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7 result(s) for "Carcinogens, Environmental toxicity Texas."
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Tainted Earth
Smelting is an industrial process involving the extraction of metal from ore. During this process, impurities in ore-including arsenic, lead, and cadmium-may be released from smoke stacks, contaminating air, water, and soil with toxic-heavy metals. The problem of public health harm from smelter emissions received little official attention for much for the twentieth century. Though people living near smelters periodically complained that their health was impaired by both sulfur dioxide and heavy metals, for much of the century there was strong deference to industry claims that smelter operations were a nuisance and not a serious threat to health. It was only when the majority of children living near the El Paso, Texas, smelter were discovered to be lead-exposed in the early 1970s that systematic, independent investigation of exposure to heavy metals in smelting communities began. Following El Paso, an even more serious led poisoning epidemic was discovered around the Bunker Hill smelter in northern Idaho. In Tacoma, Washington, a copper smelter exposed children to arsenic-a carcinogenic threat. Thoroughly grounded in extensive archival research,Tainted Earthtraces the rise of public health concerns about nonferrous smelting in the western United States, focusing on three major facilities: Tacoma, Washington; El Paso, Texas; and Bunker Hill, Idaho. Marianne Sullivan documents the response from community residents, public health scientists, the industry, and the government to pollution from smelters as well as the long road to protecting public health and the environment. Placing the environmental and public health aspects of smelting in historical context, the book connects local incidents to national stories on the regulation of airborne toxic metals. The nonferrous smelting industry has left a toxic legacy in the United States and around the world. Unless these toxic metals are cleaned up, they will persist in the environment and may sicken people-children in particular-for generations to come. The twentieth-century struggle to control smelter pollution shares many similarities with public health battles with such industries as tobacco and asbestos where industry supported science created doubt about harm, and reluctant government regulators did not take decisive action to protect the public's health.
Risk of Cancer for Workers Exposed to Antimony Compounds: A Systematic Review
Background: Antimony (Sb) trioxide and antimony trisulfide are “2B: Possibly carcinogenic to humans” and “3: Unclassifiable” according to the International Agency for Research on Cancer (IARC). The U.S. National Toxicology Program (NTP) concluded that antimony trioxide “is reasonably anticipated to be a human carcinogen based on studies in rats and mice”. We investigated the cancer hazard of antimony compounds for workers, a population with high exposure to antimony substances. Methods: Using the “Guidelines for performing systematic reviews in the development of toxicity factors” (Texas Commission on Environmental Quality (TCEQ) 2017) as a guidance, we established a human and an animal toxicology data stream in Medline and ToxLine. Data from this review were applied in a human health risk assessment. Results: A final pool of 10 occupational and 13 animal toxicology articles resulted after application of TCEQ guidelines. Conclusions: Antimony carcinogenicity evidence involving workers is inadequate, based on confounding, small sample sizes, incomparability across studies, and inadequate reference populations. An increased lung cancer risk cannot be excluded. Evidence for lung neoplasms caused by antimony trioxide inhalation in experimental animals is sufficient. Overall, carcinogenicity in workers is probable (International Agency for Research on Cancer (IARC) 2A). It remains unclear from what occupational exposure duration and dose this effect arises and whether exposure threshold values should be reconsidered.
Cancer risk associated with soil distribution of polycyclic aromatic hydrocarbons within three environmental justice neighborhoods in Houston, Texas
Residents and advocacy groups began voicing concerns over the environmental quality located in the neighborhoods of Kashmere Gardens, Fifth Ward, and Denver Harbor in Houston, TX, following the confirmation of a cancer cluster in 2019 and another in 2021. These neighborhoods are in close proximity to a railyard and former wood treatment plant known to have utilized coal tar creosote and contain polycyclic aromatic hydrocarbons (PAHs). This research took core soil samples in September and October 2020 from 46 sites to assess for the presence and concentration of the U.S. Environmental Protection Agency’s (USEPA) 7 Carcinogenic PAHs. Results showed the cumulative concentration of these PAHs in each sample was variable with a range of 13,767 ng/g to 328 ng/g and a mean of 2,517.2 ng/g ± 3122. A regional soil screening evaluation revealed that 40 of the 46 soil samples were in excess of the USEPAs most conservative screening levels of 1.0 × 10−6 increased cancer risk, but none exceeding levels considered actionable for remediation. This study is a fundamental first step for quantifying the environmental pollutants in this minority-majority community. Findings revealed a low risk of cancer risk based on current PAH concentrations alone but cannot assess contributions from other contaminants or from past, possibly higher, levels of contamination. Further research is needed to identify the potential casual pathways of the observed cancer cluster and to explore possible remediation needs.
Life Cycle Environmental Impact of Biomass Co-Firing with Coal at a Power Plant in the Greater Houston Area
Electricity generation from coal is one of the leading contributors to greenhouse gas emissions in the U.S. and has adverse effects on the environment. Biomass from forest residue can be co-fired with coal to reduce the impact of fossil-fuel power plants on the environment. W. A. Parish power plant (WAP, Richmond, TX, USA) located in the greater Houston area is the largest coal and natural gas-based power generation facility in Texas and is the subject of the current study. A life cycle assessment (LCA) study was performed with SimaPro® and IMPACT 2002+ method, for the replacement of 5%, 10%, and 15% coal (energy-basis) with forest residue at the WAP power plant in Texas. Results from the LCA study indicate that life cycle air emissions of CO2, CO, SO2, PM2.5, NOX, and VOC could reduce by 13.5%, 6.4%, 9.5%, 9.2%, 11.6%, and 7.7% respectively when 15% of coal is replaced with forest residue. Potential life cycle impact decreased across 9 mid-point impact categories of, human/aquatic toxicity, respiratory organics/inorganics, global warming, non-renewable energy, mineral extraction, aquatic acidification, and terrestrial acidification/nitrification. The potential impact across damage/end-point categories of human health, ecosystem quality, climate change, and resources reduced by 8.7%, 3.8%, 13.2%, and 14.8% respectively for 15% co-firing ratio.
Human DNA Adduct Measurements: State of the Art
Human DNA adduct formation (covalent modification of DNA with chemical carcinogens) is a promising biomarker for elucidating the molecular epidemiology of cancer. Classes of compounds for which human DNA adducts have been observed include polycyclic aromatic hydrocarbons (PAHs), nitrosamines, mycotoxins, aromatic amines, heterocyclic amines, ultraviolet light, and alkylating cancer chemotherapeutic agents. Most human DNA adduct exposure monitoring has been performed with either32P-postlabeling or immunoassays, neither of which is able to chemically characterize specific DNA adducts. Recently developed combinations of methods with chemical and physical end points have allowed identification of specific adducts in human tissues. Studies are presented that demonstrate that high ambient levels of benzo[a]pyrene are associated with high levels of DNA adducts in human blood cell DNA and that the same DNA adduct levels drop when the ambient PAH levels decrease significantly. DNA adduct dosimetry, which has been achieved with some dietary carcinogens and cancer chemotherapeutic agents, is described, as well as studies correlating DNA adducts with other biomarkers. It is likely that some toxic, noncarcinogenic compounds may have genotoxic effects, including oxidative damage, and that adverse health outcomes other than cancer may be correlated with DNA adduct formation. The studies presented here may serve as useful prototypes for exploration of other toxicological end points.
Polycyclic Aromatic Hydrocarbons (PAHs), Nitro-PAHs and Related Environmental Compounds: Biological Markers of Exposure and Effects
Lung cancer caused by polycyclic aromatic hydrocarbons (PAHs), nitro-PAHs and related environmental agents is a major problem in industrialized nations. The high case-fatality rate of the disease, even with the best supportive treatment, underscores the importance of primary lung cancer prevention. Development of biomarkers of exposure and effects to PAHs and related compounds is now underway and includes measurement of urinary metabolites of specific PAHs as well as detection of protein and DNA adducts as indicators of effective dose. Validation of these markers in terms of total environmental dose requires that concurrent measures of air levels and potential dermal exposure be made. In addition, the interrelationships between PAH biomarkers must be determined, particularly when levels of the marker in surrogate molecules (e.g., protein) or markers from surrogate tissues (e.g., lymphocyte DNA) are used to assess the risk to the target organ, the lung. Two approaches to biomarker studies will be reviewed in this article: the progress made using blood lymphocytes as surrogates for lung tissues and the progress made developing noninvasive markers of carcinogen-DNA adduct levels in lung-derived cells available in bronchial-alveolar lavage and in sputum. Data are presented from studies in which exfoliated urothelial cells were used as a surrogate tissue to assess exposure to human urinary bladder carcinogens in occupational groups.