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Publications in this journal

• Particulate Matter, DNA Methylation in Nitric Oxide Synthase, and Childhood Respiratory Disease.

  Authors: Carrie V Breton, Muhammad T Salam, Xinhui Wang, Hyang-Min Byun, Kimberly D Siegmund, Frank D Gilliland

  Environmental health perspectives.

  Background: Air pollutants have been associated with childhood asthma and wheeze. Epigenetic regulation of nitric oxide synthase, the gene responsible for nitric oxide production, may be affected byBackground: Air pollutants have been associated with childhood asthma and wheeze. Epigenetic regulation of nitric oxide synthase, the gene responsible for nitric oxide production, may be affected by air pollutants and contribute to the pathogenesis of asthma and wheeze. Objectives: To investigate the association between air pollutants, DNA methylation, and respiratory outcomes in children. Methods: Based on residential address and buccal sample collection date, 7 day, 1 month, 6 month and 1 year cumulative average PM2.5 and PM10 exposures were estimated for 940 participants in the Children's Health Study. Methylation of 12 CpG sites in 3 NOS genes was measured using a bisulfite-polymerase chain reaction Pyrosequencing assay. Beta regression models were used to estimate associations between air pollutants, % DNA methylation, and respiratory outcomes. Results: A 5 µg/m3 increase in PM2.5 was associated with a 0.20% (95% CI -0.32, -0.07) to 1.0% (95% CI -1.61, -0.56) lower DNA methylation at NOS2A Position 1, 0.06% (95% CI -0.18, 0.06) to 0.58% (95% CI -1.13, -0.02) lower methylation at Position 2, and 0.34% (95% CI -0.57, -0.11) to 0.89% (95% CI -1.57, -0.21) lower methylation at Position 3, depending on the length of exposure and CpG locus. One year PM2.5 exposure was associated with 0.33% (95% CI 0.01, 0.65) higher in average DNA methylation of 4 loci in the NOS2A CpG island. A 5 µg/m3 increase in 7 day and 1 year PM2.5 was associated with 0.6% (95% CI 0.13, 0.99) and 2.8% (95% CI 1.77, 3.75) higher NOS3 DNA methylation. No associations were observed for NOS1. PM10 showed similar but weaker associations with DNA methylation in these genes. Conclusions: PM2.5 exposure was associated with % DNA methylation of several CpG loci in NOS genes, suggesting an epigenetic mechanism through which these pollutants may alter production of nitric oxide.

• Mercury, Cadmium and Lead Levels in Human Placenta: a Systematic Review.

  Authors: María Dolores Esteban-Vasallo, Nuria Aragonés, Marina Pollan, Gonzalo López-Abente, Beatriz Perez-Gomez

  Environmental health perspectives.

  Background: Placental tissue may furnish information on the exposure of both mother and fetus. Mercury, cadmium and lead are toxicants of interest in pregnancy, associated with alterations in childBackground: Placental tissue may furnish information on the exposure of both mother and fetus. Mercury, cadmium and lead are toxicants of interest in pregnancy, associated with alterations in child development. Objectives: To summarize the available information regarding total mercury, cadmium and lead levels in human placenta and possible related factors. Methods: Systematic search of PubMed, Medline, EMBASE, Lilacs, OSH and Web of Science for original papers on total mercury, cadmium or lead levels in human placenta, published in English or Spanish (1976-2011). Data on study design, population characteristics, collection and analysis of placenta specimens and main results were extracted using a standardized form. Results: A total of 79 papers (73 different studies) were found. Mercury, cadmium and lead levels were reported in 24, 46 and 46 studies, respectively. Most studies included small convenience samples of healthy pregnant women. Studies were heterogeneous as to populations selected, processing of specimens and presentation of results. Mercury concentrations of over 50 ng/g were found in China (Shanghai), Japan and the Faroe Islands. Cadmium levels ranged from 1.2 ng/g to 53 ng/g, and were highest in USA, Japan and Eastern Europe. Lead showed the greatest variability, with levels ranging from 1.18 ng/g in China (Shanghai) to 500 ng/g in a polluted area of Poland. Conclusion: The use of the placenta to assess heavy metals exposure is underdeveloped. International standardized protocols are needed to enhance comparability and increase the usefulness of this promising tissue in biomonitoring studies.

• Di(2-ethylhexyl) Phthalate (DEHP) Impairs Female Fertility and Promotes Adipogenesis in C3H/N Mice.

  Authors: Juliane-Susanne Schmidt, Kristina Schaedlich, Nadia Fiandanese, Paola Pocar, Bernd Fischer

  Environmental health perspectives.

  Background: Di(2-ethylhexyl) phthalate (DEHP) and its metabolites are known to affect lipid metabolism and adipogenesis, mainly by activation of PPARs. Exposure to DEHP has been linked withBackground: Di(2-ethylhexyl) phthalate (DEHP) and its metabolites are known to affect lipid metabolism and adipogenesis, mainly by activation of PPARs. Exposure to DEHP has been linked with testicular impairment and male subfertility. However, the effects of DEHP on female reproductive health and metabolism remain to be studied in detail. Objectives: Analysis of dietary DEHP exposure on metabolism and fertility in female mice. Methods: In two independent approaches, female C3H/N mice were exposed via their diet to DEHP [0.05, 5, 500 mg/kg bw/day] for 8 weeks. Food intake, weight gain and litter size were recorded. After exposure, liver, visceral fat, and plasma were analyzed by qRTPCR and ELISA in F0 females (Study I) and F0 dams and their F1 offspring (Study II). Results: In Study I, F0 females had a significant increase in body weight, food intake, and visceral adipose tissue in all exposure groups compared with controls. In liver tissue, PPARα and PPARγ transcripts were significantly changed in the 500mg group. In the same group, PPARγ mRNA was significantly reduced in liver but not in fat tissue. Leptin and FABP4 mRNA were increased in adipose tissue, while adiponectin was decreased. In Study II, we detected a 100% abortion rate in F0 dams in the 500mg group. F1 offspring exposed in utero and during lactation had an increase in visceral fat tissue and body weight. Conclusion: DEHP impaired fertility in high concentrations and increased body weight and visceral fat depots in female C3H/N mice in environmentally relevant dosages. Although DEHP exposure was only in utero and during lactation, metabolic changes induced by DEHP did also occur in the offspring of diet-exposed females.

• Ambient Temperature and Biomarkers of Heart Failure: A Repeated Measures Analysis.

  Authors: Elissa H Wilker, Gloria Yeh, Gregory A Wellenius, Roger B Davis, Russell S Phillips, Murray A Mittleman

  Environmental health perspectives.

  Background: Extreme temperatures have been associated with hospitalization and death among individuals with heart failure, but few studies have explored the underlying mechanisms. Objectives: WeBackground: Extreme temperatures have been associated with hospitalization and death among individuals with heart failure, but few studies have explored the underlying mechanisms. Objectives: We hypothesized that outdoor temperature in the Boston area (one to four day moving averages) would be associated with higher levels of biomarkers of inflammation and myocyte injury in a repeated-measures study of individuals with stable heart failure. Methods: We analyzed data from a completed clinical trial that randomized 100 patients to 12 weeks of tai chi classes or time-matched education control. B-natriuretic peptide (BNP), C-reactive protein (CRP) and tumor necrosis factor were measured at baseline, 6 and 12 weeks. Endothelin-1 was measured at baseline and 12 weeks. We used fixed effects models to evaluate associations with temperature measures and adjusted for time-varying covariates. Results: Higher apparent temperature was associated with higher levels of BNP beginning with two day moving averages and reached statistical significance for three and four day moving averages. CRP results followed a similar pattern, but were delayed by one day. A 5° C change in three and four day moving averages of apparent temperature was associated with 11.3% (95%CI: 1.1, 22.5, p=.03) and 11.4% (95%CI: 1.2, 22.5, p=.03) higher BNP. A 5° C change in the four day moving average of apparent temperature was associated with 21.6% (95%CI: 2.5, 44.2, p=.03) higher CRP. No clear associations with tumor necrosis factor or endothelin-1 were observed. Conclusions: Among patients undergoing treatment for heart failure, we observed positive associations between temperature and both BNP and CRP, predictors of heart failure prognosis and severity.

• A Three-Stage Algorithm to Make Toxicologically Relevant Activity Calls from Quantitative High Throughput Screening Data.

  Authors: Keith R Shockley

  Environmental health perspectives.

  Background: The ability of a substance to induce a toxicological response is better understood by analyzing the response profile over a broad range of concentrations than at a single concentration.Background: The ability of a substance to induce a toxicological response is better understood by analyzing the response profile over a broad range of concentrations than at a single concentration. In vitro quantitative high throughput screening (qHTS) assays are multiple-concentration experiments with an important role in the National Toxicology Program's (NTP) efforts to advance toxicology from a predominantly observational science at the level of disease-specific models to a more predictive science based on broad inclusion of biological observations. Objective: To develop a systematic approach to classify substances from large scale concentration-response data into statistically supported and toxicologically relevant activity categories. Methods: The first stage of the approach finds active substances with robust concentration-response profiles within the tested concentration range. The second stage finds substances with activity at the lowest tested concentration not captured in the first stage. The third and final stage separates statistically significant (but not robustly statistically significant) profiles from responses that lack statistically compelling support, or "inactives". The performance of the proposed algorithm was evaluated with simulated qHTS data sets. Results: The proposed approach performed well for 14 point concentration-response curves with typical levels of residual error (σ ≤ 25%) or when maximal response (|RMAX|) was greater than 25% of the positive control response. The approach also worked well in most cases for smaller sample sizes when |RMAX| ≥ 50%, even with as few as 4 data points. Conclusions: The three-stage classification algorithm performed better than one-stage classification approaches based on overall F-tests, t-tests or linear regression.

• Evaluation of Developmental Toxicants and Signaling Pathways in a Functional Test Based on the Migration of Human Neural Crest Cells.

  Authors: Bastian Zimmer, Gabsang Lee, Nina V Stiegler, Kesavan Meganathan, Agapios Sachinidis, Lorenz Studer, Marcel Leist

  Environmental health perspectives.

  BACKGROUND: Information on the potential developmental toxicity (DT) of the majority of chemicals is scarce, and test capacities for further animal-based testing are limited. Therefore, newBACKGROUND: Information on the potential developmental toxicity (DT) of the majority of chemicals is scarce, and test capacities for further animal-based testing are limited. Therefore, new approaches with higher throughput are required. A screening strategy based on the use of relevant human cell types has been proposed by the EPA and others. As impaired neural crest (NC) function is one of the known causes for teratologic effects, testing of toxicant effects on NC is desirable for a DT test battery. OBJECTIVE: To develop a robust and widely applicable human-relevant NC function assay, allowing sensitive screening of environmental toxicants, and a definition of toxicity pathways. METHODS: We generated NC cells from human embryonic stem cells, and after establishing a migration assay of NC (MINC), we tested environmental toxicants as well as inhibitors of physiological signal transduction pathways. RESULTS: Methylmercury (50 nM), valproic acid (> 10 µM) and Lead-acetate (1 µM) affected migration of NC more potently than migration of other cell types. The MINC assay correctly identified the neural crest toxicants triadimefon and triadimenol, additionally it showed different sensitivities to various organic and inorganic mercury compounds. Applying classic pharmacologic inhibitors and large-scale microarray gene expression profiling, we found several signaling pathways that are relevant for the migration of NC in the MINC. CONCLUSIONS: The MINC assay faithfully models human NC migration, and reveals impairment of this function by developmental toxicants with good sensitivity and specificity.

• Plasmid-Mediated Quinolone Resistance Genes and Antibiotic Residues in Wastewater and Soil Adjacent to Swine Feedlots: Potential Transfer to Agricultural Lands.

  Authors: Juan Li, Thanh Wang, Bing Shao, Jianzhong Shen, Shaochen Wang, Yongning Wu

  Environmental health perspectives.

  BACKGROUND: Inappropriate use of antibiotics in swine feed could cause accelerated emergence of antibiotic resistance genes, and agricultural application of swine waste could spread antibioticBACKGROUND: Inappropriate use of antibiotics in swine feed could cause accelerated emergence of antibiotic resistance genes, and agricultural application of swine waste could spread antibiotic resistance genes to the surrounding environment. OBJECTIVES: This study was conducted to investigate the distribution of plasmid-mediated quinolone resistance (PMQR) genes from swine feedlots and their surrounding environment. METHODS: We used a culture-independent method to identify PMQR genes and estimate their levels in wastewater from seven swine feedlot operations and corresponding wastewater-irrigated farm fields. Concentrations of (fluoro)quinolones in wastewater and soil samples were determined by ultra-performance liquid chromatography-electrospray tandem mass spectrometry. RESULTS：The predominant PMQR genes in the samples were qnrD, qepA and oqxB, whereas qnrS and oqxA were present only in wastewater samples. Absolute concentrations of all PMQR genes combined ranged from 1.66×107 to 4.06×108 copies/mL in wastewater and 4.06×106 to 9.52×107 copies/g in soil. Concentrations of (fluoro)quinolones ranged from 4.57 to 321 ng/mL in wastewater and below detection limit to 23.4 ng/g in soil. Significant correlations were found between the relative abundance of PMQR genes and (fluoro)quinolone concentrations (r =0.71, p=0.005) and the relative abundance of PMQR genes in paired wastewater and agricultural soil samples (r =0.91, p =0.005). CONCLUSIONS: Swine feedlot wastewater may be a source of PMQR genes that could facilitate the spread of antibiotic resistance. To our knowledge, this is the first study to examine the occurrence of PMQR genes in animal husbandry environments using a culture-independent method.

• Maternal Exposure to Polycyclic Aromatic Hydrocarbons and 5'-CpG Methylation of Interferon-γ in Cord White Blood Cells.

  Authors: Wan-Yee Tang, Linda Levin, Glenn Talaska, Yuk Yin Cheung, Julie Herbstman, Deliang Tang, Rachel L Miller, Frederica Perera, Shuk-Mei Ho

  Environmental health perspectives.

  Background: Maternal factors are implicated in the onset of childhood asthma. Differentiation of naïve CD4+ T lymphocytes into pro-allergic T helper 2 cells induces interleukin (IL)4 expression andBackground: Maternal factors are implicated in the onset of childhood asthma. Differentiation of naïve CD4+ T lymphocytes into pro-allergic T helper 2 cells induces interleukin (IL)4 expression and inhibits interferon (IFN)γ expression accompanied by concordant methylation changes in the promoters of these genes. However, it has yet to be established if maternal exposure to polycyclic aromatic hydrocarbons (PAHs) can alter these gene promoters epigenetically during fetal development. Objectives: This study sought to elucidate the relationship between maternal PAH exposure and promoter methylation status of IFNγ and IL4. Methods: We assessed the effects of benzo[a]pyrene (BaP), a representative airborne PAH, on the methylation status of the IFNγ and IL4 promoters in Jurkat cells and two lung adenocarcinoma cell lines, and on gene expression. In addition we evaluated methylation status of the IFNγ promoter in cord white blood cells from 53 participants in the Columbia Center for Children's Environmental Health cohort. Maternal PAH exposure was estimated by personal air monitoring during pregnancy. Results: In vitro exposure of the cell models to low, non-cytotoxic doses (0.1 and 1 nM) of BaP elicited increased promoter hypermethylation and reduced expression of IFNγ, but not IL4. IFNγ promoter methylation in cord white blood cells was associated with maternal PAH exposure in the cohort study subsample. Conclusion: Consistent with the results for the cell lines, maternal exposure to PAHs was associated with hypermethylation of IFNγ in cord blood DNA from cohort children. These findings support a potential role of epigenetics in fetal reprogramming by PAH-induced environmental diseases.

• Profiling Environmental Chemicals for Activity in the Antioxidant Response Element Signaling Pathway Using a High-Throughput Screening Approach.

  Authors: Sunita J Shukla, Ruili Huang, Steven O Simmons, Raymond R Tice, Kristine L Witt, Danielle Vanleer, Ram Ramabhadran, Christopher P Austin, Menghang Xia

  Environmental health perspectives.

  BACKGROUND: Oxidative stress has been implicated in the pathogenesis of a variety of diseases ranging from cancer to neurodegeneration, highlighting the need to identify chemicals that can induceBACKGROUND: Oxidative stress has been implicated in the pathogenesis of a variety of diseases ranging from cancer to neurodegeneration, highlighting the need to identify chemicals that can induce this effect. The antioxidant response element (ARE) signaling pathway plays an important role in the amelioration of oxidative stress. Thus, assays that detect the up-regulation of this pathway could be useful for identifying chemicals that induce oxidative stress. OBJECTIVES: To utilize cell-based reporter methods and informatics tools to efficiently screen a large collection of environmental chemicals and identify compounds that induce oxidative stress. METHODS: We utilized two cell-based ARE assay reporters, ß-lactamase and luciferase, to screen a U.S. National Toxicology Program 1408 (1340 unique) compound library for their ability to induce oxidative stress in HepG2 cells using quantitative high throughput screening (qHTS). RESULTS: Roughly 3% (34 of 1340 unique) of compounds demonstrated activity across both cell-based assays. Based on biological activity and structure-activity relationship profiles, we selected 50 compounds for re-testing in the two ARE assays and in an additional follow-up assay that employed a mutated ARE linked to ß-lactamase. Based on this strategy, we identified 30 compounds that demonstrated activity in the ARE-bla and ARE-luc assays and were able to determine structural features conferring compound activity across assays. CONCLUSIONS: Our results support the robustness of utilizing two different cell-based approaches for identifying compounds that induce ARE signaling. These methods are useful for prioritizing chemicals for further in-depth mechanism-based toxicity testing.

• Controlled Exposure Study of Air Pollution and T Wave Alternans in Volunteers without Cardiovascular Disease.

  Authors: Marjan Kusha, Stephane Masse, Talha Farid, Bruce Urch, Frances S Silverman, Robert D Brook, Diane R Gold, Iqwal Mangat, Mary Speck, Krishnakumar Nair, Kwaku Poku, Chris Meyer, Murray A Mittleman, Gregory A Wellenius, Kumaraswamy Nanthakumar

  Environmental health perspectives.

  Background: Epidemiological studies have assessed T wave alternans (TWA) as a possible mechanism of cardiac arrhythmias related to air pollution in high risk subjects and have reported associationsBackground: Epidemiological studies have assessed T wave alternans (TWA) as a possible mechanism of cardiac arrhythmias related to air pollution in high risk subjects and have reported associations with increased TWA magnitude. Objective: In this controlled human exposure study we assessed the impact of exposure to concentrated ambient particulate matter (CAP) and ozone (O3) on T wave alternans in resting volunteers without pre-existing cardiovascular disease. Methods: 17 participants without pre-existing cardiac disease were randomized to filtered air (FA), CAP (150 μg/m3), O3 (120 ppb), or combined CAP+O3 exposures for 2 hours. Continuous electrocardiograms (ECGs) were recorded at rest and T wave alternans (TWA) was computed by modified moving average analysis with QRS alignment for the artifact free intervals of 20 beats along the V2 andV5 leads. Exposure-induced changes in the highest TWA magnitude (TWAMax) were estimated for the first and last 5 minutes of each exposure (TWAMax_Early and TWAMax_Late respectively). ∆TWAMax (Late - Early) were compared among exposure groups using analysis of variance (ANOVA). Results: Mean values for ∆TWAMax were -2.1 ± 0.4, -2.7 ± 1.1, -1.9 ± 1.5 and -1.2 ± 1.5 in FA, CAP, O3 and CAP+O3 exposure groups respectively; with no significant difference between pollutant exposures and FA. Conclusion: In our study of 17 volunteers without pre-existing cardiovascular disease, we did not observe significant changes in T wave alternans after 2-hour exposures to CAP, O3, or combined CAP+O3. This finding, however, does not preclude the possibility of pollution-related effects on TWA at elevated heart rates, such as during exercise, or the possibility of delayed responses.

• Respiratory Health Effects of Airborne Particulate Matter: The Role of Particle Size, Composition and Oxidative Potential - The RAPTES Project.

  Authors: Maciej Strak, Nicole A H Janssen, Krystal J Godri, Ilse Gosens, Ian S Mudway, Flemming R Cassee, Erik Lebret, Frank J Kelly, Roy M Harrison, Bert Brunekreef, Maaike Steenhof, Gerard Hoek

  Environmental health perspectives.

  Background. Specific characteristics of particulate matter (PM) responsible for associations with respiratory health observed in epidemiological studies are not well established. High correlationsBackground. Specific characteristics of particulate matter (PM) responsible for associations with respiratory health observed in epidemiological studies are not well established. High correlations among and differential measurement errors of individual components contribute to this uncertainty. Objectives. Investigate which PM characteristics have the most consistent associations with acute changes in respiratory function in healthy volunteers. Methods. We used a semi-experimental design to accurately assess exposure. We increased exposure contrast and reduced correlations among PM characteristics by exposing volunteers at 5 different locations- an underground train station, two traffic sites, a farm and an urban background site. Each of the 31 volunteers was exposed for 5 hours, while exercising intermittently, 3-7 times at different locations from March-October 2009. We measured PM10, PM2.5, particle number concentrations (PNC), absorbance, elemental/organic carbon, trace metals, secondary inorganic components, endotoxin content, gaseous pollutants, and PM oxidative potential (OP). Lung function (FEV1, FVC, FEF25-75, PEF) and fractional exhaled nitric oxide (FENO) were measured before and at three time points after exposure. Data were analyzed with mixed linear regression. Results. An interquartile increase in PNC (33,000 particles/cm3) was associated with an 11% (95% confidence interval (CI): 5% to 17%) and 12% (95% CI: 6% to 17%) FENO increase over baseline immediately and two hours post-exposure, respectively. A 7% (95% CI: 0.5% to 14%) increase persisted until the following morning. These associations were robust and insensitive to adjustment for other pollutants. Similarly consistent associations were seen between FVC and FEV1 with PNC, NO2 and NOX. Conclusions. Changes in PNC, NO2 and NOX were associated with evidence of acute airway inflammation (FENO) and impaired lung function. PM mass concentration and PM10 OP were not predictive of the observed acute responses.

• Bisphenol A Induces Gene Expression Changes and Proliferative Effects through GPER in Breast Cancer Cells and Cancer-Associated Fibroblasts.

  Authors: Marco Pupo, Assunta Pisano, Rosamaria Lappano, Maria Francesca Santolla, Ernestina Marianna De Francesco, Sergio Abonante, Camillo Rosano, Marcello Maggiolini

  Environmental health perspectives.

  BACKGROUND: Bisphenol-A (BPA) is the principal constituent of baby bottles, reusable water bottles, metal cans and plastic food containers. BPA exerts estrogen-like activity interacting with theBACKGROUND: Bisphenol-A (BPA) is the principal constituent of baby bottles, reusable water bottles, metal cans and plastic food containers. BPA exerts estrogen-like activity interacting with the classical estrogen receptors (ERα and ERβ) and through the G protein-coupled receptor named Gpr30/Gper. In this regard, recent studies have shown that Gper was involved in the proliferative effects induced by BPA in both normal and tumor cells. OBJECTIVES: We studied the transduction signaling pathways through which BPA influences cell proliferation and migration in breast cancer cells and cancer-associated fibroblasts (CAFs). METHODS AND RESULTS: We used as a model system the SKBR3 breast cancer cells and CAFs that lack the classical ERs. Specific pharmacological inhibitors and gene-silencing procedures were used to show that BPA induces the expression of the Gper target genes c-FOS, EGR-1 and CTGF through the Gper/egfr/erk transduction pathway in SKBR3 breast cancer cells and CAFs. Moreover, we demonstrate that Gper is required for the growth effects and migration stimulated by BPA in both cell types. CONCLUSIONS: Our results indicate that Gper is involved in the biological action elicited by BPA in breast cancer cells and CAFs. Hence, Gper-mediated signaling should be included among the transduction mechanisms through which BPA may stimulate cancer progression.

• Current Status of the Epidemiologic Evidence Linking Polychlorinated Biphenyls and Non-Hodgkin Lymphoma, and the Role of Immune Dysregulation.

  Authors: Shira Kramer, Stephanie Moller Hikel, Kristen Adams, David Hinds, Katherine Moon

  Environmental health perspectives.

  Background: While case-control studies conducted to date have largely affirmed the relationship between polychlorinated biphenyls (PCBs) and non-Hodgkin lymphoma (NHL), occupational cohort studies ofBackground: While case-control studies conducted to date have largely affirmed the relationship between polychlorinated biphenyls (PCBs) and non-Hodgkin lymphoma (NHL), occupational cohort studies of PCB-exposed workers have been generally interpreted as negative, thereby raising doubts about a potential causal association. A common theme of immune dysregulation unifies many of NHL's strongest risk factors, and several authors have posited that sub-clinical immune dysregulation may increase NHL risk by decreasing host resistance, reducing control of cellular proliferation and differentiation, and diminishing tumor surveillance mechanisms. Objectives: The goals of this review are: I) to evaluate the epidemiological research examining the association between PCB exposure and NHL and discuss the contribution to the weight of evidence of case-control studies and occupational cohort studies; and II) to summarize the evidence for immune dysregulation as a means by which PCBs may cause NHL. Methods: We performed a literature search using PubMed and 7 additional online biomedical and toxicological referencing libraries to identify literature published through August 2011. Discussion and Conclusions: Overall, we conclude that the weight of evidence supports a causal role of PCBs in lymphomagenesis. The strongest epidemiological evidence for the relationship between PCBs and NHL comes from case-control studies conducted among the general population. Epidemiological and toxicological data demonstrating immunosuppressive and inflammatory effects of PCBs further contribute to the weight of evidence by providing a plausible explanation for how PCBs can cause NHL through immune dysregulation.

• Environmental Lead after Hurricane Katrina.

  Authors: Howard W Mielke

  Environmental health perspectives. 120(5):a188.

• Environmental Lead: Rabito et al. Respond.

  Authors: Felicia A Rabito, Janet C Rice, Whitney Arroyave

  Environmental health perspectives. 120(5):a188-a189.

• Studies Raise Questions about Pavement Sealers.

  Authors: Bob Weinhold

  Environmental health perspectives. 120(5):a192-a193.

• Landscape Fire Smoke as a Cause of Death: Burning Vegetation Estimated to Kill Hundreds of Thousands Worldwide.

  Authors: Bob Weinhold

  Environmental health perspectives. 120(5):a204.

• Hearts over Time: Cardiovascular Mortality Risk Linked to Long-Term PM2.5 Exposure.

  Authors: Tanya Tillett

  Environmental health perspectives. 120(5):a205.

• Migration Associated with Climate Change: Modern Face of an Ancient Phenomenon.

  Authors: Julia R Barrett

  Environmental health perspectives. 120(5):a205.

• Environment and Reproductive Health in China: Challenges and Opportunities.

  Authors: Weihua Li, Bo Chen, Xuncheng Ding

  Environmental health perspectives. 120(5):a184-a185.

• Common Bacterium Induces Histamine Production in Neutrophils.

  Authors: Carol Potera

  Environmental health perspectives. 120(5):a190.

• Shark Fin Consumption May Expose People to Neurotoxic BMAA.

  Authors: Wendee Holtcamp

  Environmental health perspectives. 120(5):a191.

• The Beat.

  Authors: Erin E Dooley

  Environmental health perspectives. 120(5):a192-a193.

• Satellite-based Estimates of Ambient Air Pollution and Global Variations in Childhood Asthma Prevalence.

  Authors: H Ross Anderson, Barbara K Butland, Aaron van Donkelaar, Michael Brauer, David P Strachan, Tadd Clayton, Rita van Dingenen, Markus Amann, Bert Brunekreef, Aaron Cohen, Frank Dentener, Christopher Lai, Lok N Lamsal, Randall V Martin

  Environmental health perspectives.

  Background: The effect of ambient air pollution on global variations and trends in asthma prevalence is unclear. Objectives: To investigate community-level associations between asthma prevalence dataBackground: The effect of ambient air pollution on global variations and trends in asthma prevalence is unclear. Objectives: To investigate community-level associations between asthma prevalence data from the International Study of Asthma and Allergies in Childhood (ISAAC) and satellite-based estimates of particulate matter with aerodynamic diameter <2.5 µm (PM2.5) and nitrogen dioxide (NO2), and modelled estimates of ozone. Methods: We assigned satellite-based estimates of PM2.5 and NO2 at a spatial resolution of 0.1˚ x 0.1˚ and modelled estimates of ozone at a resolution of 1˚ x 1˚ to 183 ISAAC centres. We used centre-level prevalence of severe asthma as the outcome and multilevel models to adjust for gross national income (GNI) and centre- and country-level sex, climate and population density. We examined associations (adjusting for GNI) between air pollution and asthma prevalence over time in centres with data from ISAAC Phase One (mid-1900's) and Phase Three (2001 - 2003). Results: For the 13-14 year age group (128 centres in 28 countries) the estimated average within-country change in centre-level asthma prevalence per 100 children per 10% increase in centre-level PM2.5 and NO2 was -0.043 (-0.139, 0.053) and 0.017 (-0.030, 0.064) respectively. For ozone the estimated change in prevalence per ppbV was -0.116 (-0.234, 0.001). Equivalent results for the 6-7 year age-group (83 centres in 20 countries) though slightly different were not significantly positive. For the 13-14 year age-group, change in centre-level asthma prevalence over time per 100 children per 10% increase in PM2.5 from Phase One to Phase Three was -0.139 (-0.347, 0.068). The corresponding association with ozone (per ppbV) was -0.171 (-0.275, -0.067). Conclusion: In contrast to reports from within-community studies of individuals exposed to traffic pollution we did not find evidence of a positive association between ambient air pollution and asthma prevalence as measured at the community level.

• Offshore Exploration to Commence in the Arctic: Can Shell's Oil-Spill Response Plans Keep Up?

  Authors: Charles W Schmidt

  Environmental health perspectives. 120(5):a194-a199.

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