Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 3 de 3
Filtrar
Mais filtros

Base de dados
Tipo de documento
País de afiliação
Intervalo de ano de publicação
1.
Environ Res ; 130: 34-42, 2014 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-24566076

RESUMO

BACKGROUND: During the Vietnam War, approximately 20 million gallons of herbicides, including ~10.5 million gallons of dioxin-contaminated Agent Orange, were sprayed by about 34 UC-123 aircraft that were subsequently returned to the United States, without decontamination or testing, to three Air Force reserve units for transport operations (~1971-1982). In 1996, observed dioxin contamination led to withdrawal of these UC-123s from public auction and to their smelting in 2009. Current Air Force and Department of Veterans Affairs policies stipulate that "dried residues" of chemical herbicides and dioxin had not lead to meaningful exposures to flight crew and maintenance personnel, who are thus ineligible for Agent Orange-related benefits or medical examinations and treatment. Sparse monitoring data are available for analysis. METHODS: Three complementary approaches for modeling potential exposures to dioxin in the post-Vietnam war aircraft were employed: (1) using 1994 and 2009 Air Force surface wipe data to model personnel exposures and to estimate dioxin body burden for dermal-oral exposure for dried residues using modified generic US Environmental Protection Agency intake algorithms; (2) comparing 1979 Air Force 2,4- dichlorophenoxyacetic acid and 2,4-5-trichlorophenoxyacetic acid air samples to saturated vapor pressure concentrations to estimate potential dioxin exposure through inhalation, ingestion and skin contact with contaminated air and dust; and (3) applying emission models for semivolatile organic compounds from contaminated surfaces to estimate airborne contamination. RESULTS: Model (1): Body-burden estimates for dermal-oral exposure were 0.92 and 5.4pg/kg body-weight-day for flight crew and maintainers. The surface wipe concentrations were nearly two orders of magnitude greater than the US Army guidance level. Model (2): measured airborne concentrations were at least five times greater than saturated vapor pressure, yielding dioxin estimates that ranged from 13.2-27.0pg/m(3), thus supporting the likelihood of dioxin dust adsorption. Model (3): Theoretical models yielded consistent estimates to Model 2, 11-49pg/m(3), where the range reflects differences in experimental value of dioxin vapor pressure and surface area used. Model (3) results also support airborne contamination and dioxin dust adsorption. CONCLUSIONS: Inhalation, ingestion and skin absorption in aircrew and maintainers were likely to have occurred during post-Vietnam use of the aircraft based on the use of three complementary models. Measured and modeled values for dioxin exceeded several available guidelines. Deposition-aerosolization-redeposition homeostasis of semivolatile organic compound contaminants, particularly dioxin, is likely to have continually existed within the aircraft. Current Air Force and Department of Veterans Affairs policies are not consistent with the available industrial hygiene measurements or with the widely accepted models for semivolatile organic compounds.


Assuntos
Ácido 2,4,5-Triclorofenoxiacético/análise , Ácido 2,4-Diclorofenoxiacético/análise , Dioxinas/análise , Exposição Ambiental/análise , Herbicidas/análise , Militares , Modelos Teóricos , Dibenzodioxinas Policloradas/análise , Ácido 2,4,5-Triclorofenoxiacético/toxicidade , Ácido 2,4-Diclorofenoxiacético/toxicidade , Agente Laranja , Aeronaves , Dioxinas/toxicidade , Herbicidas/toxicidade , Humanos , Masculino , Dibenzodioxinas Policloradas/toxicidade , Estados Unidos , Guerra do Vietnã
2.
Rev Environ Health ; 23(1): 1-37, 2008.
Artigo em Inglês | MEDLINE | ID: mdl-18557596

RESUMO

What do we currently know about the occupational and environmental causes of cancer? As of 2007, the International Agency for Research on Cancer (IARC) identified 415 known or suspected carcinogens. Cancer arises through an extremely complicated web of multiple causes, and we will likely never know the full range of agents or combinations of agents. We do know that preventing exposure to individual carcinogens prevents the disease. Declines in cancer rates-such as the drop in male lung cancer cases from the reduction in tobacco smoking or the drop in bladder cancer among cohorts of dye workers from the elimination of exposure to specific aromatic amines-provides evidence that preventing cancer is possible when we act on what we know. Although the overall age-adjusted cancer incidence rates in the United States among both men and women have declined in the last decade, the rates of several types of cancers are on the rise; some of which are linked to environmental and occupational exposures. This report chronicles the most recent epidemiologic evidence linking occupational and environmental exposures with cancer. Peer-reviewed scientific studies published from January 2005 to June 2007 were reviewed, supplementing our state-of-the-evidence report published in September 2005. Despite weaknesses in certain individual studies, we consider the evidence linking the increased risk of several types of cancer with specific exposures somewhat strengthened by recent publications, among them brain cancer from exposure to non-ionizing radiation, particularly radiofrequency fields emitted by mobile telephones; breast cancer from exposure to the pesticide dichlorodiphenyltrichloroethane (DDT) before puberty; leukemia from exposure to 1,3-butadiene; lung cancer from exposure to air pollution; non-Hodgkin's lymphoma (NHL) from exposure to pesticides and solvents; and prostate cancer from exposure to pesticides, polyaromatic hydrocarbons (PAHs), and metal working fluids or mineral oils. In addition to NHL and prostate cancer, early findings from the National Institutes of Health Agricultural Health Study suggest that several additional cancers may be linked to a variety of pesticides. Our report also briefly describes the toxicological evidence related to the carcinogenic effect of specific chemicals and mechanisms that are difficult to study in humans, namely exposures to bis-phenol A and epigenetic, trans-generational effects. To underscore the multi-factorial, multi-stage nature of cancer, we also present a technical description of cancer causation summarizing current knowledge in molecular biology. We argue for a new cancer prevention paradigm, one based on an understanding that cancer is ultimately caused by multiple interacting factors rather than a paradigm based on dubious attributable fractions. This new cancer prevention paradigm demands that we limit exposure to avoidable environmental and occupational carcinogens, in combination with additional important risk factors like diet and lifestyle. The research literature related to environmental and occupational causes of cancer is constantly growing, and future updates will be carried out in light of new biological understanding of the mechanisms and new methods for studying exposures in human populations. The current state of knowledge is sufficient to compel us to act on what we know. We repeat the call of ecologist Sandra Steingraber: "From the right to know and the duty to inquire flows the obligation to act."


Assuntos
Exposição Ambiental/efeitos adversos , Poluentes Ambientais/toxicidade , Neoplasias/epidemiologia , Doenças Profissionais/epidemiologia , Distribuição por Idade , Causalidade , Humanos , Neoplasias/etiologia , Neoplasias/prevenção & controle , Doenças Profissionais/etiologia , Exposição Ocupacional/efeitos adversos , Política , Prevenção Primária , Distribuição por Sexo
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA