Volume 27, Issue 2-3

No abstract available.

To evaluate the possible impact that the BP Deepwater Horizon Gulf oil spill might have had on pollution levels in the State of Mississippi, the Mississippi Department of Environmental Quality (MDEQ), and the US Environmental Protection Agency (EPA) analyzed surface water and ambient air quality pollutant data taken from MDEQ and EPA monitoring sites on the Mississippi Gulf Coast. The data were compared with acute, chronic, and human health air and water quality standards to determine whether the pollutant levels occurring during the oil spill could cause ecological and/or human health effects. The water quality data indicated levels of nickel, vanadium, volatile organic compounds (VOCs), and semivolatile organic compounds analyzed remained below acute and chronic levels for both aquatic life and human health. The air quality sampling data showed that the levels of VOCs and polycyclic aromatic hydrocarbons associated with the oil spill were well below EPA chronic and human health screening levels. A comparison of the air quality monitoring data taken before and after the oil spill showed that the concentrations of ozone and fine particulate matter were elevated for brief periods but remained below actionable levels.

Reducing harm from secondhand smoke (SHS) exposure is especially critical for children. Current strategies aimed at reducing SHS exposure in workplaces and public spaces have been successful in reducing adult exposure, yet infants and children, who are greatly susceptible to the adverse health effects of SHS exposure, continue to be among the most exposed in the USA. Novel strategies are needed that can work in combination with those aimed at removing SHS exposure from children, our single highest priority. The overall aim of this monograph is to demonstrate how nutrition has the potential to ameliorate adverse SHS-related outcomes in children. This aim is accomplished by providing evidence for the following: susceptibility to SHS exposure is greatest during critical windows of lung and immune system development; dietary factors act on SHS mechanisms and have the potential to reduce the risk of related adverse outcomes; the key mechanisms of adverse SHS-related outcomes include reduced nutrient status, oxidative stress, compromised immune function, and chronic inflammation; identification of nutrition-related interventions for SHS-exposed populations is a timely issue and requires future research. Our primary aim should be to eliminate SHS exposure. Until infants and children are no longer exposed to SHS, however, we propose investigating nutrition-focused interventions as a method to reduce the risk of SHS-related health outcomes for infants and children.

Benzene is a widespread, naturally occurring substance of environmental concern as systemic exposure in humans is proven to be carcinogenic. Dermal exposure is a common and significant route of systemic entry and percutaneous absorption is critical in exposure risk assessment. This article reviews the scientific principles, methodologies, and research behind the multiple steps of the percutaneous absorption of benzene in animals and man and the application of this information to optimize exposure risk assessments. A focus on occupational exposures to benzene is made with an exploration of the limitations of current preventative measures and hazard assessments. Finally, recommendations for future research to fill existing knowledge gaps are made.

Year 2011 noted the first definable ozone “hole” in the Arctic region, serving as an indicator to the continued threat of dangerous ultraviolet radiation (UVR) exposure caused by the deterioration of stratospheric ozone in the northern hemisphere. Despite mandates of the Montreal Protocol to phase out the production of ozone-depleting chemicals (ODCs), the relative stability of ODCs validates popular notions of persistent stratospheric ozone for several decades. Moreover, increased UVR exposure through stratospheric ozone depletion is occurring within a larger context of physiologic stress and climate change across the biosphere. In this review, we provide commentaries on stratospheric ozone depletion with relative comparisons between the well-known Antarctic ozone hole and the newly defined ozone hole in the Arctic. Compared with the Antarctic region, the increased UVR exposure in the Northern Hemisphere poses a threat to denser human populations across North America, Europe, and Asia. In this context, we discuss emerging targets of UVR exposure that can potentially offset normal biologic rhythms in terms of taxonomically conserved photoperiod-dependent seasonal signaling and entrainment of circadian clocks. Consequences of seasonal shifts during critical life history stages can alter fitness and condition, whereas circadian disruption is increasingly becoming associated as a causal link to increased carcinogenesis. We further review the significance of genomic alterations via UVR-induced modulations of phase I and II transcription factors located in skin cells, the aryl hydrocarbon receptor (AhR), and the nuclear factor (erythroid-derived 2)-related factor 2 (Nrf2), with emphasis on mechanism that can lead to metabolic shifts and cancer. Although concern for adverse health consequences due to increased UVR exposure are longstanding, recent advances in biochemical research suggest that AhR and Nrf2 transcriptional regulators are likely targets for UVR-mediated dysregulations of rhythmicity and homeostasis among animals, including humans.

This review introduces a potential unifying concept involving the risk of chronic diseases in which early-life exposure to endocrine-disrupting chemicals (EDCs) can program host responses for misregulated inflammation. Inflammation is a part of host defense against pathogenic challenges and one of the processes necessary for normal tissue homeoregulation and for reproduction (e.g., implantation, labor). Deviations from tightly regulated inflammation present a significant health risk because unresolved inflammation can compromise tissue function and increase the risk for later-life cancer in the affected target tissue. The critical windows of innate immune vulnerability during prenatal and neonatal maturation are when developmental programming and the trajectory for childhood and adult inflammatory responses are largely established. Misregulated inflammation is a common thread that links most significant chronic diseases and conditions across all physiologic systems as well as the associated comorbid conditions. As a result, chronic diseases exist both as a myriad of conditions and as an integrated, dysfunctionally connected unit. Because the hormone microenvironment exerts a significant effect on resident innate immune cell function, endocrine disruption is likely to produce misregulated inflammation in tissues. Among the factors determining specific health risks and disease outcomes across a lifetime are the age of exposure, sex, genetic background, and transgenerational epigenetic experiences. Additional research into early-life EDC exposure and misregulation of inflammation appears to be a useful avenue for reducing environmental health risks.

Inflammatory response is implicated as a biologic mechanism that links particulate matter (PM) air pollution with health effects. C-reactive protein (CRP), an important acutephase reactant with profound proinflammatory properties, is used clinically as an indicator of the presence and intensity of inflammation. In vitro and in vivo animal studies suggest that CRP levels increase in response to PM exposure, but there was no consistency in epidemiologic studies. Herein, a systematic review was conducted to examine the association between PM exposure and serum CRP levels in humans. Elevated CRP levels were consistently found among children, and CRP elevations were also observed among healthy adults, albeit requiring higher peak levels of PM exposure. PM-induced CRP responses were not consistently found in adults with chronic inflammatory conditions, perhaps because of the use of anti-inflammatory medications in this population. Of the eight examined randomized trials, only one trial with a longer intervention period supported the effect of PM exposure on CRP concentrations. To provide conclusive evidence, further epidemiologic studies are needed to better quantify the magnitude of CRP level changes in response to PM with well-defined study populations and better control of various confounding factors.