergic disease outcomes among NYC children. We hypothesized that, among NYC children, (1) sensitization to Alternaria alternata would be associated with increased asthma symptoms, (2) domestic exposure to A alternata would be associated with increased Feno, and (3) the association with Feno would be modified by neighborhood EC concentrations.

Background: Rhinitis and conjunctivitis are often linked to asthma development through an allergic pathway. However, runny nose and watery eyes can result from nonallergic mechanisms. These mechanisms can also underlie exercise-induced wheeze (EIW), which has been associated with urgent medical visits for asthma, independent of other indicators of asthma severity or control. Objective: To test the hypothesis that rhinitis or watery eyes without cold symptoms (RWWC) in infancy predict development of EIW and urgent respiratory-related medical visits at school age, independent of seroatopy. Methods: Within a prospective birth cohort of low-income, urban children (n = 332), RWWC was queried during the first year of life. Relative risks (RRs) for EIW, emergency department (ED) visits, and hospitalizations for asthma and other breathing difficulties at 5 to 7 years of age were estimated with multivariable models. Seroatopy was determined at 7 years of age. Results: Infant RWWC was common (49% of children) and predicted school-age EIW (RR, 2.8; P

Background: Secondhand smoke (SHS) and ambient air pollution (AAP) exposures have been associated with increased prevalence and severity of asthma and DNA modifications of immune cells. In the current study, we examined the association between SHS and AAP with DNA methylation and expression of interferon-gamma (IFN-γ) and forkhead box protein 3 (Foxp3) in T cell populations. Methods: Subjects 7–18 years old were recruited from Fresno (high AAP; n = 62) and Stanford, CA (low AAP; n = 40) and divided into SHS-exposed (Fresno: n = 31, Stanford: n = 6) and non-SHS-exposed (nSHS; Fresno: n = 31, Stanford: n = 34) groups. T cells purified from peripheral blood were assessed for levels of DNA methylation and expression of IFN-γ (in effector T cells) or Foxp3 (in regulatory T cells). Results: Analysis showed a significant increase in mean % CpG methylation of IFN-γ and Foxp3 associated with SHS exposure (IFN-γ: FSHS 62.10%, FnSHS 41.29%, p

An estimated 3 million infants and children younger than 5 years die every year from pneumonia in developing countries.1 Exposure to household air pollution emitted from biomass fuels has been implicated in about a third of these cases.2 Observational and case-control studies have reported an association between exposure to household air pollution and lower respiratory tract infections.3 However, until now, no randomised controlled intervention trials had been done in children. In The Lancet, Kirk R Smith and colleagues of the Randomised Exposure Study of Pollution Indoors and Respiratory Effects (RESPIRE) report a randomised trial that aimed to reduce household air pollution and its subsequent effects on early childhood pneumonia. 4 The RESPIRE trial, which was undertaken in the Guatemalan highlands from 2002–04, introduced chimney stoves (planchas) in homes using traditional wood fires for cooking. 534 homes with pregnant women or infants younger than 4 months were randomly assigned to either planchas or control (traditional wood fires); the primary outcome was the reduction of physician-diagnosed pneumonia in children with use of standardised criteria. Study participants were followed up until 18 months of age, with weekly visits by fieldworkers, and subsequent referral to local physicians who were masked to intervention status for the assessment and diagnosis of pneumonia.

Background: Social and environmental stressors, may modify associations between environmental pollutants and asthma symptoms. We examined if neighborhood asthma prevalence (higher: HAPN vs. lower: LAPN), a surrogate for underlying risk factors for asthma, modified the relationship between pollutants and urgent asthma visits. Methods: Through zip code, home addresses were linked to New York City Community Air Survey’s land use regression model for street-level, annual average nitrogen dioxide (NO2), particulate matter (PM2.5), elemental carbon (EC); summer average ozone (O3); winter average sulfur dioxide (SO2) concentrations. Poisson regression models were fit to estimate the association (prevalence ratio, PR) between pollutant exposures and seeking urgent asthma care. Results: All pollutants, except O3 were higher in HAPN than LAPN (P0.05). Conclusions: Relationships between modeled street-level pollutants and urgent asthma were stronger in LAPN compared to HAPN. Social stressors that may be more prevalent in HAPN than LAPN, could play a greater role in asthma exacerbations in HAPN versus pollutant exposure alone.

Background: Studies suggest that phthalate exposures may adversely affect child respiratory health. Objectives: We evaluated associations between asthma diagnosed in children between 5 and 11 years of age and prenatal exposures to butylbenzyl phthalate (BBzP), di-n-butyl phthalate (DnBP), di(2-ethylhexyl) phthalate (DEHP), and diethyl phthalate (DEP). Methods: Phthalate metabolites were measured in spot urine collected from 300 pregnant inner-city women. Children were examined by an allergist or pulmonologist based on the first parental report of wheeze, other respiratory symptoms, and/or use of asthma rescue/controller medication in the preceding 12 months on repeat follow-up questionnaires. Standardized diagnostic criteria were used to classify these children as either having or not having current asthma at the time of the physician examination. Children without any report of wheeze or the other asthma-like symptoms were classified as nonasthmatics at the time of the last negative questionnaire. Modified Poisson regression analyses were used to estimate relative risks (RR) controlling for specific gravity and potential confounders. Results: Of 300 children, 154 (51%) were examined by a physician because of reports of wheeze, other asthma-like symptoms, and/or medication use; 94 were diagnosed with current asthma and 60 without current asthma. The remaining 146 children were classified as nonasthmatic. Compared with levels in nonasthmatics, prenatal metabolites of BBzP and DnBP were associated with a history of asthma-like symptoms (p < 0.05) and with the diagnosis of current asthma: RR = 1.17 (95% CI: 1.01, 1.35) and RR = 1.25 (95% CI: 1.04, 1.51) per natural log-unit increase, respectively. Risk of current asthma was > 70% higher among children with maternal prenatal BBzP and DnBP metabolite concentrations in the third versus the first tertile. Conclusion: Prenatal exposure to BBzP and DnBP may increase the risk of asthma among inner-city children. However, because this is the first such finding, results require replication.

Consideration of the relationship between residential floor level and concentration of traffic-related airborne pollutants may predict individual residential exposure among inner city dwellers more accurately. Our objective was to characterize the vertical gradient of residential levels of polycyclic aromatic hydrocarbons (PAH; dichotomized into Σ8PAHsemivolatile (MW 178–206), and Σ8PAHnonvolatile (MW 228–278), black carbon (BC), PM2.5 (particulate matter) by floor level (FL), season and building type. We hypothesize that PAH, BC and PM2.5 concentrations may decrease with higher FL and the vertical gradients of these compounds would be affected by heating season and building type. PAH, BC and PM2.5 were measured over a two-week period outdoor and indoor of the residences of a cohort of 5–6 year old children (n = 339) living in New York City’s Northern Manhattan and the Bronx. Airborne-pollutant levels were analyzed by three categorized FL groups (0–2nd, 3rd–5th, and 6th–32nd FL) and two building types (low-rise versus high-rise apartment building). Indoor Σ8PAHnonvolatile and BC levels declined with increasing FL. During the nonheating season, the median outdoor Σ8PAHnonvolatile, but not Σ8PAHsemivolatile, level at 6th–2nd FL was 1.5–2 times lower than levels measured at lower FL. Similarly, outdoor and indoor BC concentrations at 6th–32nd FL were significantly lower than those at lower FL only during the nonheating season (p less than 0.05). In addition, living in a low-rise building was associated significantly with higher levels of Σ8PAHnonvolatile and BC. These results suggest that young inner city children may be exposed to varying levels of air pollutants depending on their FL, season, and building type.

Background: Outdoor ambient polycyclic aromatic hydrocarbon (PAH) concentrations are variable throughout an urban environment. However, little is known about how variation in semivolatile and nonvolatile PAHs related to the built environment (open space vs. semi-closed space) contributes to differences in concentrations. Methods: We simultaneously collected 14, two-week samples of PAHs from the outside of windows facing the front (adjacent to the street) open side of a New York City apartment building and the alley, semi-closed side of the same apartment unit between 2007 and 2012. We also analyzed samples of PAHs measured from 35 homes across Northern Manhattan and the Bronx, 17 from street facing windows with a median floor level of 4 (range 2–26) and 18 from alley-facing windows with a median floor level of 4 (range 1–15). Results: Levels of nonvolatile ambient PAHs were significantly higher when measured from a window adjacent to a street (an open space), compared to a window 30 feet away, adjacent to an alley (a semi-closed space) (street geometric mean (GM) 1.32 ng/m3, arithmetic mean ± standard deviation (AM ± SD) 1.61 ± 1.04 ng/m3; alley GM 1.10 ng/m3, AM ± SD 1.37 ± 0.94 ng/m3). In the neighborhood-wide comparison, nonvolatile PAHs were also significantly higher when measured adjacent to streets compared with adjacent to alley sides of apartment buildings (street GM 1.10 ng/m3, AM ± SD 1.46 ± 1.24 ng/m3; alley GM 0.61 ng/m3, AM ± SD 0.81 ± 0.80 ng/m3), but not semivolatile PAHs. Conclusions: Ambient PAHs, nonvolatile PAHs in particular, are significantly higher when measured from a window adjacent to a street compared to a window adjacent to an alley, despite both locations being relatively close to street traffic. This study highlights small-scale spatial variations in ambient PAH concentrations that may be related to the built environment (open space vs. semi-closed space) from which the samples are measured, as well as the relative distance from street traffic, that could impact accurate personal exposure assessments.

Multiple studies have suggested that prenatal exposure to either allergens or air pollution may increase the risk for the development of allergic immune responses in young offspring. However, the effects of prenatal environmental exposures on adult offspring have not been well-studied. We hypothesized that combined prenatal exposure to Aspergillus fumigatus (A. fumigatus) allergen and diesel exhaust particles will be associated with altered IgE production, airway inflammation, airway hyperreactivity (AHR), and airway remodeling of adult offspring. Following sensitization via the airway route to A. fumigatus and mating, pregnant BALB/c mice were exposed to additional A. fumigatus and/or diesel exhaust particles. At age 9-10 weeks, their offspring were sensitized and challenged with A. fumigatus. We found that adult offspring from mice that were exposed to A. fumigatus or diesel exhaust particles during pregnancy experienced decreases in IgE production. Adult offspring of mice that were exposed to both A. fumigatus and diesel exhaust particles during pregnancy experienced decreases in airway eosinophilia. These results suggest that, in this model, allergen and/or diesel administration during pregnancy may be associated with protection from developing systemic and airway allergic immune responses in the adult offspring.

The biological mechanisms responsible for the onset and exacerbation of asthma symptoms in children may involve the epigenetic regulation of inflammatory genes after environmental exposures. Using buccal cells, we hypothesized that DNA methylation in promoter regions of two asthma genes, inducible nitric oxide synthase (iNOS) and interferon γ (IFNγ), can vary over several days. Repeat buccal samples were collected 4 to 7 days apart from 34 children participating in the Columbia Center for Children's Environmental Health (CCCEH) birth cohort study. Several field duplicates (sequential collection of two samples in the field) and replicates (one sample pyrosequenced twice) also were collected to ensure consistency with collection and laboratory procedures. DNA methylation was assessed by pyrosequencing a PCR of bisulfite-treated DNA. We found that replicate and field duplicate samples were correlated strongly (r = 0.86 to 0.99, P < 0.05), while repeat samples demonstrated low within-subject correlations (r = 0.19 to 0.56, P = 0.06 to 0.30). Our data reveal DNA methylation as a dynamic epigenetic mechanism that can be accessed safely and reproducibly in an inner city pediatric cohort using non-invasive buccal swabs and pyrosequencing technology.

Background: Urban landscape elements, particularly trees, have the potential to affect airflow, air quality, and production of aeroallergens. Several large-scale urban tree planting projects have sought to promote respiratory health, yet evidence linking tree cover to human health is limited. Objectives: We sought to investigate the association of tree canopy cover with subsequent development of childhood asthma, wheeze, rhinitis, and allergic sensitization. Methods: Birth cohort study data were linked to detailed geographic information systems data characterizing 2001 tree canopy coverage based on LiDAR (light detection and ranging) and multispectral imagery within 0.25 km of the prenatal address. A total of 549 Dominican or African-American children born in 1998–2006 had outcome data assessed by validated questionnaire or based on IgE antibody response to specific allergens, including a tree pollen mix. Results: Tree canopy coverage did not significantly predict outcomes at 5 years of age, but was positively associated with asthma and allergic sensitization at 7 years. Adjusted risk ratios (RRs) per standard deviation of tree canopy coverage were 1.17 for asthma (95% CI: 1.02, 1.33), 1.20 for any specific allergic sensitization (95% CI: 1.05, 1.37), and 1.43 for tree pollen allergic sensitization (95% CI: 1.19, 1.72). Conclusions: Results did not support the hypothesized protective association of urban tree canopy coverage with asthma or allergy-related outcomes. Tree canopy cover near the prenatal address was associated with higher prevalence of allergic sensitization to tree pollen. Information was not available on sensitization to specific tree species or individual pollen exposures, and results may not be generalizable to other populations or geographic areas.

The application of benzo(a)pyrene (BaP)-toxic equivalent factor to polycyclic aromatic hydrocarbons (PAH) concentrations can provide a more accurate risk assessment from environmental exposure to PAH. We hypothesized that BaP-equivalent toxicity determined following residential air monitoring among young urban children may vary by season. Residential indoor and outdoor air levels of PAH measured over two-weeks in a cohort of 5–6 year old children (n = 260) in New York City were normalized to the cancer and mutagen potency equivalent factor of BaP (BaP = 1). Data are presented as carcinogenic equivalents (BaP-TEQ) and mutagenic equivalents (BaP-MEQ) for the sum of 8 PAH (∑8PAH; MW ³ 228) and individual PAH and compared across heating versus nonheating seasons. Results show that heating compared to nonheating season was associated significantly with higher (BaP-TEQ)∑8PAH and (BaP-MEQ)∑8PAH both indoors and outdoors (p less than 0.001). Outdoor (BaP-TEQ)∑8PAH and (BaP-MEQ)∑8PAH were significantly higher than the corresponding indoor measures during the heating season (p less than 0.01). These findings suggest that at levels encountered in New York City air, especially during the heating season, residential exposure to PAH may pose an increased risk of cancer and mutation.