RESUMO
Respiratory virus infections are related to over 80% of childhood asthma exacerbations. They enhance pro-inflammatory mediator release, especially for sensitized individuals exposed to pollens/molds. Using a time-series study design, we investigated possible effect modification by respiratory virus infections of the associations between aeroallergens/PM2.5 and asthma exacerbation rates. Outpatient, emergency department (ED), and inpatient visits for asthma exacerbation among children with asthma (28,540/24,444 [warm/cold season]), as well as viral infection counts were obtained from electronic health records of the Children's Hospital of Philadelphia from 2011 to 2016. Rate ratios (RRs, 90th percentile vs. 0) for late-season grass pollen were 1.00 (0.85-1.17), 1.04 (0.95-1.15), and 1.12 (0.96-1.32), respectively, for respiratory syncytial virus (RSV) counts within each tertile. However, similar trends were not observed for weed pollens/molds or PM2.5. Overall, our study provides little evidence supporting effect modification by respiratory viral infections.
Assuntos
Poluentes Atmosféricos , Alérgenos , Asma , Material Particulado , Infecções Respiratórias , Humanos , Asma/epidemiologia , Criança , Material Particulado/análise , Philadelphia/epidemiologia , Alérgenos/imunologia , Masculino , Feminino , Pré-Escolar , Infecções Respiratórias/epidemiologia , Infecções Respiratórias/virologia , Infecções Respiratórias/imunologia , Poluentes Atmosféricos/análise , Adolescente , Estações do Ano , Pólen/imunologia , LactenteRESUMO
Although prediagnostic circulating concentrations of the immune activation markers soluble CD27 (sCD27), sCD30 and chemokine ligand-13 (CXCL13) have been associated with non-Hodgkin lymphoma (NHL) risk, studies have been limited by sample size in associations with NHL subtypes. We pooled data from eight nested case-control studies to investigate subtype-specific relationships for these analytes. Using polytomous regression, we calculated odds ratios (ORs) with 95% confidence intervals (CIs) relating study-specific analyte tertiles to selected subtypes vs controls (n = 3310): chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL; n = 623), diffuse large B cell lymphoma (DLBCL; n = 621), follicular lymphoma (FL; n = 398), marginal zone lymphoma (MZL; n = 138), mantle cell lymphoma (MCL; n = 82) and T cell lymphoma (TCL; n = 92). We observed associations with DLBCL for elevated sCD27 [OR for third vs first tertile (ORT3 ) = 2.2, 95% CI = 1.6-3.1], sCD30 (ORT3 = 2.0, 95% CI = 1.6-2.5) and CXCL13 (ORT3 = 2.3, 95% CI = 1.8-3.0). We also observed associations with sCD27 for CLL/SLL (ORT3 = 3.3, 95% CI = 2.4-4.6), MZL (ORT3 = 7.7, 95% CI = 3.0-20.1) and TCL (ORT3 = 3.4, 95% CI = 1.5-7.7), and between sCD30 and FL (ORT3 = 2.7, 95% CI = 2.0-3.5). In analyses stratified by time from phlebotomy to case diagnosis, the sCD27-TCL and all three DLBCL associations were equivalent across both follow-up periods (<7.5, ≥7.5 years). For other analyte-subtype comparisons, associations were stronger for the follow-up period closer to phlebotomy, particularly for indolent subtypes. In conclusion, we found robust evidence of an association between these immune markers and DLBCL, consistent with hypotheses that mechanisms related to immune activation are important in its pathogenesis. Our other findings, particularly for the rarer subtypes MZL and TCL, require further investigation.
Assuntos
Leucemia Linfocítica Crônica de Células B , Linfoma Folicular , Linfoma Difuso de Grandes Células B , Linfoma de Célula do Manto , Linfoma não Hodgkin , Adulto , Humanos , Leucemia Linfocítica Crônica de Células B/complicações , Linfoma não Hodgkin/etiologia , Biomarcadores , Estudos de Casos e ControlesRESUMO
While past research suggests that urban greenspace is associated with weaker income-based mortality inequities, little is known about associations with racial inequities, which may be distinct owing to historical and contemporary forms of racism. We quantified the extent to which different measures of greenspace modified socioeconomic and racial/ethnic inequities in all-cause and cardiovascular disease mortality. For every residential census tract in Philadelphia, PA (N = 376), we linked counts of all-cause and cardiovascular mortality (years 2008-2015) with measures of greenspace (proportion tree canopy or grass/shrub cover, proportion residents reporting park access, and the normalized difference vegetation index measure of overall greenness) and American Community Survey-based measures of sociodemographic composition (proportion of residents living in poverty, proportion identifying as non-Hispanic Black, and the index of concentration at the extremes (ICE) representing racialized economic deprivation). We used age- and sex-adjusted negative binomial models, with the natural logarithm of age-specific population counts as an offset, to quantify the magnitude of inequities by each composition variable, overall and stratified by categories of each greenspace measure. Inequities in mortality were weaker among neighborhoods with higher proportion grass/shrub cover or overall greenness. The most substantially narrowed inequities were those by the ICE. Mortality inequities did not differ substantially by perceived park access, and tree canopy was associated with weaker ICE-based inequities only. In this ecologic analysis, neighborhood greenspace was associated with weaker mortality inequities. However, associations varied across greenspace type and sociodemographic composition metrics, with generally stronger associations with overall greenness and grass/shrub coverage, and for ICE-basedinequities.
Assuntos
Parques Recreativos , Pobreza , Humanos , Philadelphia/epidemiologia , Renda , Características de Residência , ÁrvoresRESUMO
Fine particulate matter (PM2.5) and aeroallergens (i.e., pollen, molds) are known triggers of asthma exacerbation. Despite mechanistic evidence suggesting synergistic effects between PM2.5 and asthma exacerbation, little epidemiologic work has been performed in children, which has exhibited inconsistency. We conducted a time-series study to explore their interactions using electronic health records (EHR) data in Philadelphia, PA, for asthma diagnoses in outpatient, emergency department [ED], and inpatient settings. Daily asthma exacerbation cases (28,540 asthma exacerbation case encounters) were linked to daily ambient PM2.5 and daily aeroallergen levels during the aeroallergen season of a six-year period (mid-March to October 2011-2016). Asthma exacerbation counts were modeled using quasi-Poisson regression, where PM2.5 and aeroallergens were fitted with distributed lag non-linear functions (lagged from 0 to 14-days), respectively, when modeled as the primary exposure variables. Regression models were adjusted for mean daily temperature/relative humidity, long-term and seasonal trends, day-of-week, and major U.S. holidays. Increasing gradient of RR estimates were observed for only a few primary exposure risk factors [PM2.5 (90th vs. 5th percentile)/aeroallergens (90th percentile vs. 0)], across different levels of effect modifiers. For example, RRs for the association between late-season grass pollen (lag1) and asthma exacerbation were higher at higher levels of PM2.5, 5-days preceding the exacerbation event (low PM2.5: RR = 1.01, 95% CI: 0.93-1.09; medium PM2.5: 1.04, 95% CI: 0.96-1.12; high PM2.5: 1.09, 95% CI: 1.01-1.19). However, most of the highest RRs for aeroallergens were instead observed for days with low- or medium- PM2.5 levels; likewise, when PM2.5 was modeled as the primary exposure with aeroallergens as the effect modifier. Most of the RR estimates did not exhibit gradients that suggested synergism, and were of relatively high imprecision. Overall, our study suggested no evidence for interactions between PM2.5 and aeroallergens in their relationships with childhood asthma exacerbation.
Assuntos
Poluentes Atmosféricos , Poluição do Ar , Asma , Humanos , Criança , Poluentes Atmosféricos/toxicidade , Philadelphia , Asma/induzido quimicamente , Material Particulado/análise , Alérgenos/toxicidade , Poluição do Ar/análise , Exposição Ambiental/análiseRESUMO
Vegetation may influence asthma exacerbation through effects on aeroallergens, localized climates, air pollution, or children's behaviors and stress levels. We investigated the association between residential vegetation and asthma exacerbation by conducting a matched case-control study based on electronic health records of asthma patients, from the Children's Hospital of Philadelphia (CHOP). Our study included 17,639 exacerbation case events and 34,681 controls selected from non-exacerbation clinical visits for asthma, matched to cases by age, sex, race/ethnicity, public payment source, and residential proximity to the CHOP main campus ED and hospital. Overall greenness, tree canopy, grass/shrub cover, and impervious surface were assessed near children's homes (250 m) using satellite imagery and high-resolution landcover data. We used generalized estimating equations to estimate odds ratios (OR) and 95% confidence intervals (CI) for associations between each vegetation/landcover measure and asthma exacerbation, with adjustment for seasonal and sociodemographic factors-for all cases, and for cases defined by diagnosis setting and exacerbation frequency. Lower odds of asthma exacerbation were observed in association with greater levels of tree canopy near the home, but only for children who experienced multiple exacerbations in a year (OR = 0.94 per 10.2% greater tree canopy coverage, 95% CI = 0.90-0.99). Our findings suggest possible protection for asthma patients from tree canopy, but differing results by case frequency suggest that potential benefits may be specific to certain subpopulations of asthmatic children.
Assuntos
Poluição do Ar , Asma , Poluição do Ar/efeitos adversos , Asma/epidemiologia , Estudos de Casos e Controles , Criança , Humanos , Razão de Chances , ÁrvoresRESUMO
OBJECTIVES: High ambient temperatures may contribute to acute asthma exacerbation, a leading cause of morbidity in children. We quantified associations between hot-season ambient temperatures and asthma exacerbation in children ages 0-18 years in Philadelphia, PA. METHODS: We created a time series of daily counts of clinical encounters for asthma exacerbation at the Children's Hospital of Philadelphia linked with daily meteorological data, June-August of 2011-2016. We estimated associations between mean daily temperature (up to a 5-day lag) and asthma exacerbation using generalised quasi-Poisson distributed models, adjusted for seasonal and long-term trends, day of the week, mean relative humidity,and US holiday. In secondary analyses, we ran models with adjustment for aeroallergens, air pollutants and respiratory virus counts. We quantified overall associations, and estimates stratified by encounter location (outpatient, emergency department, inpatient), sociodemographics and comorbidities. RESULTS: The analysis included 7637 asthma exacerbation events. High mean daily temperatures that occurred 5 days before the index date were associated with higher rates of exacerbation (rate ratio (RR) comparing 33°C-13.1°C days: 1.37, 95% CI 1.04 to 1.82). Associations were most substantial for children ages 2 to <5 years and for Hispanic and non-Hispanic black children. Adjustment for air pollutants, aeroallergens and respiratory virus counts did not substantially change RR estimates. CONCLUSIONS: This research contributes to evidence that ambient heat is associated with higher rates of asthma exacerbation in children. Further work is needed to explore the mechanisms underlying these associations.
Assuntos
Poluentes Atmosféricos , Poluição do Ar , Asma , Adolescente , Poluentes Atmosféricos/efeitos adversos , Poluentes Atmosféricos/análise , Poluição do Ar/efeitos adversos , Poluição do Ar/análise , Alérgenos/efeitos adversos , Asma/epidemiologia , Asma/etiologia , Criança , Pré-Escolar , Temperatura Alta , Humanos , Lactente , Recém-Nascido , Philadelphia/epidemiologia , Temperatura , Fatores de TempoRESUMO
OBJECTIVES: Given mixed evidence for carcinogenicity of current-use herbicides, we studied the relationship between occupational herbicide use and risk of non-Hodgkin's lymphoma (NHL) in a large, pooled study. METHODS: We pooled data from 10 case-control studies participating in the International Lymphoma Epidemiology Consortium, including 9229 cases and 9626 controls from North America, the European Union and Australia. Herbicide use was coded from self-report or by expert assessment in the individual studies, for herbicide groups (eg, phenoxy herbicides) and active ingredients (eg, 2,4-dichlorophenoxyacetic acid (2,4-D), glyphosate). The association between each herbicide and NHL risk was estimated using logistic regression to produce ORs and 95% CIs, with adjustment for sociodemographic factors, farming and other pesticides. RESULTS: We found no substantial association of all NHL risk with ever-use of any herbicide (OR=1.10, 95% CI: 0.94 to 1.29), nor with herbicide groups or active ingredients. Elevations in risk were observed for NHL subtypes with longer duration of phenoxy herbicide use, such as for any phenoxy herbicide with multiple myeloma (>25.5 years, OR=1.78, 95% CI: 0.74 to 4.27), 2,4-D with diffuse large B-cell lymphoma (>25.5 years, OR=1.47, 95% CI: 0.67 to 3.21) and other (non-2,4-D) phenoxy herbicides with T-cell lymphoma (>6 years, lagged 10 years, OR=3.24, 95% CI: 1.03 to 10.2). An association between glyphosate and follicular lymphoma (lagged 10 years: OR=1.48, 95% CI: 0.98 to 2.25) was fairly consistent across analyses. CONCLUSIONS: Most of the herbicides examined were not associated with NHL risk. However, associations of phenoxy herbicides and glyphosate with particular NHL subtypes underscore the importance of estimating subtype-specific risks.
Assuntos
Herbicidas , Linfoma não Hodgkin , Exposição Ocupacional , Praguicidas , Humanos , Herbicidas/efeitos adversos , Exposição Ocupacional/efeitos adversos , Linfoma não Hodgkin/induzido quimicamente , Linfoma não Hodgkin/epidemiologia , Agricultura , Estudos de Casos e Controles , Fatores de RiscoRESUMO
Evidence for the human health effects of pesticides is needed to inform risk assessment. We studied the relationship between occupational insecticide use and risk of non-Hodgkin lymphoma (NHL) by pooling data from nine case-control studies participating in the InterLymph Consortium, including 7909 cases and 8644 controls from North America, the European Union and Australia. Insecticide use was coded using self-report or expert assessment, for insecticide groups (eg, organophosphates, pyrethroids) and active ingredients (eg, malathion, permethrin). Associations with insecticides were estimated using logistic regression to produce odds ratios (ORs) and 95% confidence intervals (CI) for all NHL and NHL subtypes, with adjustment for study site, demographic factors and use of other pesticides. Occupational insecticide use, overall, was not associated with risk of NHL. Use of organophosphate insecticides was associated with increased risk of all NHL and the subtype follicular lymphoma, and an association was found with diazinon, in particular (ever use: OR = 2.05, 95%CI: 1.24-3.37). The carbamate insecticide, carbaryl, was associated with risk of all NHL, and the strongest associations were found with T-cell NHL for ever-use (OR = 2.44, 95%CI: 1.13-5.28) and longer duration (>8 years vs never: OR = 2.90, 95%CI: 1.02-8.25). There was no association of NHL with other broad groups of insecticides, including organochlorines and pyrethroids, and some inverse associations were estimated in relation to historical DDT use. Our findings contribute to the totality of evidence available to help inform risk decisions by public health and regulatory agencies of importance given continued, widespread use of organophosphate and carbamate insecticides.
Assuntos
Inseticidas/intoxicação , Linfoma não Hodgkin/diagnóstico , Doenças Profissionais/diagnóstico , Exposição Ocupacional/efeitos adversos , Saúde Ocupacional/estatística & dados numéricos , Adulto , Idoso , Austrália , Estudos de Casos e Controles , União Europeia , Feminino , Humanos , Linfoma não Hodgkin/etiologia , Linfoma não Hodgkin/prevenção & controle , Masculino , Pessoa de Meia-Idade , América do Norte , Doenças Profissionais/etiologia , Doenças Profissionais/prevenção & controle , Exposição Ocupacional/análise , Razão de Chances , Medição de Risco/métodos , Medição de Risco/estatística & dados numéricos , Fatores de RiscoRESUMO
BACKGROUND: Water total trihalomethanes (TTHMs) are disinfectant byproducts found in municipal water supplies. TTHM exposure has been linked to cancer and may be associated with adverse reproductive outcomes. A non-optimal cervicovaginal microbiota and low cervicovaginal beta-defensin-2 levels are associated with increased risk of spontaneous preterm birth. Whether TTHM exposure increases the risk of spontaneous preterm birth or alters the cervicovaginal microbial or immune state is unknown. OBJECTIVE: Investigate associations of water TTHM levels with spontaneous preterm birth, a non-optimal cervicovaginal microbiota, and beta-defensin-2 levels in a completed, diverse, urban pregnancy cohort. We hypothesized that higher TTHM levels would be associated with spontaneous preterm birth, a non-optimal cervicovaginal microbiota, and lower beta-defensin-2 levels. DESIGN: Methods: This was a secondary analysis of participants (n = 474) in the Motherhood & Microbiome (M&M) study (n = 2000), who lived in Philadelphia and had cervicovaginal samples analyzed for cervicovaginal microbiota composition and beta-defensin-2 levels. The microbiota was classified into community state types (CSTs). CST IV (non-optimal microbiota) is characterized by a paucity of Lactobacillus species and wide array of anaerobes. Municipal water TTHM levels were obtained from 16 sites monthly across the city of Philadelphia to establish mean residential water supply levels for each participant for the first four months of pregnancy (prior to vaginal swab collection at 16-20 weeks' gestation). Associations of water TTHM levels with spontaneous preterm birth and a non-optimal cervicovaginal microbiota birth were analyzed using multivariable logistic regression. Multivariable linear regression was used to model associations of water TTHM levels with log-transformed cervicovaginal beta-defensin-2 levels. Since water TTHM levels vary by season and beta-defensin-2 levels have been shown to differ by race, stratified models by warm (April-September) and cold (October-March) seasons as well as by self-identified race were utilized. RESULTS: Participants' water supply TTHM levels (mean µg/L [SD]) were higher in the warm (53.5 [9.4]) than cold (33.4 [7.5]) season (p < 0.0001). TTHM levels were non-significantly higher among Black participants than non-Black participants (44.8 [13.5] vs. 41.8 [11.8], p = 0.07). No associations were detected between TTHM with spontaneous preterm birth (per SD increment of TTHM, aOR 0.94, 95%CI: 0.66, 1.34) or with CST IV (aOR 0.94, 95%CI: 0.86, 1.16). Counter to our hypothesis, we observed positive associations of water TTHM with log-transformed cervicovaginal beta-defensin-2 levels in unadjusted models (ß 0.20 [95%CI: 0.02, 0.39]) per SD increment of TTHM), but the association was null after adjustment for season. However, in models adjusted for covariates including season and stratified by race, TTHM was significantly associated with lower beta-defensin-2 levels among non-Black participants (ß -0.75 [95%CI: -1.43, -0.08]) but not among Black participants (ß 0.17 [95%CI: -0.15, 0.49]), interaction p = 0.013). CONCLUSION: We did not detect associations of water TTHM levels with spontaneous preterm birth or the structure of the cervicovaginal microbiota. However, the finding of a significant interaction between TTHM and race on beta-defensin-2 levels suggest that environmental exposures may contribute to differences in reproductive tract innate immune function by race. Future studies to delineate environmental contributions to the cervicovaginal microbial-immune state, a potentially important biologic underpinning for preterm birth, are warranted.
Assuntos
Desinfetantes , Microbiota , Nascimento Prematuro , Feminino , Humanos , Recém-Nascido , Gravidez , Nascimento Prematuro/induzido quimicamente , Nascimento Prematuro/epidemiologia , Trialometanos/toxicidade , Abastecimento de ÁguaRESUMO
Fine particulate matter (PM2.5) and ozone (O3) air pollutants are known risk factors for asthma exacerbation. We studied the association of these air pollutants with pediatric asthma exacerbation in the Philadelphia metropolitan region, and evaluated potential effect modification by children's characteristics (e.g., race/ethnicity, atopic conditions) and environmental factors (e.g., neighborhood tree canopy, meteorological factors, aeroallergens). We conducted a time-stratified case-crossover study of 54,632 pediatric (age ≤18 years) asthma exacerbation cases occurring from 2011 to 2014, identified through electronic health records (EHR) of the Children's Hospital of Philadelphia (CHOP) health system. We applied conditional logistic regression to estimate associations between air pollution and asthma exacerbation, using daily census-tract level pollutant concentrations estimated from the EPA Fused Air Quality Surface Using Downscaling (FAQSD) files. The associations were estimated within warm (Apr-Sep) and cold (Oct-Mar) months for unlagged exposure and for cumulative effects up to 5 days after exposure, with adjustment for temperature, relative humidity, and holidays. We found small increases in odds of asthma exacerbation with higher pollutant concentrations, with positive associations (OR, comparing concentrations of 75th to 25th percentile) observed for PM2.5 during both warm (1.03, 95% CI: 0.98-1.08) and cold months (1.05, 95% CI: 1.02-1.07), and for O3 during cold months (1.08, 95% CI: 1.02-1.14). The exposure-response relationship with PM2.5 during the cold months was essentially linear, whereas thresholds of effect were observed for the other associations at low-medium pollutant concentrations. Results were robust to multi-pollutant modeling and adjustment for additional covariates. We found no effect modification by most children's characteristics, while effect sizes were higher on days with detected tree and grass pollens during warm months. Our results suggest that even small decreases in pollutant concentrations could potentially reduce risk of childhood asthma exacerbation - an important finding, given the high burden of childhood asthma and known disparities in asthma control.
Assuntos
Poluentes Atmosféricos , Poluição do Ar , Asma , Ozônio , Adolescente , Poluentes Atmosféricos/análise , Poluentes Atmosféricos/toxicidade , Poluição do Ar/efeitos adversos , Poluição do Ar/análise , Asma/induzido quimicamente , Asma/epidemiologia , Criança , Estudos Cross-Over , Exposição Ambiental/efeitos adversos , Exposição Ambiental/análise , Humanos , Ozônio/análise , Ozônio/toxicidade , Material Particulado/análise , Material Particulado/toxicidade , Philadelphia/epidemiologiaRESUMO
OBJECTIVE: To quantify the association between heat and infant mortality and identify factors that influence infant vulnerability to heat. METHODS: We conducted a time-stratified case-crossover analysis of associations between ambient temperature and infant mortality in Philadelphia, Pennsylvania, during the warm months of 2000 through 2015. We used conditional logistic regression models to estimate associations of infant mortality with daily temperatures on the day of death (lag 0) and for averaging periods of 0 to 1 to 0 to 3 days before the day of death. We explored modification of associations by individual and census tract-level characteristics and by amounts of green space. RESULTS: Risk of infant mortality increased by 22.4% (95% confidence interval [CI] = 5.0%, 42.6%) for every 1°C increase in minimum daily temperature over 23.9°C on the day of death. We observed limited evidence of effect modification across strata of the covariates. CONCLUSIONS: Our results contribute to a growing body of evidence that infants are a subpopulation that is particularly vulnerable to climate change effects. Further research using large data sets is critically needed to elucidate modifiable factors that may protect infants against heat vulnerability.
Assuntos
Calor Extremo/efeitos adversos , Mortalidade Infantil/tendências , Pobreza , População Urbana , Estudos Cross-Over , Feminino , Humanos , Lactente , Mortalidade Infantil/etnologia , Recém-Nascido , Masculino , Philadelphia , Estações do AnoRESUMO
Extreme precipitation events may be an important environmental trigger for asthma exacerbations in children. We used a time stratified case-crossover design and data from a large electronic health record database at the Children's Hospital of Philadelphia (CHOP) to estimate associations of daily heavy precipitation (defined as > 95th percentile of the summertime distribution) with asthma exacerbation among children. We defined control days as those falling on the same day of the week within the same month and year as the case. We restricted our primary analyses to the summer months in years 2011-2016 and used conditional logistic regression models to estimate associations between heavy precipitation and acute asthma exacerbations in both outpatient (primary care, specialty care, and emergency department) and inpatient settings. We investigated numerous individual-level (e.g., age, sex, eczema diagnosis) and environmental measures (e.g., greenspace, particulate matter) as potential effect modifiers. The analysis include 13,483 asthma exacerbations in 10,434 children. Odds of asthma exacerbation were 11% higher on heavy precipitation vs. no precipitation days (95% CI: 1.02-1.21). There was little evidence of effect modification by most measures. These results suggest that heavy summertime precipitation events may contribute to asthma exacerbations. Further research using larger datasets from other health systems is needed to confirm these results, and to explore underlying mechanisms.
Assuntos
Asma , Registros Eletrônicos de Saúde , Asma/epidemiologia , Criança , Estudos Cross-Over , Serviço Hospitalar de Emergência , Humanos , Material ParticuladoRESUMO
Despite mounting evidence that urban greenspace protects against mortality in adults, few studies have explored the relationship between greenspace and death among infants. Here, we describe results from an analysis of associations between greenness and infant mortality in Philadelphia, PA. We used images of the normalized difference vegetation index (NDVI), derived from processed satellite data, to estimate greenness density in each census tract. We linked these data with census tract level counts of total infant mortality cases (n = 963) and births (n = 113,610) in years 2010-2014, and used Bayesian spatial areal unit, conditional autoregressive models to estimate associations between greenness and infant mortality. The models included a set of random effects to account for spatial autocorrelation between neighboring census tracts. Infant mortality counts were modeled using a Poisson distribution, and the logarithm of total births in each census tract was specified as the offset term. The following variables were included as potential confounders and effect modifiers: percentage non-Hispanic black, percentage living below the poverty line, an indicator of housing quality, and population density. In adjusted models, the rate of infant mortality was 27% higher in less green compared to more green tracts (95% CI 1.02-1.59). These results contribute further evidence that greenspace may be a health promoting environmental asset.
Assuntos
Meio Ambiente , Mortalidade Infantil/tendências , Plantas , Adulto , Teorema de Bayes , Feminino , Habitação , Humanos , Lactente , Masculino , Philadelphia/epidemiologia , Densidade Demográfica , Análise EspacialRESUMO
Evidence from a small number of studies suggests that longer telomere length measured in peripheral leukocytes is associated with an increased risk of non-Hodgkin lymphoma (NHL). However, these studies may be biased by reverse causation, confounded by unmeasured environmental exposures and might miss time points for which prospective telomere measurement would best reveal a relationship between telomere length and NHL risk. We performed an analysis of genetically inferred telomere length and NHL risk in a study of 10 102 NHL cases of the four most common B-cell histologic types and 9562 controls using a genetic risk score (GRS) comprising nine telomere length-associated single-nucleotide polymorphisms. This approach uses existing genotype data and estimates telomere length by weighing the number of telomere length-associated variant alleles an individual carries with the published change in kb of telomere length. The analysis of the telomere length GRS resulted in an association between longer telomere length and increased NHL risk [four B-cell histologic types combined; odds ratio (OR) = 1.49, 95% CI 1.22-1.82,P-value = 8.5 × 10(-5)]. Subtype-specific analyses indicated that chronic lymphocytic leukemia or small lymphocytic lymphoma (CLL/SLL) was the principal NHL subtype contributing to this association (OR = 2.60, 95% CI 1.93-3.51,P-value = 4.0 × 10(-10)). Significant interactions were observed across strata of sex for CLL/SLL and marginal zone lymphoma subtypes as well as age for the follicular lymphoma subtype. Our results indicate that a genetic background that favors longer telomere length may increase NHL risk, particularly risk of CLL/SLL, and are consistent with earlier studies relating longer telomere length with increased NHL risk.
Assuntos
Estudos de Associação Genética/métodos , Predisposição Genética para Doença , Linfoma de Células B/genética , Linfoma de Células B/patologia , Telômero/patologia , Adolescente , Adulto , Fatores Etários , Idoso , Idoso de 80 Anos ou mais , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Estudos ProspectivosRESUMO
OBJECTIVES: Although many studies have investigated the association between trichloroethylene (TCE) exposure and non-Hodgkin's lymphoma (NHL), less is known about other chlorinated solvents. We extended our previous analysis of occupational TCE exposure in a multicentre population-based case-control study of NHL to investigate associations with five additional chlorinated solvents: 1,1,1,-trichloroethane, carbon tetrachloride, chloroform, methylene chloride and perchloroethylene. METHODS: Cases (n=1189) and controls (n=982) provided detailed information on their occupational histories and workplace exposure to chlorinated solvents for selected occupations using job-specific interview modules. An industrial hygienist used this information and a review of the literature to assess occupational exposure to chlorinated solvents. We computed ORs and 95% CIs for different exposure metrics, with the unexposed group as the referent. We also computed ORs by NHL subtype. RESULTS: High cumulative hours exposed to carbon tetrachloride was associated with NHL (>520 hours: OR 1.9; 95% CI 1.0 to 3.6; Ptrend=0.04). This association remained after restricting to jobs with high-intensity exposure (OR 2.0; 95% CI 1.1 to 3.8; P=0.03) and ≥90% exposure probability (OR 2.1; 95% CI 1.0 to 4.3; P=0.03), adjusting for TCE (OR 2.1; 95% CI 1.0- to 4.1; P=0.04) and incorporating a 15-year lag (OR 1.9; 95% CI 1.0 to 3.6; P=0.06). The other evaluated chlorinated solvents were not associated with NHL. CONCLUSIONS: This is the first study using high-quality quantitative exposure assessment methods to identify a statistically significant elevated association between occupational exposure to carbon tetrachloride and NHL. Our findings, although limited by a small number of exposed cases, offer evidence that carbon tetrachloride may be a lymphomagen.
Assuntos
Linfoma não Hodgkin/induzido quimicamente , Doenças Profissionais/induzido quimicamente , Exposição Ocupacional/efeitos adversos , Solventes/efeitos adversos , Adulto , Idoso , Estudos de Casos e Controles , Feminino , Humanos , Modelos Logísticos , Linfoma não Hodgkin/epidemiologia , Masculino , Pessoa de Meia-Idade , Doenças Profissionais/epidemiologia , Fatores de Risco , Estados Unidos/epidemiologiaRESUMO
OBJECTIVES: To investigate the association between occupational exposure to aromatic hydrocarbon solvents and risk of multiple myeloma (MM) in a large, consortium-based study. METHODS: We pooled data on 2854 cases and 10 743 controls from nine studies participating in the InterLymph consortium. Occupational exposures to benzene, toluene and xylene were assigned by a job-exposure matrix, coupled with 'correction' of exposure probability by self-reported or expert-assessed exposure from the individual studies. Cumulative intensity was calculated as the job-specific exposure intensity multiplied by job duration, summed across jobs. Associations were estimated using logistic regression, with inclusion of covariates for study matching factors and other potential confounders. We repeated our main analysis using random-effects meta-analysis to evaluate heterogeneity of effect. RESULTS: Benzene, toluene and xylene were each associated with MM. For the three solvents, the highest quartile of high-probability cumulative intensity exposure (vs unexposed) was associated with 42% to 63% increased risks of MM. Associations with toluene and xylene exposures were fairly consistent and robust to sensitivity analyses. The estimated effect for benzene was moderately heterogeneous between the studies. Each solvent's association with MM was stronger for exposure occurring within 20 years of diagnosis than with exposure lagged by more than 20 years. CONCLUSIONS: Our study adds important evidence for a role of aromatic hydrocarbon solvents in causation of MM. The difficulty in disentangling individual compounds in this group and a lack of data on potential carcinogenicity of toluene and xylene, in widespread current use, underscore a need for further epidemiological evaluation.
Assuntos
Hidrocarbonetos Aromáticos/toxicidade , Mieloma Múltiplo/induzido quimicamente , Doenças Profissionais/induzido quimicamente , Exposição Ocupacional/efeitos adversos , Solventes/toxicidade , Idoso , Estudos de Casos e Controles , Feminino , Humanos , Modelos Logísticos , Masculino , Pessoa de Meia-Idade , Exposição Ocupacional/análise , Fatores de RiscoRESUMO
BACKGROUND: Landscape characteristics, including vegetation and impervious surfaces, influence urban microclimates and may lead to within-city differences in the adverse health effects of high ambient temperatures. OBJECTIVE: Our objective was to quantitatively summarize the epidemiologic literature that assessed microclimate indicators as effect measure modifiers (EMM) of the association between ambient temperature and mortality or morbidity. METHODS: We systematically identified papers and abstracted relative risk estimates for hot and cool microclimate indicator strata. We calculated the ratio of the relative risks (RRR) and 95% confidence intervals (95% CI) to assess differences in health effects across strata, and pooled the RRR estimates using random effects meta-analyses. RESULTS: Eleven papers were retained. In the pooled analyses, people living in hotter areas within cities (based on land surface temperature or modeled estimates of air temperature) had 6% higher risk of mortality/morbidity compared to those in cooler areas (95% CI: 1.03-1.09). Those living in less vegetated areas had 5% higher risk compared to those living in more vegetated areas (95% CI: 1.00-1.11). DISCUSSION: There is epidemiologic evidence that those living in hotter, and less vegetated areas of cities have higher risk of morbidity or mortality from higher ambient temperature. Further research with improved assessment of landscape characteristics and investigation of the joint effects of physiologic adaptation and landscape will advance the current understanding. CONCLUSION: This review provides quantitative evidence that intra-urban differences in landscape characteristics and micro-urban heat islands contribute to within-city variability in the health effects of high ambient temperatures.
Assuntos
Planejamento Ambiental , Nível de Saúde , Temperatura Alta , Microclima , Cidades , Exposição Ambiental , Humanos , Temperatura , Saúde da População UrbanaRESUMO
BACKGROUND: Seasonal variations are often observed for respiratory tract infections; however, limited information is available regarding seasonal patterns of acquisition of common cystic fibrosis (CF)-related respiratory pathogens. We previously reported differential seasonal acquisition of Pseudomonas aeruginosa in young children with CF and no such variation for methicillin-susceptible Staphylococcus aureus acquisition. The purpose of this study was to describe and compare the seasonal incidence of acquisition of other respiratory bacterial pathogens in young children with CF. METHODS: We conducted a retrospective study to describe and compare the seasonal incidence of methicillin-resistant Staphylococcus aureus (MRSA), Stenotrophomonas maltophilia, Achromobacter xylosoxidans, and Haemophilus influenzae acquisition in young CF patients residing in the U.S. using the Cystic Fibrosis Foundation National Patient Registry, 2003-2009. Log-linear overdispersed Poisson regression was used to evaluate seasonal acquisition of each of these pathogens. RESULTS: A total of 4552 children met inclusion criteria. During follow-up 910 (20%), 1161 (26%), 228 (5%), and 2148 (47%) children acquired MRSA, S. maltophilia, A. xylosoxidans and H. influenzae, respectively. Compared to winter season, MRSA was less frequently acquired in spring (Incidence Rate Ratio [IRR]: 0.79; 95% Confidence Interval [CI]: 0.65, 0.96) and summer (IRR: 0.69; 95% CI: 0.57, 0.84) seasons. Similarly, a lower rate of A. xylosoxidans acquisition was observed in spring (IRR: 0.59; 95% CI: 0.39, 0.89). For H. influenzae, summer (IRR: 0.88; 95% CI: 0.78, 0.99) and autumn (IRR: 0.78; 95% CI: 0.69, 0.88) seasons were associated with lower acquisition rates compared to winter. No seasonal variation was observed for S. maltophilia acquisition. CONCLUSION: Acquisition of CF-related respiratory pathogens displays seasonal variation in young children with CF, with the highest rate of acquisition for most pathogens occurring in the winter. Investigation of factors underlying these observed associations may contribute to our understanding of the aetiology of these infections and guide future infection control strategies.
Assuntos
Fibrose Cística/microbiologia , Infecções Respiratórias/epidemiologia , Infecções Respiratórias/microbiologia , Achromobacter denitrificans/isolamento & purificação , Achromobacter denitrificans/patogenicidade , Pré-Escolar , Clima , Fibrose Cística/complicações , Feminino , Infecções por Haemophilus/epidemiologia , Infecções por Haemophilus/microbiologia , Haemophilus influenzae/isolamento & purificação , Haemophilus influenzae/patogenicidade , Humanos , Masculino , Staphylococcus aureus Resistente à Meticilina/isolamento & purificação , Staphylococcus aureus Resistente à Meticilina/patogenicidade , Infecções por Pseudomonas/epidemiologia , Infecções por Pseudomonas/microbiologia , Pseudomonas aeruginosa/isolamento & purificação , Pseudomonas aeruginosa/patogenicidade , Estudos Retrospectivos , Estações do Ano , Infecções Estafilocócicas/epidemiologia , Infecções Estafilocócicas/microbiologia , Staphylococcus aureus/isolamento & purificação , Staphylococcus aureus/patogenicidade , Stenotrophomonas maltophilia/isolamento & purificação , Stenotrophomonas maltophilia/patogenicidade , Estados UnidosRESUMO
BACKGROUND: The role of air pollution in increasing susceptibility to respiratory tract infections in the cystic fibrosis (CF) population has not been well described. We recently demonstrated that chronic PM2.5 exposure is associated with an increased risk of initial Pseudomonas aeruginosa acquisition in young children with CF. The purpose of this study was to determine whether PM2.5 exposure is a risk factor for acquisition of other respiratory pathogens in young children with CF. METHODS: We conducted a retrospective study of initial acquisition of methicillin susceptible and methicillin resistant Staphylococcus aureus (MSSA and MRSA), Stenotrophomonas maltophilia and Achromobacter xylosoxidans in U.S. children <6 years of age with CF using the CF Foundation Patient Registry, 2003-2009. Multivariable Weibull regression with interval-censored outcomes was used to evaluate the association of PM2.5 concentration in the year prior to birth and risk of acquisition of each organism. RESULTS: During follow-up 63%, 17%, 24%, and 5% of children acquired MSSA, MRSA, S. maltophilia, and A. xylosoxidans, respectively. A 10 µg/m3 increase in PM2.5 exposure was associated with a 68% increased risk of MRSA acquisition (Hazard Ratio: 1.68; 95% Confidence Interval: 1.24, 2.27). PM2.5 was not associated with acquisition of other respiratory pathogens. CONCLUSIONS: Fine particulate matter is an independent risk factor for initial MRSA acquisition in young children with CF. These results support the increasing evidence that air pollution contributes to pulmonary morbidities in the CF community.
Assuntos
Poluição do Ar , Portador Sadio/epidemiologia , Fibrose Cística/epidemiologia , Exposição Ambiental/estatística & dados numéricos , Infecções por Bactérias Gram-Negativas/epidemiologia , Material Particulado , Infecções Respiratórias/epidemiologia , Infecções Estafilocócicas/epidemiologia , Achromobacter denitrificans , Portador Sadio/microbiologia , Criança , Pré-Escolar , Estudos de Coortes , Fibrose Cística/microbiologia , Feminino , Infecções por Bactérias Gram-Negativas/microbiologia , Humanos , Lactente , Masculino , Staphylococcus aureus Resistente à Meticilina , Análise Multivariada , Análise de Regressão , Infecções Respiratórias/microbiologia , Estudos Retrospectivos , Infecções Estafilocócicas/microbiologia , Stenotrophomonas maltophilia , Estados UnidosRESUMO
Family clusters of multiple myeloma (MM) suggest disease heritability. Nevertheless, patterns of inheritance and the importance of genetic versus environmental risk factors in MM aetiology remain unclear. We pooled data from eleven case-control studies from the International Multiple Myeloma Consortium to characterize the association of MM risk with having a first-degree relative with a history of a lympho-haematapoietic cancer. Unconditional logistic regression models, adjusted for study, sex, age and education level, were used to estimate associations between MM risk and having a first-degree relative with a history of non-Hodgkin lymphoma, Hodgkin lymphoma, leukaemia or MM. Sex, African American race/ethnicity and age were explored as effect modifiers. A total of 2843 cases and 11 470 controls were included. MM risk was elevated in association with having a first-degree relative with any lympho-haematapoietic cancer (Odds Ratio (OR) = 1·29, 95% Confidence Interval (CI): 1·08-1·55). The association was particularly strong for having a first-degree relative with MM (OR = 1·90, 95% CI: 1·26-2·87), especially among men (OR = 4·13, 95% CI: 2·17-7·85) and African Americans (OR = 5·52, 95% CI: 1·87-16·27).These results support the hypothesis that genetic inheritance plays a role in MM aetiology. Future studies are warranted to characterize interactions of genetic markers with environmental exposures.