The application of PTR-MS and non-targeted analysis to characterize VOCs emitted from a plastic recycling facility fire.

Background: On April 11th, 2023, the My Way Trading (MWT) recycling facility in Richmond, Indiana caught fire, mandating the evacuation of local residents and necessitating the U.S. Environmental Protection Agency (EPA) to conduct air monitoring.

Association of arsenic exposure with measles antibody titers in US children: Influence of sex and serum folate levels.

Exposure to arsenic during childhood is associated with various adverse health conditions. However, little is known about the effect of arsenic exposure on vaccine-related humoral immunity in children. We analyzed data from the National Health and Nutrition Examination Survey (2003-2004 and 2009-2010) to study the relationship between urinary arsenic and measles antibody levels in 476 US children aged 6-11.

Air Pollutant Patterns and Human Health Risk following the East Palestine, Ohio, Train Derailment.

On February 3, 2023, a train carrying numerous hazardous chemicals derailed in East Palestine, OH, spurring temporary evacuation of residents and a controlled burn of some of the hazardous cargo. Residents reported health symptoms, including headaches and respiratory, skin, and eye irritation. Initial data from U.

Maternal exposure to ultrafine particles enhances influenza infection during pregnancy.

Background: Interactions between air pollution and infectious agents are increasingly recognized and critical to identify, especially to protect vulnerable populations. Pregnancy represents a vulnerable period for influenza infection and air pollution exposure, yet interactions during pregnancy remain unclear. Maternal exposure to ultrafine particles (UFPs, [Formula: see text] 100 nm diameter), a class of particulate matter ubiquitous in urban environments, elicits unique pulmonary immune responses.

Ultrafine Particulate Exposure Yields Sex- and Dose-Specific Responses to Neonatal Respiratory Syncytial Virus Infection.

Exposure to particulate matter (PM) is associated with lower respiratory tract infections. The role of ultrafine particles (UFPs, ≤0.1 μm) in respiratory disease is not fully elucidated, especially in models of immunologically immature populations.

NRF2-Dependent Placental Effects Vary by Sex and Dose following Gestational Exposure to Ultrafine Particles.

Exposure to ultrafine particles (UFPs, PM) during pregnancy triggers placental oxidative stress and inflammation, similar to fine PM (PM). The gene encodes a redox-sensitive transcription factor that is a major regulator of antioxidant and anti-inflammatory responses. Disruption of NRF2 is known to substantially enhance PM-driven oxidant and inflammatory responses; however, specific responses to UFP exposure, especially during critical windows of susceptibility such as pregnancy, are not fully characterized; To investigate the role of NRF2 in regulating maternal antioxidant defenses and placental responses to UFP exposure, wildtype (WT) and pregnant mice were exposed to either low dose (LD, 100 µg/m) or high dose (HD, 500 µg/m) UFP mixture or filtered air (FA, control) throughout gestation; HD-exposed female offspring exhibited significantly reduced fetal and placental weights.

NRF2 Protects against Altered Pulmonary T Cell Differentiation in Neonates Following In Utero Ultrafine Particulate Matter Exposure.

Early life exposure to particulate matter (PM) air pollution negatively impacts neonatal health. The underlying mechanisms following prenatal exposure, particularly to ultrafine particles (UFP, diameter ≤ 0.1 μm), are not fully understood; To evaluate the role of in response to in utero UFP exposure, we exposed time-mated -deficient () or wildtype (WT) mice to filtered air (FA) or 100 μg/m ultrafine PM daily throughout pregnancy.

Gestational Exposure to Ultrafine Particles Reveals Sex- and Dose-Specific Changes in Offspring Birth Outcomes, Placental Morphology, and Gene Networks.

Particulate matter (PM) causes adverse developmental outcomes following prenatal exposure, but the underlying biological mechanisms remain uncertain. Here we elucidate the effects of diesel exhaust ultrafine particle (UFP) exposure during pregnancy on placental and fetal development. Time-mated C57Bl/6n mice were gestationally exposed to UFPs at a low dose (LD, 100 µg/m3) or high dose (HD, 500 µg/m3) for 6 h daily.

Polycyclic Aromatic Hydrocarbons in Houston Parks After Hurricane Harvey.

Unprecedented inland precipitation and catastrophic flooding associated with Hurricane Harvey potentially redistributed contaminants from industrial sites and transportation infrastructure to recreational areas that make up networks of green infrastructure, creeks, and waterways used for flood control throughout the Greater Houston Area. Sediment samples were collected in parks located near the Buffalo Bayou watershed 1 week after Hurricane Harvey made landfall and again 7 weeks later. Total concentrations of the U.

Air pollution and children's health-a review of adverse effects associated with prenatal exposure from fine to ultrafine particulate matter.

Background: Particulate matter (PM), a major component of ambient air pollution, accounts for a substantial burden of diseases and fatality worldwide. Maternal exposure to PM during pregnancy is particularly harmful to children's health since this is a phase of rapid human growth and development.

Method: In this review, we synthesize the scientific evidence on adverse health outcomes in children following prenatal exposure to the smallest toxic components, fine (PM) and ultrafine (PM) PM.

Maternal exposure to polycyclic aromatic hydrocarbons in South Texas, evaluation of silicone wristbands as personal passive samplers.

Background: Prenatal exposure to polycyclic aromatic hydrocarbons (PAHs) is associated with adverse health effects in children. Valid exposure assessment methods with accurate spatial and temporal resolution across pregnancy is a critical need for advancing environmental health studies.

Objective: The objective of this study was to quantify maternal PAH exposure in pregnant women residing in McAllen, Texas where the prematurity rate and childhood asthma prevalence rates are high.

Application of the navigation guide systematic review methodology to evaluate prenatal exposure to particulate matter air pollution and infant birth weight.

Low birth weight is an important risk factor for many co-morbidities both in early life as well as in adulthood. Numerous studies report associations between prenatal exposure to particulate matter (PM) air pollution and low birth weight. Previous systematic reviews and meta-analyses report varying effect sizes and significant heterogeneity between studies, but did not systematically evaluate the quality of individual studies or the overall body of evidence.

Gestational exposure to particulate air pollution exacerbates the growth phenotypes induced by preconception paternal alcohol use: a multiplex model of exposure.

It is now clear that parental histories of drug use, toxicant exposure, and social stress all have a significant influence on the health and development of the next generation. However, the ability of epigenetic parental life memories to interact with subsequent gestational exposures and cumulatively modify the developmental trajectory of the offspring remains an unexplored perspective in toxicology. Studies from our laboratory have identified male-specific postnatal growth restriction in a mouse model of chronic, preconception paternal alcohol exposure.

Development of broad-acting clays for the tight adsorption of benzo[a]pyrene and aldicarb.

People and animals can be unintentionally exposed to complex mixtures of hazardous chemicals that can threaten the safety of food and water supplies following natural and man-made disasters and emergencies. Our research has focused on the development of broad-acting adsorbents that will tightly bind environmental contaminants in the gastrointestinal tract and decrease their bioavailability to humans and animals during these events. In this study, benzo[a]pyrene (BaP) and aldicarb were used as representative chemicals due to their high toxicity and extensive distribution in the environment.

Serum miR-182 is a predictive biomarker for dichotomization of risk of hepatocellular carcinoma in rats.

Exploration of animal models leads to discoveries that can reveal candidate biomarkers for translation to human populations. Herein, a model of hepatocarcinogenesis and protection was used in which rats treated with aflatoxin (AFB ) daily for 28 days (200 µg/kg BW) developed tumors compared with rats completely protected from tumors by concurrent administration of the chemoprotective agent, 1-[2-cyano-3-,12-dioxooleana-1,9(11)-dien-28-oyl]imidazole (CDDO-Im). Differential expression of miRNAs in tumors (AFB ) and nontumor (AFB  + CDDO-Im) bearing livers and their levels in sera over the life-course of the animals was determined.

Adverse organogenesis and predisposed long-term metabolic syndrome from prenatal exposure to fine particulate matter.

Exposure to fine particulate matter (PM) during pregnancy is associated with high risks of birth defects/fatality and adverse long-term postnatal health. However, limited mechanistic data are available to assess the detailed impacts of prenatal PM exposure. Here we evaluate fine PM exposure during pregnancy on prenatal/postnatal organogenesis in offspring and in predisposing metabolic syndrome for adult life.

In utero ultrafine particulate matter exposure causes offspring pulmonary immunosuppression.

Early life exposure to fine particulate matter (PM) in air is associated with infant respiratory disease and childhood asthma, but limited epidemiological data exist concerning the impacts of ultrafine particles (UFPs) on the etiology of childhood respiratory disease. Specifically, the role of UFPs in amplifying Th2- and/or Th17-driven inflammation (asthma promotion) or suppressing effector T cells (increased susceptibility to respiratory infection) remains unclear. Using a mouse model of in utero UFP exposure, we determined early immunological responses to house dust mite (HDM) allergen in offspring challenged from 0 to 4 wk of age.

Profound changes in miRNA expression during cancer initiation by aflatoxin B and their abrogation by the chemopreventive triterpenoid CDDO-Im.

Aflatoxin B (AFB ) is a potent human and animal hepatocarcinogen. To investigate the effects of aflatoxin on miRNA expression during the initiation phase of carcinogenesis, next-generation sequencing was used to analyze liver tissues from F344 rats exposed to 200 μg/kg per day AFB for 4 week. A panel of miRNAs was identified that was upregulated with AFB treatment compared to controls: rno-miR-434-3p, rno-miR-411-5p, rno-miR-221-3p, rno-miR-127-3p, rno-miR-205, rno-miR-429, rno-miR-34a-5p, rno-miR-181c-3p, rno-miR-200b-3p, and rno-miR-541-5p.

Genetic or pharmacologic activation of Nrf2 signaling fails to protect against aflatoxin genotoxicity in hypersensitive GSTA3 knockout mice.

Mice are resistant to aflatoxin hepatotoxicity, primarily due to high expression of glutathione S-transferases (GSTs), and in particular the GSTA3 subunit. Nuclear factor erythroid 2 related factor 2 (Nrf2) signaling, which controls a broad-based cytoprotective response, was activated either genetically or pharmacologically in an attempt to rescue GSTA3 knockout mice from aflatoxin genotoxicity. Genetic activation of Nrf2 signaling was attained in a GSTA3: hepatocyte-specific Keap1 double knockout (DKO) mouse whereas pharmacologic activation of Nrf2 was achieved through pretreatment of mice with the triterpenoid 1-[2-cyano-3-,12-dioxoleana-1,9(11)-dien-28-oyl] imidazole (CDDO-Im) prior to aflatoxin B1 exposure.

Complete protection against aflatoxin B(1)-induced liver cancer with a triterpenoid: DNA adduct dosimetry, molecular signature, and genotoxicity threshold.

In experimental animals and humans, aflatoxin B1 (AFB1) is a potent hepatic toxin and carcinogen. The synthetic oleanane triterpenoid 1-[2-cyano-3-,12-dioxooleana-1,9(11)-dien-28-oyl]imidazole (CDDO-Im), a powerful activator of Keap1-Nrf2 signaling, protects against AFB1-induced toxicity and preneoplastic lesion formation (GST-P-positive foci). This study assessed and mechanistically characterized the chemoprotective efficacy of CDDO-Im against AFB1-induced hepatocellular carcinoma (HCC).

Reduction in the urinary aflatoxin M1 biomarker as an early indicator of the efficacy of dietary interventions to reduce exposure to aflatoxins.

Aflatoxin B1 is a persistent public health issue in Ghana. Assessment of AFB1 intervention efficacy is currently dependent on long-term biomarkers. This study was designed to determine whether daily AFM1 biomarker levels could be utilized as an early detection method for intervention efficacy.

Aflatoxin and PAH exposure biomarkers in a U.S. population with a high incidence of hepatocellular carcinoma.

The incidence of hepatocellular carcinoma (HCC) is significantly elevated in a Hispanic community in Bexar County, Texas. Chronic exposure to dietary aflatoxins (AFs) is a major risk factor for HCC; increased risk has been linked to polycyclic aromatic hydrocarbon (PAH) co-exposure and hepatitis virus infection. The aims of this study were to assess AF and PAH exposures, investigate dietary factors that may contribute to increased AF exposure, and determine the prevalence of hepatitis virus infection in Bexar Co.

HIV and hepatocellular and esophageal carcinomas related to consumption of mycotoxin-prone foods in sub-Saharan Africa.

Background: Promotion of the HIV epidemic by aflatoxin is postulated but not yet established. Sub-Saharan populations commonly consume food contaminated by mycotoxins, particularly aflatoxins (predominantly found in peanut, maize, rice, and cassava) and fumonisins, which occur primarily in maize. Aflatoxin promotes hepatocellular cancer, and fumonisin may promote esophageal cancer.

PAH exposure in a Ghanaian population at high risk for aflatoxicosis.

It was postulated that a population in sub-Saharan Africa, known to be at high risk for aflatoxicosis due to frequent ingestion of aflatoxin (AF)-contaminated foods could also be exposed to polycyclic aromatic hydrocarbons (PAHs) from a variety of environmental sources. Previously, participants in this population were shown to be highly exposed to AFs, and this exposure was significantly reduced by intervention with NovaSil clay (NS). Objectives of this study were 1) to assess PAH exposure in participants from the AF study using urinary biomarker 1-hydroxypyrene (1-OHP); 2) examine the effect of NS clay and placebo (cellulose) treatment on 1-OHP levels; and 3) determine potential association(s) between AF and PAH exposures.