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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.

Due to their unique chemical properties, per- and polyfluoroalkyl substances (PFAS) have been used extensively as industrial surfactants and processing aids. While several types of PFAS have been voluntarily phased out by their manufacturers, these chemicals continue to be of ecological and public health concern due to their persistence in the environment and their presence in living organisms. Moreover, while the compounds referred to as “legacy” PFAS remain in the environment, alternative compounds have emerged as replacements for their legacy predecessors and are now detected in numerous matrices. In this review, we discuss the historical uses of PFAS, recent advances in analytical techniques for analysis of these compounds, and the fate of PFAS in the environment. In addition, we evaluate current biomonitoring studies of human exposure to legacy and emerging PFAS and examine the associations of PFAS exposure with human health impacts, including cancer- and non-cancer-related outcomes. Special focus is given to short-chain perfluoroalkyl acids (PFAAs) and ether-substituted, polyfluoroalkyl alternatives including hexafluoropropylene oxide dimer acid (HFPO-DA; tradename GenX), 4,8-dioxa-3H-perfluorononanoic acid (DONA), and 6:2 chlorinated polyfluoroethersulfonic acid (6:2 Cl-PFESA; tradename F-53B).

Mycotoxins are the most frequently occurring natural contaminants in human and animal diet. Among them, deoxynivalenol (DON), produced by Fusarium, is one of the most prevalent and thus represent an important health risk. Recent detection methods revealed new mycotoxins and new molecules derivated from the \"native\" mycotoxin. The main derivates of DON are the acetylated forms produced by the fungi (3-and 15acetyl-DON), the biologically \"modified\" forms produced by the plant (deoxynivalenol-3-β-D-glucopyranoside), or after bacteria transformation (de-epoxy DON, 3-epi-DON and 3-keto-DON) as well as the chemical \"modified\" forms (norDON A-C and DON-sulfonates). High proportions of acetylated and modified forms of DON co-occur with DON, increasing the exposure and the health risk. DON and its acetylated and modified forms are rapidly absorbed following ingestion. At the molecular level DON binds to the ribosome, induces a ribotoxic stress leading to the activation of MAP kinases, cellular cell-cycle arrest and apoptosis. The toxic effects of DON include emesis and anorexia, alteration of intestinal and immune functions, reduced absorption of the nutrients as well as increased susceptibility to infection and chronic diseases. In contrast to DON, very little information exists concerning the acetylated and modified forms; some can be converted back to DON, their ability to bind to the ribosome and to induce cellular effect varied according to the toxin. Except for the acetylated forms, their toxicity and impact on human and animal health are poorly documented.

A growing number of well-designed epidemiological and molecular studies provide substantial evidence that the pesticides used in agricultural, commercial, and home and garden applications are associated with excess cancer risk. This risk is associated both with those applying the pesticide and, under some conditions, those who are simply bystanders to the application. In this article, the epidemiological, molecular biology, and toxicological evidence emerging from recent literature assessing the link between specific pesticides and several cancers including prostate cancer, non-Hodgkin lymphoma, leukemia, multiple myeloma, and breast cancer are integrated. Although the review is not exhaustive in its scope or depth, the literature does strongly suggest that the public health problem is real. If we are to avoid the introduction of harmful chemicals into the environment in the future, the integrated efforts of molecular biology, pesticide toxicology, and epidemiology are needed to help identify the human carcinogens and thereby improve our understanding of human carcinogenicity and reduce cancer risk. [PUBLICATION ABSTRACT]

Acrolein alters cell proliferation, cell death, or nutrient supply, inhibiting tumour suppressor genes and activating proto-oncogenes in cultured human and rodent cells, and inducing hyperplasia and metaplasia in the rodent respiratory system.2,3 Overall, there is “strong” evidence that acrolein exhibits multiple key characteristics of carcinogens, primarily from studies with human primary cells and studies in experimental systems, supported by studies in humans on DNA adducts. An electrophilic α,β-unsaturated aldehyde (enal), crotonaldehyde forms cyclic adducts in DNA as well as DNA interstrand and DNA–protein cross-links. α-Methyl-γ-hydroxy-1,N2-propanodeoxyguanosine has been detected in human saliva, urine, blood, mammary tissue, oral (gingival) tissue, liver, and placenta.4,5 Adduct levels were significantly elevated in tobacco smokers.4 Crotonaldehyde-derived DNA adducts have also been detected in human cells in vitro and in rodents. Crotonaldehyde is genotoxic, exhibiting clastogenicity in human primary cells and human cell lines,8 dominant lethality and chromosomal aberrations in rodents, and gene mutations in cultured rodent cells, Drosophila melanogaster, Salmonella typhimurium, and plasmid systems.

Environmental exposure to bisphenol A (BPA) affects mammary gland development in rodents and primates. Prenatal exposure to environmentally relevant doses of BPA increased the number of intraductal hyperplasias and ductal carcinomas in situ by 50 days of age in Wistar-Furth rats. We aimed to determine whether BPA exposure of dams during gestation only or throughout lactation affects the incidence of mammary gland neoplasia in female offspring. We treated pregnant Sprague-Dawley rats with BPA at 0, 0.25, 2.5, 25, or 250 μg BPA/kg BW/day from gestational day (GD) 9 to birth and from GD9 to postnatal day (PND) 21. Mammary glands from BPA-exposed offspring were examined at four time points for preneoplastic and neoplastic lesions. To assess circulating BPA levels, we exposed pregnant rats to vehicle or 250 μg BPA/kg BW/day during gestation only or during gestation/lactation and analyzed sera from dams, fetuses, and nursing pups for total and unconjugated BPA. Total and unconjugated BPA were detected in sera from 100% of dams and fetuses and 33% of pups exposed to 250 μg BPA/kg BW/day. Unconjugated BPA levels in exposed dams and fetuses (gestational) and in exposed dams and pups (gestational/lactational) were within levels found in humans. Preneoplastic lesions developed in BPA-exposed female offspring across all doses as early as PND50. Unexpectedly, mammary gland adenocarcinomas developed in BPA-exposed offspring by PND90. Our findings suggest that developmental exposure to environmentally relevant levels of BPA during gestation and lactation induces mammary gland neoplasms in the absence of any additional carcinogenic treatment. Thus, BPA may act as a complete mammary gland carcinogen.

Genotoxicity of chemical compounds is primarily associated with the interaction with DNA, formation of mutations, damage to chromosomes and initiating carcinogenesis processes. Currently, many compounds found in the environment are considered to be genotoxic agents, among them chromium: trivalent (III) and hexavalent (VI). The genotoxicity of hexavalent (VI) chromium has been proven in numerous epidemiological, in vitro and in vivo studies. The main source of Cr (VI) is environmental pollution associated with its use in various industries. On the other hand, the role of chromium (III) as a microelement is widely discussed. Due to its beneficial properties, associated with maintaining adequate blood glucose levels and supporting weight loss, it is widely used in the form of dietary supplements, often in doses exceeding the daily requirement. However, the safety of chromium compounds is disputable. Data about the mechanism of genotoxic effects are still incomplete. The aim of this review is to present the current knowledge about the induction of genotoxicity from two forms of chromium: trivalent (III) and hexavalent (VI). Chromium (VI) is a carcinogen with proven mutagenic and genotoxic effects, but this issue is still being investigated by scientists. In recent years, numerous studies have also been conducted on the genotoxic effect of chromium (III). Due to the still unexplained mechanism of the genotoxic action and incomplete knowledge about the transformation of chromium in the body, further research is needed, especially due to the growing popularity of Cr (III) compounds and their consumption in the form of dietary supplements and doubts as to the safety of its use, as well as environmental exposure to Cr (VI).

Background: Exposure to arsenic, an established human carcinogen, through consumption of highly contaminated drinking water is a worldwide public health concern. Several mechanisms by which arsenical compounds induce tumorigenesis have been proposed, including oxidative stress, genotoxic damage, and chromosomal abnormalities. Recent studies have suggested that epigenetic mechanisms may also mediate toxicity and carcinogenicity resulting from arsenic exposure. Objective: We examined the evidence supporting the roles of the three major epigenetic mechanisms—DNA methylation, histone modification, and microRNA (miRNA) expression—in arsenic toxicity and, in particular, carcinogenicity. We also investigated future research directions necessary to clarify epigenetic and other mechanisms in humans. Data sources and synthesis: We conducted a PubMed search of arsenic exposure and epigenetic modification through April 2010 and summarized the in vitro and in vivo research findings, from both our group and others, on arsenic-associated epigenetic alteration and its potential role in toxicity and carcinogenicity. Conclusions: Arsenic exposure has been shown to alter methylation levels of both global DNA and gene promoters; histone acetylation, methylation, and phosphorylation; and miRNA expression, in studies analyzing mainly a limited number of epigenetic end points. Systematic epigenomic studies in human populations exposed to arsenic or in patients with arsenic-associated cancer have not yet been performed. Such studies would help to elucidate the relationship between arsenic exposure, epigenetic dysregulation, and carcinogenesis and are becoming feasible because of recent technological advancements.