This article is the first in a series of three that describes the development and delivery of the Environmental Health and Land Reuse (EHLR) Basic Training and the first pilot of the EHLR Immersion Training. The EHLR Basic Training is based on the 5-step Land Reuse Model from the Agency for Toxic Substances and Disease Registry (ATSDR). Through a collaboration with the National Environmental Health Association (NEHA), we developed the EHLR Basic Training in two modalities: virtual/live (maintained by ATSDR) and online/asynchronous (maintained by NEHA). The modules include: (1) Engaging With Your Community, (2) Evaluating Environmental and Health Risks, (3) Communicating Environmental and Health Risks, (4) Redesigning With Health in Mind, and (5) Measuring Success: Evaluating Environmental and Health Change. From June 2019-August 2022, ATSDR and NEHA delivered 10 EHLR Classroom Basic Trainings, launched the EHLR Online Basic Training, and developed the EHLR Immersion Training. We piloted the EHLR Immersion Training in July 2022, March 2023, and July 2023. Our participants included science, technology, engineering, and mathematics (STEM) students from Dine College who were in a Summer Intern Program; tribal environmental professionals; NEHA members in environmental health careers; and environmental professionals, students, and community members who were engaged in environmental work or environmental justice. We have learned that individual training modules can be used for specific learning needs among our participants. Perhaps more importantly, we have learned that undergraduate students and community members can and should be engaged in EHLR Training. The results of the evaluation and longterm follow-up of the EHLR Training will be presented in the second and third articles in this series.

Nano-sized titanium dioxide particles (TiO(2) NPs) are a high-production volume nanomaterial widely used in the paints, cosmetics, food and photovoltaics industry. However, the potential carcinogenic effects of TiO(2) NPs in the lung are still unclear despite the vast number of in vitro and in vivo studies investigating TiO(2) NPs. Here, we systematically reviewed the existing in vitro and in vivo mechanistic evidence of TiO(2) NP lung carcinogenicity using the ten key characteristics of carcinogens for identifying and classifying carcinogens. A total of 346 studies qualified for the quality and reliability assessment, of which 206 were considered good quality. Using a weight-of-evidence approach, these studies provided mainly moderate to high confidence for the biological endpoints regarding genotoxicity, oxidative stress and chronic inflammation. A limited number of studies investigated other endpoints important to carcinogenesis, relating to proliferation and transformation, epigenetic alterations and receptor-mediated effects. In summary, TiO(2) NPs might possess the ability to induce chronic inflammation and oxidative stress, but it was challenging to compare the findings in the studies due to the wide variety of TiO(2) NPs differing in their physicochemical characteristics, formulation, exposure scenarios/test systems, and experimental protocols. Given the limited number of high-quality and high-reliability studies identified within this review, there is a lack of good enough mechanistic evidence for TiO(2) NP lung carcinogenicity. Future toxicology/carcinogenicity research must consider including positive controls, endotoxin testing (where necessary), statistical power analysis, and relevant biological endpoints, to improve the study quality and provide reliable data for evaluating TiO(2) NP-induced lung carcinogenicity.

This article is the first in a series of three that describes the development and delivery of the Environmental Health and Land Reuse (EHLR) Basic Training and the first pilot of the EHLR Immersion Training. The EHLR Basic Training is based on the 5-step Land Reuse Model from the Agency for Toxic Substances and Disease Registry (ATSDR). Through a collaboration with the National Environmental Health Association (NEHA), we developed the EHLR Basic Training in two modalities: virtual/live (maintained by ATSDR) and online/asynchronous (maintained by NEHA). The modules include: 1) Engaging With Your Community, 2) Evaluating Environmental and Health Risks, 3) Communicating Environmental and Health Risks, 4) Redesigning With Health in Mind, and 5) Measuring Success: Evaluating Environmental and Health Change. From June 2019-August 2022, ATSDR and NEHA delivered 10 EHLR Classroom Basic Trainings, launched the EHLR Online Basic Training, and developed the EHLR Immersion Training. We piloted the EHLR Immersion Training in July 2022, March 2023, and July 2023. Our participants included science, technology, engineering, and mathematics (STEM) students from Dine College who were in a Summer Intern Program; tribal environmental professionals; NEHA members in environmental health careers; and environmental professionals, students, and community members who were engaged in environmental work or environmental justice. We have learned that individual training modules can be used for specific learning needs among our participants. Perhaps more importantly, we have learned that undergraduate students and community members can and should be engaged in EHLR Training. The results of the evaluation and longterm follow-up of the EHLR Training will be presented in the second and third articles in this series. © 2024, National Environmental Health Association. All rights reserved.

OBJECTIVES: In 2016, the Centers for Disease Control and Prevention supported 5 local health departments (LHDs) to implement teen dating violence and youth violence primary prevention strategies across multiple levels of the social-ecological model and build capacity for the expansion of such prevention efforts at the local level. The objective of this study was to estimate the total cost of implementing primary prevention strategies for all LHDs across 3 years of program implementation. METHODS: We used a microcosting analytic approach to identify resources and compute costs for all prevention strategies implemented by LHDs. We computed the total program cost, total and average cost per strategy by social-ecological model level, and average cost of implementation per participant served by the program. All costs were inflated via the monthly Consumer Price Index and reported in August 2020 dollars. RESULTS: For 3 years of program implementation, the total estimated cost of implementing teen dating violence and youth violence primary prevention strategies was >$7.1 million across all 5 LHDs. The largest shares of program-related costs were program staff (55.9%-57.0%) and contracts (22.4%-25.5%). Among prevention strategies, the largest share of total costs was for strategies implemented at the community level of the social-ecological model (42.8%). CONCLUSIONS: The findings from this analysis provide a first look at the total costs of implementing comprehensive teen dating violence and youth violence primary prevention strategies and serve as a foundation for investments in local violence prevention funding for young people.

Urban agriculture presents the opportunity for increased availability of local, fresh foods; however, exposure to lead soil contamination can occur through gardening in urban environments. Through a community-engaged partnership, we implemented Soil Screening, Health, Outreach and Partnerships (soilSHOPs), in-person and virtually, to screen soils for lead in Atlanta, Georgia. These soilSHOPs inform best practices for increasing awareness about lead exposure and grounding interventions in residents' lived experiences and also led the US Environmental Protection Agency to identify a Superfund site.

The article focuses on the Environmental Health and Land Reuse (EHLR) Certificate Program, an initiative that aims to increase knowledge about the danger of brownfield sites. Topics include the partnership of Agency for Toxic Substances and Disease Registry (ATSDR) with stakeholders throughout the Navajo Nation, the environmental health and land reuse training under the Summer Internship Program (SIP), and the challenges brought by COVID-19 pandemic in implementing the virtual SIP.

OBJECTIVE: The aim of the study was to assess occupational health effects 1 month after responding to a natural gas pipeline explosion. METHODS: First responders to a pipeline explosion in Kentucky were interviewed about pre- and post-response health symptoms, post-response health care, and physical exertion and personal protective equipment (PPE) use during the response. Logistic regression was used to examine associations between several risk factors and development of post-response symptoms. RESULTS: Among 173 first responders involved, 105 (firefighters [58%], emergency medical services [19%], law enforcement [10%], and others [12%]) were interviewed. Half (53%) reported at least 1 new or worsening symptom, including upper respiratory symptoms (39%), headache (18%), eye irritation (17%), and lower respiratory symptoms (16%). The majority (79%) of symptomatic responders did not seek post-response care. Compared with light-exertion responders, hard-exertion responders (48%) had significantly greater odds of upper respiratory symptoms (aOR: 2.99, 95% CI: 1.25-7.50). Forty-four percent of responders and 77% of non-firefighter responders reported not using any PPE. CONCLUSIONS: Upper respiratory symptoms were common among first responders of a natural gas pipeline explosion and associated with hard-exertion activity. Emergency managers should ensure responders are trained in, equipped with, and properly use PPE during these incidents and encourage responders to seek post-response health care when needed.

Taenia saginata, Taenia solium and Taenia asiatica (beef, pork and Asian tapeworms, respectively) are parasitic flatworms of major public health and food safety importance. Among them, T. asiatica is a newly recognized species that split from T. saginata via an intermediate host switch approximately 1.14 Myr ago. Here we report the 169- and 168-Mb draft genomes of T. saginata and T. asiatica. Comparative analysis reveals that high rates of gene duplications and functional diversifications might have partially driven the divergence between T. asiatica and T. saginata. We observe accelerated evolutionary rates, adaptive evolutions in homeostasis regulation, tegument maintenance and lipid uptakes, and differential/specialized gene family expansions in T. asiatica that may favour its hepatotropism in the new intermediate host. We also identify potential targets for developing diagnostic or intervention tools against human tapeworms. These data provide new insights into the evolution of Taenia parasites, particularly the recent speciation of T. asiatica.

OBJECTIVE: To estimate the hospitalization rate of severe acute respiratory infection (SARI) cases attributable to influenza in Jingzhou city, Hubei province from 2010 to 2012. METHODS: SARI surveillance was conducted at four hospitals in Jingzhou city, Hubei province from 2010 to 2012. Inpatients meeting the SARI case definition and with informed consent were enrolled to collect their demographic information, clinical features, treatment, and disease outcomes, with their respiratory tract specimens collected for PCR test of influenza virus. RESULTS: From April, 2010 to September, 2012, 19 679 SARI cases enrolled were residents of Jingzhou, and nasopharyngeal swab was collected from 18 412 (93.6%) cases of them to test influenza virus and 13.3% were positive for influenza. During the three consecutive 2010-2012 flu seasons, laboratory-confirmed influenza was associated with 102 per 100 000, 132 per 100 000 and 244 per 100 000, respectively. As for the hospitalization rate attributable to specific type/subtype of influenza virus, 48 per 100 000, 30 per 100 000 and 24 per 100 000 were attributable to A (H3N2), A (H1N1) pdm2009, and influenza B, respectively in 2010-2011 season; 42 per 100 000 [A (H3N2)] and 90 per 100 000 (influenza B) in 2011-2012 season; 90 per 100 000 [A (H3N2)] and one per 100 000 [influenza B] from April, 2010 to September, 2012. SARI hospitalization caused by influenza A or B occurred both mainly among children younger than five years old, with the peak in children aged 0.5 year old. CONCLUSION: Influenza could cause a substantial number of hospitalizations and different viral type/subtype result in different hospitalizations over influenza seasons in Jingzhou city, Hubei province. Children less than five years old should be prioritized for influenza vaccination in China.

Genome-wide association studies (GWAS) have mapped risk alleles for at least ten distinct cancers to a small region of 63,000 bp on chromosome 5p15.33. This region harbors the TERT and CLPTM1L genes; the former encodes the catalytic subunit of telomerase reverse transcriptase and the latter may play a role in apoptosis. To investigate further the genetic architecture of common susceptibility alleles in this region, we conducted an agnostic subset-based meta-analysis (ASSET) across six distinct cancers in 34,248 cases and 45,036 controls. Based on sequential conditional analysis, we identified as many as six independent risk loci marked by common single nucleotide polymorphisms (SNPs): five in the TERT gene (region 1: rs7726159, P=2.10x10-39; region 3: rs2853677, P=3.30x10-36 and PConditional=2.36x10-8; region 4: rs2736098, P=3.87x10-12 and PConditional=5.19x10-6, region 5: rs13172201, P=0.041 and PConditional=2.04x10-6; and region 6: rs10069690, P=7.49x10-15 and PConditional=5.35x10-7) and one in the neighboring CLPTM1L gene (region 2: rs451360; P=1.90x10-18 and PConditional=7.06x10-16). Between three and five cancers mapped to each independent locus with both risk-enhancing and protective effects. Allele specific effects on DNA methylation were seen for a subset of risk loci indicating that methylation and subsequent effects on gene expression may contribute to the biology of risk variants on 5p15.33. Our results provide strong support for extensive pleiotropy across this region of 5p15.33, to an extent not previously observed in other cancer susceptibility loci.

As part of our continuing effort to highlight innovative approaches to improving the health and environment of communities, the Journal is pleased to bring back the bimonthly column from the U.S. Agency for Toxic Substances and Disease Registry (ATSDR). The ATSDR, based in Atlanta, Georgia, is a federal public health agency of the U.S. Department of Health and Human Services and shares a common office of the Director with the National Center for Environmental Health at the Centers for Disease Control and Prevention (CDC). ATSDR serves the public by using the best science, taking responsive public health actions, and providing trusted health information to prevent harmful exposures and diseases related to toxic substances. The purpose of this column is to inform readers of ATSDR's activities and initiatives to better understand the relationship between exposure to hazardous substances in the environment and their impact on human health and how to protect public health. We believe that the column will provide a valuable resource to our readership by helping to make known the considerable resources and expertise that ATSDR has available to assist communities, states, and others to assure good environmental health practice for all is served. The conclusions of this article are those of the author(s) and do not necessarily represent the views of ATSDR, CDC, or the U.S. Department of Health and Human Services. Gary D. Perlman is an environmental health scientist for ATSDR. He is a commissioned officer with the U.S. Public Health Service and has been deployed in support of numerous environmental disasters including hurricanes Katrina, Rita, Isabelle, and Irene, as well as the Deepwater Horizon oil spill. Laurel Berman is the national brownfields coordinator with ATSDR. She coordinates the ATSDR Brownfields/Land-Reuse Health Initiative. Kathryn Leann Lemley Bing is an environmental health scientist and an ATSDR regional representative in Atlanta. She has specialized expertise working in brownfield/land-reuse communities.

Modified vaccinia virus Ankara (MVA) is a safe, attenuated orthopoxvirus that is being developed as a vaccine vector but has demonstrated limited immunogenicity in several early-phase clinical trials. Our objective was to rationally improve the immunogenicity of MVA-based HIV/AIDS vaccines via the targeted deletion of specific poxvirus immune-modulatory genes. Vaccines expressing codon-optimized HIV subtype C consensus Env and Gag antigens were generated from MVA vector backbones that (i) harbor simultaneous deletions of four viral immune-modulatory genes, encoding an interleukin-18 (IL-18) binding protein, an IL-1beta receptor, a dominant negative Toll/IL-1 signaling adapter, and CC-chemokine binding protein (MVADelta4-HIV); (ii) harbor a deletion of an additional (fifth) viral gene, encoding uracil-DNA glycosylase (MVADelta5-HIV); or (iii) represent the parental MVA backbone as a control (MVA-HIV). We performed head-to-head comparisons of the cellular and humoral immune responses that were elicited by these vectors during homologous prime-boost immunization regimens utilizing either high-dose (2 x 10(8) PFU) or low-dose (1 x 10(7) PFU) intramuscular immunization of rhesus macaques. At all time points, a majority of the HIV-specific T cell responses, elicited by all vectors, were directed against Env, rather than Gag, determinants, as previously observed with other vector systems. Both modified vectors elicited up to 6-fold-higher frequencies of HIV-specific CD8 and CD4 T cell responses and up to 25-fold-higher titers of Env (gp120)-specific binding (nonneutralizing) antibody responses that were relatively transient in nature. While the correlates of protection against HIV infection remain incompletely defined, our results indicate that the rational deletion of specific genes from MVA vectors can positively alter their cellular and humoral immunogenicity profiles in nonhuman primates.

Gliomas account for approximately 80 % of all primary malignant brain tumors and, despite improvements in clinical care over the last 20 years, remain among the most lethal tumors, underscoring the need for gaining new insights that could translate into clinical advances. Recent genome-wide association studies (GWAS) have identified seven new susceptibility regions. We conducted a new independent GWAS of glioma using 1,856 cases and 4,955 controls (from 14 cohort studies, 3 case-control studies, and 1 population-based case-only study) and found evidence of strong replication for three of the seven previously reported associations at 20q13.33 (RTEL), 5p15.33 (TERT), and 9p21.3 (CDKN2BAS), and consistent association signals for the remaining four at 7p11.2 (EGFR both loci), 8q24.21 (CCDC26) and 11q23.3 (PHLDB1). The direction and magnitude of the signal were consistent for samples from cohort and case-control studies, but the strength of the association was more pronounced for loci rs6010620 (20q,13.33; RTEL) and rs2736100 (5p15.33, TERT) in cohort studies despite the smaller number of cases in this group, likely due to relatively more higher grade tumors being captured in the cohort studies. We further examined the 85 most promising single nucleotide polymorphism (SNP) markers identified in our study in three replication sets (5,015 cases and 11,601 controls), but no new markers reached genome-wide significance. Our findings suggest that larger studies focusing on novel approaches as well as specific tumor subtypes or subgroups will be required to identify additional common susceptibility loci for glioma risk.

In an analysis of 31,717 cancer cases and 26,136 cancer-free controls from 13 genome-wide association studies, we observed large chromosomal abnormalities in a subset of clones in DNA obtained from blood or buccal samples. We observed mosaic abnormalities, either aneuploidy or copy-neutral loss of heterozygosity, of >2 Mb in size in autosomes of 517 individuals (0.89%), with abnormal cell proportions of between 7% and 95%. In cancer-free individuals, frequency increased with age, from 0.23% under 50 years to 1.91% between 75 and 79 years (P = 4.8 x 10(-8)). Mosaic abnormalities were more frequent in individuals with solid tumors (0.97% versus 0.74% in cancer-free individuals; odds ratio (OR) = 1.25; P = 0.016), with stronger association with cases who had DNA collected before diagnosis or treatment (OR = 1.45; P = 0.0005). Detectable mosaicism was also more common in individuals for whom DNA was collected at least 1 year before diagnosis with leukemia compared to cancer-free individuals (OR = 35.4; P = 3.8 x 10(-11)). These findings underscore the time-dependent nature of somatic events in the etiology of cancer and potentially other late-onset diseases.

Chronic arsenic exposure remains a human health risk; however a clear mode of action to understand gene signaling-driven arsenic carcinogenesis is currently lacking. This study chronically exposed human lung epithelial BEAS-2B cells to low-dose arsenic trioxide to elucidate cancer promoting gene signaling networks associated with arsenic-transformed (B-As) cells. Following a 6 month exposure, exposed cells were assessed for enhanced cell proliferation, colony formation, invasion ability and in vivo tumor formation compared to control cell lines. Collected mRNA was subjected to whole genome expression microarray profiling followed by in silico Ingenuity Pathway Analysis (IPA) to identify lung carcinogenesis modes of action. B-As cells displayed significant increases in proliferation, colony formation and invasion ability compared to BEAS-2B cells. B-As injections into nude mice resulted in development of primary and secondary metastatic tumors. Arsenic exposure resulted in widespread up-regulation of genes associated with mitochondrial metabolism and increased reactive oxygen species protection suggesting mitochondrial dysfunction. Carcinogenic initiation via reactive oxygen species and epigenetic mechanisms was further supported by altered DNA repair, histone, and ROS-sensitive signaling. NF-kappaB, MAPK and NCOR1 signaling disrupted PPARalpha/delta-mediated lipid homeostasis. A 'pro-cancer' gene signaling network identified increased survival, proliferation, inflammation, metabolism, anti-apoptosis and mobility signaling. IPA-ranked signaling networks identified altered p21, EF1alpha, Akt, MAPK, and NF-kappaB signaling networks promoting genetic disorder, altered cell cycle, cancer and changes in nucleic acid and energy metabolism. In conclusion, transformed B-As cells with their whole genome expression profile provide an in vitro arsenic model for future lung cancer signaling research and data for chronic arsenic exposure risk assessment.