Bernard D. Goldstein

Potential public health hazards, exposures and health effects from unconventional natural gas development.

The rapid increase in unconventional natural gas (UNG) development in the United States during the past decade has brought wells and related infrastructure closer to population centers. This review evaluates risks to public health from chemical and nonchemical stressors associated with UNG, describes likely exposure pathways and potential health effects, and identifies major uncertainties to address with future research. The most important occupational stressors include mortality, exposure to hazardous materials and increased risk of industrial accidents. For communities near development and production sites the major stressors are air pollutants, ground and surface water contamination, truck traffic and noise pollution, accidents and malfunctions, and psychosocial stress associated with community change. Despite broad public concern, no comprehensive population-based studies of the public health effects of UNG operations exist. Major uncertainties are the unknown frequency and duration of human exposure, future extent of development, potential emission control and mitigation strategies, and a paucity of baseline data to enable substantive before and after comparisons for affected populations and environmental media. Overall, the current literature suggests that research needs to address these uncertainties before we can reasonably quantify the likelihood of occurrence or magnitude of adverse health effects associated with UNG production in workers and communities.

Erythropoietic Protoporphyria: Lipid Peroxidation and Red Cell Membrane Damage Associated with Photohemolysis

The mechanism by which long wavelength ultraviolet light hemolyzes red cells obtained from patients with erythropoietic protoporphyria (EPP) was investigated. Previous studies had suggested that irradiation of these red cells with wavelengths of light capable of eliciting dermatological manifestations led to oxygen-dependent colloid osmotic hemolysis through the formation of peroxides. In the present report, lipid peroxidation during in vitro irradiation of EPP red cells with long ultraviolet light was demonstrated by: (a) the formation of 2-thiobarbituric acid reactants; (b) the presence of conjugated diene bonds in red cell lipid; and (c) the selective loss of unsaturated fatty acids proportional to the number of carbon-carbon double bonds in each. Irradiation of EPP red cells was also shown to result in the formation of hydrogen peroxide.Before photohemolysis there was a decline in cell membrane sulfhydryl groups and a loss in activity of the cell membrane enzyme acetylcholinesterase. These parameters provide further evidence suggesting that the cell membrane is a primary site of the photohemolytic effect of long ultraviolet light in EPP red cells. Further evaluation of the radiation-induced inactivation of EPP red cell acetylcholinesterase was performed by radiating mixtures containing bovine erythrocyte acetylcholinesterase and protoporphyrin IX. These studies revealed that the rate of decline in enzyme activity is accelerated by the addition of linoleic acid, an unsaturated fatty acid, but not by palmitic acid, a saturated fatty acid. Partial protection against both photohemolysis and acetylcholinesterase decline is provided by alpha-to-copherol. This lipid antioxidant loses its activity during the irradiation of EPP red cells suggesting that it is utilized in this process.

The inhalation toxicology of benzene: Incidence of hematopoietic neoplasms and hematotoxicity in AKRJ and C57BL6J mice

Abstract AKR J mice and C57BL 6J mice were given lifetime exposures to 100 and 300 ppm benzene, respectively. Peripheral blood cell counts were obtained biweekly throughout the exposures. Anemia and lymphocytopenia were produced in benzene-exposed AKR mice. Twenty percent of the exposed AKR mice developed bone marrow hypoplasia, compared to 2% for the controls. The benzene exposures did not alter the incidence or induction time of the viral-induced lymphomas commonly seen in AKR mice. In C57BL mice, exposure to benzene produced anemia, lymphocytopenia, and neutrophilia accompanied by a left shift. Thirteen (33%) of the exposed C57BL mice developed bone marrow hyperplasia and in four of these mice, hyperplasia was essentially limited to granulopoietic elements. None of the control C57BL mice developed bone marrow hyperplasia. In benzene-exposed C57BL mice there was a significant increase in the incidence of hematopoietic neoplasms including six cases (15%) of thymic lymphoma. Although two control mice (5%) died with lymphoma neither of these tumors involved the thymus. Thymic lymphoma is rare in C57BL mice but can be produced by ionizing radiation and chemical carcinogens.

Protease inhibitors antagonize the activation of polymorphonuclear leukocyte oxygen consumption

Abstract We report that the burst of oxygen consumption, as well as the resultant production of O 2 − • and H 2 O 2 , occurring in activated human polymorphonuclear leukocytes is inhibited by various compounds which have in common the ability to antagonize the effects of proteolytic enzymes. This effect of protease inhibitors was observed with a variety of stimuli, both phagocytic and non-phagocytic, used to activate O 2 − • production in human polymorphonuclear leukocytes. Inhibition was also noted in rat polymorphonuclear leukocytes and alveolar macrophages. The results indicate that proteolysis may be involved in activating the burst of oxygen consumption following stimulation of phagocytic cells.

Stimulation of human polymorphonuclear leukocyte superoxide anion radical production by tumor promoters

Comparison was made of the ability of the potent tumor promoter phorbol myristate acetate (PMA), as well as less active PMA analogs and non-phorbol ester tumor promoters, to stimulate superoxide anion radical (O-.2) production by human polymorphonuclear leukocytes (PMN). The rate of O-.2 production was found to correlate with the tumor-promoting activity of the phorbol esters as opposed to their inflammatory activity. Mezerein and telocidin B were slightly better stimulators of O-.2 production than PMA. Acetic acid was inactive. These data are discussed in terms of a possible role for O-.2 and other reactive oxygen species in tumor promotion.

The Gulf Oil Spill

The 2010 Gulf Oil spill was an occupational, environmental, and community health disaster. This review summarizes the contaminants of concern, toxicologic consequences for humans and the ecosystem, lessons for worker safety, and mental health consequences in the community.

Ozone and Vitamin E

Vitamin E deficiency in rats is associated with a greater susceptibility to lethal levels of ozone. Exposure of rats to sublethal ozone concentrations produces an accelerated decline in serum vitamin E levels. These findings are consistent with the possibility that lipid peroxidation is a mechanism of ozone toxicity.

Electron Paramagnetic Resonance Spectroscopy

The air pollutant ozone Is believed to exert its deleterious biological effects by the formation of free radicals. However these free radicals have not been directly measured. It has also been suggested that peroxidation of cell membrane unsaturated fatty acids is an important mechanism In ozone toxicity. Utilizing electron paramagnetic resonance technique, direct ozonization of linoleic acid produced measurable free radicals after a two-hour induction period.

Effect of Ozone on Lipid Peroxidation in the Red Blood Cell.

Summary In vitro exposure of erythrocytes to ozone resulted in an increased osmotic fragility associated with the formation of TBA reactants. This suggests that lipid peroxidation may be involved in the mechanism of ozone toxicity.

Risks and Risk Governance in Unconventional Shale Gas Development

A broad assessment is provided of the current state of knowledge regarding the risks associated with shale gas development and their governance. For the principal domains of risk, we identify observed and potential hazards and promising mitigation options to address them, characterizing current knowledge and research needs. Important unresolved research questions are identified for each area of risk; however, certain domains exhibit especially acute deficits of knowledge and attention, including integrated studies of public health, ecosystems, air quality, socioeconomic impacts on communities, and climate change. For these, current research and analysis are insufficient to either confirm or preclude important impacts. The rapidly evolving landscape of shale gas governance in the U.S. is also assessed, noting challenges and opportunities associated with the current decentralized (state-focused) system of regulation. We briefly review emerging approaches to shale gas governance in other nations, and consider new governance initiatives and options in the U.S. involving voluntary industry certification, comprehensive development plans, financial instruments, and possible future federal roles. In order to encompass the multiple relevant disciplines, address the complexities of the evolving shale gas system and reduce the many key uncertainties needed for improved management, a coordinated multiagency federal research effort will need to be implemented.