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[Display omitted] Rhinitis is a prevalent, chronic nasal condition associated with asthma. However, its developmental trajectories remain poorly characterized. We sought to describe the course of rhinitis from infancy to adolescence and the association between identified phenotypes, asthma-related symptoms, and physician-diagnosed asthma. We collected rhinitis data from questionnaires repeated across 22 time points among 688 children from infancy to age 11 years and used latent class mixed modeling (LCMM) to identify phenotypes. Once children were between ages 5 and 12, a study physician determined asthma diagnosis. We collected information on the following asthma symptoms: any wheeze, exercise-induced wheeze, nighttime coughing, and emergency department visits. For each, we used LCMM to identify symptom phenotypes. Using logistic regression, we described the association between rhinitis phenotype and asthma diagnosis and each symptom overall and stratified by atopic predisposition and sex. LCMM identified 5 rhinitis trajectory groups: never/infrequent; transient; late onset, infrequent; late onset, frequent; and persistent. LCMM identified 2 trajectories for each symptom, classified as frequent and never/infrequent. Participants with persistent and late onset, frequent phenotypes were more likely to be diagnosed with asthma and to have the frequent phenotype for all symptoms (P <.01). We identified interaction between seroatopy and rhinitis phenotype for physician-diagnosed asthma (P =.04) and exercise-induced wheeze (P =.08). Severe seroatopy was more common among children with late onset, frequent and persistent rhinitis, with nearly 25% of these 2 groups exhibiting sensitivity to 4 or 5 of the 5 allergens tested. In this prospective, population-based birth cohort, persistent and late onset, frequent rhinitis phenotypes were associated with increased risk of asthma diagnosis and symptoms during adolescence. [ABSTRACT FROM AUTHOR]

[Display omitted] Descriptive epidemiological data on incidence rates (IRs) of asthma with recurrent exacerbations (ARE) are sparse. This study hypothesized that IRs for ARE would vary by time, geography, age, and race and ethnicity, irrespective of parental asthma history. The investigators leveraged data from 17,246 children born after 1990 enrolled in 59 US with 1 Puerto Rican cohort in the Environmental Influences on Child Health Outcomes (ECHO) consortium to estimate IRs for ARE. The overall crude IR for ARE was 6.07 per 1000 person-years (95% CI: 5.63-6.51) and was highest for children aged 2-4 years, for Hispanic Black and non-Hispanic Black children, and for those with a parental history of asthma. ARE IRs were higher for 2- to 4-year-olds in each race and ethnicity category and for both sexes. Multivariable analysis confirmed higher adjusted ARE IRs (aIRRs) for children born 2000-2009 compared with those born 1990-1999 and 2010-2017, 2-4 versus 10-19 years old (aIRR = 15.36; 95% CI: 12.09-19.52), and for males versus females (aIRR = 1.34; 95% CI 1.16-1.55). Black children (non-Hispanic and Hispanic) had higher rates than non-Hispanic White children (aIRR = 2.51; 95% CI 2.10-2.99; and aIRR = 2.04; 95% CI: 1.22-3.39, respectively). Children born in the Midwest, Northeast and South had higher rates than those born in the West (P <.01 for each comparison). Children with a parental history of asthma had rates nearly 3 times higher than those without such history (aIRR = 2.90; 95% CI: 2.43-3.46). Factors associated with time, geography, age, race and ethnicity, sex, and parental history appear to influence the inception of ARE among children and adolescents. [ABSTRACT FROM AUTHOR]

The last 2 years yielded a proliferation of high-quality asthma research. These include new understandings of the incidence and natural history of asthma, findings on the effects of exposure to air pollution, allergens, and intake of acetaminophen, soy isoflavones, and polyunsaturated fatty acids, and exposure to microbial products. The past 2 years have benefited from great strides in determining potential mechanisms of asthma development and asthma exacerbations. These novel understandings led to identification and development of exciting new avenues for potential therapeutic intervention. Finally, there has been significant progress made in the development of tools to facilitate the diagnosis of asthma and measurement of airway physiology and in precision diagnostic approaches. Asthma guidelines were updated and new insights into the pharmacologic management of patients, including biologics, were reported. We review the most notable advances in the natural history of asthma, risk factors for the development of asthma, underlying mechanisms, diagnostic approaches, and treatments. Although greater knowledge of the mechanisms underlying responses and nonresponses to novel therapeutics and across asthma phenotypes would be beneficial, the progress over just the past 2 years has been immense and impactful. [ABSTRACT FROM AUTHOR]

Few studies have examined longitudinal asthma incidence rates (IRs) from a public health surveillance perspective. Our aim was to calculate descriptive asthma IRs in children over time with consideration for demographics and parental asthma history. Data from 9 US birth cohorts were pooled into 1 population covering the period from 1980 to 2017. The outcome was earliest parental report of a doctor diagnosis of asthma. IRs per 1,000 person-years were calculated. The racial/ethnic backgrounds of the 6,283 children studied were as follows: 55% European American (EA), 25.5% African American (AA), 9.5% Mexican-Hispanic American (MA) and 8.5% Caribbean-Hispanic American (CA). The average follow-up was 10.4 years (SD = 8.5 years; median = 8.4 years), totaling 65,291 person-years, with 1789 asthma diagnoses yielding a crude IR of 27.5 per 1,000 person-years (95% CI = 26.3-28.8). Age-specific rates were highest among children aged 0 to 4 years, notably from 1995 to 1999, with a decline in EA and MA children in 2000 to 2004 followed by a decline in AA and CA children in 2010 to 2014. Parental asthma history was associated with statistically significantly increased rates. IRs were similar and higher in AA and CA children versus lower but similar in EA and MA children. The differential rates by sex from birth through adolescence principally resulted from a decline in rates among males but relatively stable rates among females. US childhood asthma IRs varied dramatically by age, sex, parental asthma history, race/ethnicity, and calendar year. Higher rates in the 0- to 4-year-olds group, particularly among AA/CA males with a parental history of asthma, as well as changes in rates over time and by demographic factors, suggest that asthma is driven by complex interactions between genetic susceptibility and variation in time-dependent environmental and social factors. [ABSTRACT FROM AUTHOR]

Many notable advances in drug allergy, urticaria, angioedema, and anaphylaxis were reported in 2018. Broad-spectrum antibiotic use and, consequently, antibiotic resistance are widespread, and algorithms to clarify β-lactam allergy and optimize antibiotic use were described. Meaningful data emerged on the pathogenesis of delayed drug hypersensitivity reactions. Progress not only in defining biomarkers but also in understanding the effect on quality of life and developing better treatments has been made for patients with chronic idiopathic urticaria. Patients with hereditary angioedema (HAE) have gained additional access to highly efficacious therapies, with associated improvements in quality of life, and some progress was made in our understanding of recurrent angioedema in patients with normal laboratory results. Guidelines have defined clear goals to help providers optimize therapies in patients with HAE. The epidemiology and triggers of anaphylaxis and the mechanisms underlying anaphylaxis were elucidated further. In summary, these disorders (and labels) cause substantial burdens for individual persons and even society. Fortunately, publications in 2018 have informed on advancements in diagnosis and management and have provided better understanding of mechanisms that potentially could yield new therapies. This progress should lead to better health outcomes and paths forward in patients with drug allergy, urticaria, HAE, and anaphylaxis. [ABSTRACT FROM AUTHOR]

Although real-time personal exposure monitoring devices have the ability to capture a wealth of data regarding fluctuations in pollutant levels, only a few studies have defined 'peaks' in black carbon (BC) exposure utilizing high-resolution data. Furthermore, studies to assess and characterize various features of peak exposure are very limited especially among children. A better understanding of characteristics of BC peak exposure would improve our understanding of health risks associated with BC. By capturing personal BC exposure at 5-min intervals using a real-time monitor during 24-hr monitoring periods among children in New York City (NYC), we defined 'peak characteristics' in 4 different ways across three major microenvironments (school vs. commute vs. home): 1) mean concentrations of BC across the 3 microenvironments, 2) 'p eak duration ' or time spent above the peak threshold (i.e., ≥1.5 μg/m3), 3) 'p eak intensity ' or the rate of exposure, defined as time spent above the threshold within each microenvironment divided by the total time spent in the microenvironment and 4) a novel metric of ' peak variability ', defined as frequency of peaks (i.e., data points with +50% and −50% changes compared to the preceding and the subsequent data points), divided by the total time spent in the microenvironment. While peak duration was greatest at home, the intensity of peak exposure was greatest during commute hours, despite the short time spent in commute (p < 0.05). Peak variability was highest during commute, yet lowest in home environments (p < 0.05), particularly during non-sleeping hours. Children residing in a high-density urban setting spent on average, 5.4 hr per day above our peak threshold (≥1.5 μg/m3) in their everyday environments. Policies that limit children's exposure during high traffic periods and improved efforts to increase the number of vehicles using clean air technology could reduce the intensity of peaks and peak variability in children's BC exposure. [Display omitted] • Children are exposed to high black carbon (BC) in different microenvironments. • Average BC concentration was higher during commute compared to school or home. • Peak duration , or time spent above the BC peak threshold, was highest at home. • Peak intensity , or the rate of exposure, was greatest during commute. • Peak variability , or rapid fluctuations in BC, was highest during commute, yet lowest in the home environment. [ABSTRACT FROM AUTHOR]

Despite attempts and some successes to improve air quality over the decades, current US national trends suggest that exposure to outdoor and indoor air pollution remains a significant risk factor for both the development of asthma and the triggering of asthma symptoms. Emerging science also suggests that environmental exposures during the prenatal period and early childhood years increase the risk of asthma. Multiple mechanisms mediate this risk because a wide range of deleterious air pollutants contribute to the pathogenesis of asthma across a variety of complex asthma phenotypes. In this review we will consider the role of altered innate and adaptive immune responses, gene-environment interactions, epigenetic regulation, and possibly gene-environment-epigene interactions. Gaining a greater understanding of the mechanisms that underlie the effect of exposure to air pollution on asthma, allergies, and other airway diseases can identify targets for therapy. Such interventions will include pollutant source reduction among those most exposed and most vulnerable and novel pharmaceutical strategies to reduce asthma morbidity. [ABSTRACT FROM AUTHOR]

Summary: Background: Previously, we reported that prenatal exposures to polycyclic aromatic hydrocarbons (PAH) and postnatal environmental tobacco smoke (ETS) in combination were associated with respiratory symptoms at ages 1 and 2 years. Here, we hypothesized that children exposed to both prenatal PAH and ETS may be at greater risk of asthma and seroatopy at ages 5–6 years, after controlling for current pollution exposure. Methods: Prenatal PAH exposure was measured by personal air monitoring over 48 h. ETS exposure, respiratory symptoms and asthma at ages 5–6 years were assessed through questionnaire. Immunoglobulin (Ig) E was measured by Immunocap. Results: A significant interaction between prenatal PAH and prenatal (but not postnatal) ETS exposure on asthma (p < 0.05), but not IgE, was detected. Among children exposed to prenatal ETS, a positive nonsignificant association was found between prenatal PAH exposure and asthma (OR 1.96, 95% CI [0.95–4.05]). Among children without exposure to prenatal ETS, a negative nonsignificant association was found between prenatal PAH exposure and asthma (OR 0.65, 95% CI [0.41–1.01]). Prenatal PAH exposure was not associated with asthma or IgE at age 5–6 years. Conclusions: Combined prenatal exposure to PAH and ETS appears to be associated with asthma but not seroatopy at age 5–6. Exposure to PAH alone does not appear associated with either asthma or seroatopy at age 5–6 years. Discerning the differential effects between ETS exposed and ETS nonexposed children requires further study. [Copyright &y& Elsevier]

Background: The relationships between cockroach and mouse allergen exposure, anti-cockroach and anti-mouse IgE, and wheeze, rhinitis, and atopic dermatitis in children as young as age 3 years are of public health importance but have not been thoroughly evaluated. Objective: We hypothesized that inner-city children might have anti-cockroach and anti-mouse IgE by age 3 years, and their presence would be associated with respiratory and atopic symptoms. Methods: Children were followed prospectively from birth through age 3 years (n = 404). Residential levels of cockroach and mouse allergens, sera levels of anti-cockroach and anti-mouse IgE, and parental report of wheeze, rhinitis, and atopic dermatitis were measured. Results: The odds of early wheeze were significantly higher among children who had IgE to cockroach (odds ratio [OR], 3.3; 95% CI, 1.8-6.2), mouse (OR, 4.6; 95% CI, 2.3-9.0), or both (OR, 9.7; 95% CI, 3.4-27.3). The odds of rhinitis or atopic dermatitis were also higher among children with IgE to cockroach, mouse, or both. Higher IgE class to cockroach and mouse was associated with wheeze and atopic dermatitis (tests for trend, P < .002). Conclusions: Children age 2 to 3 years who have anti-cockroach and anti-mouse IgE are at increased risk of wheeze and atopy. Moreover, a dose-response relationship was found between higher IgE class and increased prevalence of wheeze, rhinitis, or atopic dermatitis. These findings indicate the importance of reducing exposure to cockroach and mouse allergens for susceptible children. [Copyright &y& Elsevier]

Background: Cat ownership is inversely associated with atopy and asthma in some areas of the world, but the relevance of cat ownership to allergic disease in the inner city is less known. Objective: We sought to evaluate the relationship between cat ownership and the development of early sensitization and wheeze. Methods: By using a prospective birth cohort study, Dominican and African American mothers living in New York City underwent repeated questionnaires about their child from birth to age 5 years. Sera collected from children at ages 2 (n = 323), 3 (n = 336), and 5 (n = 242) years were assayed for anti-cat IgE and anti–Fel d 1 IgG antibodies. Results: Cat ownership was a significant risk factor for the development of anti-cat IgE by age 2 years (risk ratio [RR], 6.4; 95% CI, 1.9-22) but not for anti-cat IgE development between the ages of 2 and 5 years (RR, 0.88; 95% CI, 0.24-2.3). Current wheeze was significantly more common among those children with anti-cat IgE at ages 3 (RR, 3.5; 95% CI, 2.1-6.0) and 5 (RR, 3.4; 95% CI, 2.3-4.9) years. Cat ownership was inversely associated with current wheeze at age 5 years among children without anti-cat IgE (RR, 0.26; 95% CI, 0.083-0.81). Among children with anti-cat IgE, a similar trend was observed (RR, 0.57; P = .044, Fisher exact test), although one with borderline statistical significance. Conclusions: Despite a positive association with sensitization, cat ownership in this inner-city cohort was inversely associated with wheeze, potentially suggesting an IgE-independent protective mechanism in this community. [Copyright &y& Elsevier]

Background: An inverse association between domestic exposure to endotoxin and atopy in childhood has been observed. The relevance of this aspect of the hygiene hypothesis to US inner-city communities that have disproportionately high asthma prevalence has not been determined. Objectives: To measure endotoxin in the dust from inner-city homes, evaluate associations between endotoxin and housing/lifestyle characteristics, and determine whether endotoxin exposure predicted wheeze, allergic rhinitis, and eczema over the first 3 years of life. Methods: As part of an ongoing prospective birth cohort study, children of Dominican and African-American mothers living in New York City underwent repeated questionnaire measures. Dust samples collected from bedroom floors at age 12 or 36 months were assayed for endotoxin. Results: Among the samples collected from 301 participants'' homes, the geometric mean endotoxin concentration (95% CI) was 75.9 EU/mg (66-87), and load was 3892 EU/m2 (3351-4522). Lower endotoxin concentrations were associated with wet mop cleaning and certain neighborhoods. Endotoxin concentration correlated weakly with cockroach (Bla g 2: r = 0.22, P < .001) and mouse (mouse urinary protein: r = 0.28; P < .001) allergens in the dust. Children in homes with higher endotoxin concentration were less likely to have eczema at age 1 year (odds ratio, 0.70 [0.53-0.93]) and more likely to wheeze at age 2 years (odds ratio, 1.34 [1.01-1.78]). These associations were stronger among children with a maternal history of asthma. Conclusion: Endotoxin levels in this inner-city community are similar to those in nonfarm homes elsewhere. In this community, domestic endotoxin exposure was inversely associated with eczema at age 1 year, but positively associated with wheeze at age 2 years. Clinical implications: Endotoxin exposure in the inner-city community may be related to wheeze in the early life; however, given the inverse association seen with eczema, the long-term development of allergic disease is still in question. [Copyright &y& Elsevier]

Background Although maternal atopy is a risk factor for the development of peanut allergy, this phenomenon has not been well characterized experimentally, and the mechanisms underlying offspring risk are unclear. Objective We sought to determine whether offspring of mothers with peanut allergy (O-PAM mice) are more susceptible to peanut allergy than offspring of naive mothers (O-NM mice) in a murine model and, if so, whether the susceptibility is linked to T H 2-biased epigenetic alterations. Methods Five-week-old O-PAM and O-NM mice were intragastrically sensitized to and challenged with peanut. Serum peanut-specific IgE levels, plasma histamine levels, anaphylactic reactions, and splenocyte and MLN cell cytokine production were measured. DNA methylation levels of the Il4 gene promoter from splenocytes and MLN cells from sensitized offspring and splenocytes from unsensitized neonatal offspring were determined by means of pyrosequencing. Results O-PAM mice exhibited 3-fold higher peanut-specific IgE levels after peanut sensitization, as well as 5-fold higher histamine levels and significantly higher anaphylactic symptom scores after challenge than O-NM mice ( P < .05-.01). Cultured splenocytes and MLNs from O-PAM mice produced significantly more T H 2 cytokines than cells from O-NM mice ( P < .05-.01). Cells from O-PAM mice exhibited significantly reduced DNA methylation at CpG sites of the Il4 gene promoter than cells from O-NM mice. DNA methylation levels were inversely correlated with IL-4 and IgE production. O-PAM neonatal splenocyte hypomethylation of the Il4 gene promoter was also present. Conclusion This study is the first to demonstrate that increased susceptibility to peanut allergy in O-PAM mice is associated with epigenetic alteration of the Il4 gene promoter. This finding might provide insight into preventing the development of early-life allergy. [ABSTRACT FROM AUTHOR]

Studies the relationship between patent foramen ovale (PFO) and perfusion abnormalities in acute pulmonary embolism. Patient characteristics; Experimental procedure; Association of PFO with frequent tricuspid regurgitation; Correlation of degree of vascular obstruction on pulmonary angiogram.

Background: Sensitization to cockroach is one of the strongest identified risk factors for greater asthma morbidity in low-income urban communities; however, the timing of exposures relevant to the development of sensitization has not been elucidated fully. Furthermore, exposure to combustion byproducts, including polycyclic aromatic hydrocarbons (PAHs), can augment the development of allergic sensitization. Objective: We sought to test the hypotheses that domestic cockroach allergen measured prenatally would predict cockroach sensitization in early childhood and that this association would be greater for children exposed to higher PAH concentrations. Methods: Dominican and African American pregnant women living in New York City were enrolled. In the third trimester expectant mothers wore personal air samplers for measurement of 8 nonvolatile PAHs and the semivolatile PAH pyrene, and dust was collected from homes for allergen measurement. Glutathione-S-transferase μ 1 (GSTM1) gene polymorphisms were measured in children. Allergen-specific IgE levels were measured from the children at ages 2, 3, 5, and 7 years. Results: Bla g 2 in prenatal kitchen dust predicted cockroach sensitization at the ages of 5 to 7 years (adjusted relative risk [RR], 1.15; P = .001; n = 349). The association was observed only among children with greater than (RR, 1.22; P = .001) but not less than (RR, 1.07; P = .24) the median sum of 8 nonvolatile PAH levels. The association was most pronounced among children with higher PAH levels and null for the GSTM1 gene (RR, 1.54; P = .001). Conclusions: Prenatal exposure to cockroach allergen was associated with a greater risk of allergic sensitization. This risk was increased by exposure to nonvolatile PAHs, with children null for the GSTM1 mutation particularly vulnerable. [Copyright &y& Elsevier]

Background: Bisphenol A (BPA) is used widely to manufacture food container linings. Mouse models suggest exposure to BPA might increase allergic inflammation. Objectives: We hypothesized that BPA exposure, as assessed based on urinary BPA concentrations, would be associated with increased odds of wheeze and asthma and increased fraction of exhaled nitric oxide (Feno) values in children. Methods: The Columbia Center for Children''s Environmental Health recruited pregnant women for a prospective birth cohort study (n = 568). Mothers during the third trimester and children at ages 3, 5, and 7 years provided spot urine samples. Total urinary BPA concentrations were measured by using online solid-phase extraction, high-performance liquid chromatography, isotope-dilution tandem mass spectrometry. Wheeze in the last 12 months was measured by using questionnaires at ages 5, 6, and 7 years. Asthma was determined by a physician once between ages 5 and 12 years. Feno values were measured at ages 7 to 11 years. Results: Prenatal urinary BPA concentrations were associated inversely with wheeze at age 5 years (odds ratio [OR], 0.7; 95% CI, 0.5-0.9; P = .02). Urinary BPA concentrations at age 3 years were associated positively with wheeze at ages 5 years (OR, 1.4; 95% CI, 1.1-1.8; P = .02) and 6 years (OR, 1.4; 95% CI, 1.0-1.9; P = .03). BPA concentrations at age 7 years were associated with wheeze at age 7 years (OR, 1.4; 95% CI, 1.0-1.9; P = .04) and Feno values (β = 0.1; 95% CI, 0.02-0.2; P = .02). BPA concentrations at ages 3, 5, and 7 years were associated with asthma (OR, 1.5 [95% CI, 1.1-2.0], P = .005; OR, 1.4 [95% CI, 1.0-1.9], P = .03; and OR, 1.5 [95% CI, 1.0-2.1], P = .04, respectively). Conclusions: This is the first report of an association between postnatal urinary BPA concentrations and asthma in children. [Copyright &y& Elsevier]

Background: Asthma prevalence varies widely among neighborhoods within New York City. Exposure to mouse and cockroach allergens has been suggested as a cause. Objective: To test the hypotheses that children living in high asthma prevalence neighborhoods (HAPNs) would have higher concentrations of cockroach and mouse allergens in their homes than children in low asthma prevalence neighborhoods (LAPNs), and that these exposures would be related to sensitization and asthma. Methods: In the New York City Neighborhood Asthma and Allergy Study, a case-control study of asthma, children 7 to 8 years old from HAPNs (n = 120) and LAPNs (n = 119) were recruited through the same middle-income health insurance plan. Children were classified as asthma cases (n = 128) or controls without asthma (n = 111) on the basis of reported symptoms or medication use. Allergens were measured in bed dust. Results: HAPN homes had higher Bla g 2 (P = .001), Mus m 1 (P = .003), and Fel d 1 (P = .003) and lower Der f 1 (P = .001) than LAPN homes. Sensitization to indoor allergens was associated with asthma, but relevant allergens differed between LAPNs and HAPNs. Sensitization to cockroach was more common among HAPN than LAPN children (23.7% vs 10.8%; P = .011). Increasing allergen exposure was associated with increased probability of sensitization (IgE) to cockroach (P < .001), dust mite (P = .009), and cat (P = .001), but not mouse (P = .58) or dog (P = .85). Conclusion: These findings further demonstrate the relevance of exposure and sensitization to cockroach and mouse in an urban community and suggest that cockroach allergen exposure could contribute to the higher asthma prevalence observed in some compared with other New York City neighborhoods. [ABSTRACT FROM AUTHOR]

Two messenger RNA (mRNA)-based vaccines are widely used globally to prevent coronavirus disease 2019 (COVID-19). Both vaccine formulations contain PEGylated lipids in their composition, in the form of polyethylene glycol [PEG] 2000 dimyristoyl glycerol for mRNA-1273, and 2 [(polyethylene glycol)-2000]-N, N -ditetradecylacetamide for BNT162b2. It is known that some PEGylated drugs and products for human use which contain PEG are capable of eliciting immune responses that lead to to detectable PEG-specific antibodies in serum. In this study, we determined if any of the components of mRNA-1273 or BNT162b2 formulations elicited PEG-specific antibody responses in serum by enzyme linked immunosorbent assay (ELISA). We detected an increase in the reactivity to mRNA vaccine formulations in mRNA-1273 but not BNT162b2 vaccinees' sera in a prime-boost dependent manner. Furthermore, we observed the same pattern of reactivity against irrelevant lipid nanoparticles from an influenza virus mRNA formulation and found that the reactivity of such antibodies correlated well with antibody levels against high and low molecular weight PEG. Using sera from participants selected based on the vaccine-associated side effects experienced after vaccination, including delayed onset, injection site or severe allergic reactions, we found no obvious association between PEG antibodies and adverse reactions. Overall, our data shows a differential induction of anti-PEG antibodies by mRNA-1273 and BNT162b2. The clinical relevance of PEG reactive antibodies induced by administration of the mRNA-1273 vaccine, and the potential interaction of these antibodies with other PEGylated drugs remains to be explored. [ABSTRACT FROM AUTHOR]

Abstract: Exposure of black carbon (BC) is associated with a variety of adverse health outcomes. A number of optical methods for estimating BC on Teflon filters have been adopted but most assume all light absorption is due to BC while other sources of colored particulate matter exist. Recently, a four-wavelength-optical reflectance measurement for distinguishing second hand cigarette smoke (SHS) from soot-BC was developed (Brook et al., 2010; Lawless et al., 2004). However, the method has not been validated for soot-BC nor SHS and little work has been done to look at the methodological issues of the optical reflectance measurements for samples that could have SHS, BC, and other colored particles. We refined this method using a lab-modified integrating sphere with absorption measured continuously from 350 nm to 1000 nm. Furthermore, we characterized the absorption spectrum of additional components of particulate matter (PM) on PM2.5 filters including ammonium sulfate, hematite, goethite, and magnetite. Finally, we validate this method for BC by comparison to other standard methods. Use of synthesized data indicates that it is important to optimize the choice of wavelengths to minimize computational errors as additional components (more than 2) are added to the apportionment model of colored components. We found that substantial errors are introduced when using 4 wavelengths suggested by Lawless et al. to quantify four substances, while an optimized choice of wavelengths can reduce model-derived error from over 10% to less than 2%. For environmental samples, the method was sensitive for estimating airborne levels of BC and SHS, but not mass loadings of iron oxides and sulfate. Duplicate samples collected in NYC show high reproducibility (points consistent with a 1:1 line, R 2 = 0.95). BC data measured by this method were consistent with those measured by other optical methods, including Aethalometer and Smoke-stain Reflectometer (SSR); although the SSR looses sensitivity at filter loadings above 90 ng/mm2. Furthermore, positive correlations (R 2 = 0.7) were observed between EC measured by NIOSH Method 5040 on quartz filters and BC measured in co-located Teflon filter samples collected from both heating and non-heating seasons. Overall, the validation data demonstrates the usefulness of this method to evaluate BC from archived Teflon filters while potentially providing additional component information. [Copyright &y& Elsevier]

• Schools in historically redlined neighborhoods had higher levels of air pollutants, compared to those in other neighborhoods. • Levels of combustion-related air pollutants near New York City schools declined from 2009 to 2018. • Decreasing trend was less apparent in historically redlined neighborhoods. • Historical discriminatory practices still affect current environmental inequity in New York City. In the 1930's the United States (US) sponsored Home Owners' Loan Corporation (HOLC) created maps that determined risk for mortgage lending based on the racial and ethnic composition of neighborhoods leading to disinvestment in "redlined" or highest risk neighborhoods. This historical practice has perpetuated racial and economic segregation, and health disparities, that persist today. Interventions near schools where children spend large portions of the day, could impact large groups of children but schools are an often-overlooked environment for exposure. Despite a declining trend of ambient pollution in New York City (NYC) between 1998 and 2012, little is known about differences in air quality improvement near schools by historical redlining neighborhood status. Our objective was to examine if recent temporal trends of air pollution near NYC public schools differed in historically redlined neighborhoods. We examined annual average street-level concentrations of combustion-related air pollutants (black carbon (BC), particulate matter (PM 2.5), nitrogen dioxide (NO 2), and nitric oxide (NO)), within a 250-m radius around schools using NYC Community Air Survey land-use regression models (n = 1,462). Year of monitoring, historical redlining (binary), and summer ozone were included in multivariable linear regression using generalized estimating equation models. Average annual percent change (APC) in pollutant concentration was calculated. Models were further stratified by historical redlining and a multiplicative interaction term (year of monitoring × historical redlining) was used to assess effect modification. Overall, there was a decreasing trend of BC (APC = -4.40%), PM 2.5 (-3.92%), NO 2 (-2.76%), and NO (-6.20%) during the 10-year period. A smaller reduction of BC, PM 2.5 and NO was observed in redlined neighborhoods (n = 722), compared to others (n = 740): BC (APC: −4.11% vs −4.69%; P interaction < 0.01), PM 2.5 (-3.82% vs −4.11%; P interaction < 0.01), and NO (-5.73% vs −6.67%; P interaction < 0.01). Temporal trends of NO 2 did not differ by historical redlining (P interaction = 0.60). Despite significant reductions in annual average pollution concentrations across NYC, schools in historically redlined neighborhoods, compared to others, experienced smaller decrease in pollution, highlighting a potential ongoing ramification of the discriminatory practice. [ABSTRACT FROM AUTHOR]

Asthma is a heterogeneous airway inflammatory disease, which is associated with Th2 cytokine-driven inflammation and non-Th2, TNF-α mediated inflammation. Unlike Th2 mediated inflammation, TNF-α mediated asthma inflammation is generally insensitive to inhaled corticosteroids (ICS). ASHMITM, aqueous extract of three medicinal herbs— Ganoderma lucidum ( G. lucidum ), Sophora flavescens Ait ( S. flavescens ) and Glycyrrhiza uralensis Fischer ( G. uralensis ), showed a high safety profile and was clinically beneficial in asthma patients. It also suppresses both Th2 and TNF-α associated inflammation in murine asthma models. We previously determined that G. uralensis flavonoids are the key active compounds responsible for ASHMITM suppression of Th2 mediated inflammation. Until now, there are limited studies on anti-TNF-α compounds presented in ASHMITM. The objective of this study was to isolate and identify TNF-α inhibitory compounds in ASHMITM. Here we report that G. lucidum , but not the other two herbal extracts, S. flavescens or G. uralensis inhibited TNF-α production by murine macrophages; and that the methylene chloride (MC)–triterpenoid-enriched fraction, but not the polysaccharide-enriched fraction, contained the inhibitory compounds. Of the 15 triterpenoids isolated from the MC fraction, only ganoderic acid C1 (GAC1) significantly reduced TNF-α production by murine macrophages (RAW 264.7 cells) and peripheral blood mononuclear cells (PBMCs) from asthma patients. Inhibition was associated with down-regulation of NF-κB expression, and partial suppression of MAPK and AP-1 signaling pathways. Ganoderic acid C1 may have potential for treating TNF-α mediated inflammation in asthma and other inflammatory diseases. [ABSTRACT FROM AUTHOR]

Importance Polycyclic aromatic hydrocarbons are common carcinogenic and neurotoxic urban air pollutants. Toxic exposures, including air pollution, are disproportionately high in communities of color and frequently co-occur with chronic economic deprivation. Objectives We examined whether the association between child IQ and prenatal exposure to polycyclic aromatic hydrocarbons differed between groups of children whose mothers reported high vs. low material hardship during their pregnancy and through child age 5. We tested statistical interactions between hardships and polycyclic aromatic hydrocarbons, as measured by DNA adducts in cord blood, to determine whether material hardship exacerbated the association between adducts and IQ scores. Design Prospective cohort. Participants were recruited from 1998 to 2006 and followed from gestation through age 7 years. Setting Urban community (New York City) Participants A community-based sample of 276 minority urban youth Exposure measure Polycyclic aromatic hydrocarbon–DNA adducts in cord blood as an individual biomarker of prenatal polycyclic aromatic hydrocarbon exposure. Maternal material hardship self-reported prenatally and at multiple timepoints through early childhood. Main outcome measure Child IQ at 7 years assessed using the Wechsler Intelligence Scale for Children. Results Significant inverse effects of high cord PAH–DNA adducts on full scale IQ, perceptual reasoning and working memory scores were observed in the groups whose mothers reported a high level of material hardship during pregnancy or recurring high hardship into the child's early years, and not in those without reported high hardship. Significant interactions were observed between high cord adducts and prenatal hardship on working memory scores ( β = − 8.07, 95% CI (− 14.48, − 1.66)) and between high cord adducts and recurrent material hardship ( β = − 9.82, 95% CI (− 16.22, − 3.42)). Conclusion The findings add to other evidence that socioeconomic disadvantage can increase the adverse effects of toxic physical “stressors” like air pollutants. Observed associations between high cord adducts and reduced IQ were significant only among the group of children whose mothers reported high material hardship. These results indicate the need for a multifaceted approach to prevention. [ABSTRACT FROM AUTHOR]