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Advancing Environmental Justice through Community-Based Participatory Research

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... Related to larger ideas of energy justice, both Indigenous and non-Indigenous communities playing host to areas of fossil-fuel capitalism have been labelled sacrifice zones [45] -places that live with dangerous health consequences for the 'betterment' of larger society 10 (see also [27,46,47]). Targeted communities are often home to marginalized populations, including Indigenous populations of Canada [48]. ...
... Problems with the ways in which Site C and Muskrat Falls (in particular) have been planned and built have created 'green energy' sacrifice zones [27,45]. These developments that are purported to be for the betterment of larger society [46,47], target Indigenous health and ways of life (as in [49]). Continued development patterns should question the sincerity of the Federal government's commitments, while also suggesting a new form of energy injustice has arrived [24,44]. ...
... Introduction: Citizen science After decades of traditional health and environmental studies which left many communities -especially low-income and communities of color -feeling disempowered, community involvement in the production of science is being heralded as necessary for the achievement of environmental justice (Shepard 2002;Cohen and Ottinger 2011;. Citizen science (CS) is broadly defined as partnerships between scientists and laypeople (nonscientists) in which data is collected, analyzed, and shared Jordan et al. 2012). ...
... CBPR "begins with a research topic of importance to the community with the aim of combining knowledge and action for social change to improve community health and eliminate health disparities" (Minkler and Wallerstein 2008, 7). In recent years, community/academic partnerships using a CBPR approach have played an important role in bringing attention to, and addressing situations of, environmental injustice (Shepard 2002). ...
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This book examines the relationship between environmental justice and citizen science, focusing on enduring issues and new challenges in a post-truth age. Debates over science, facts, and values have always been pivotal within environmental justice struggles. For decades, environmental justice activists have campaigned against the misuses of science, while at the same time engaging in community-led citizen science. However, post-truth politics has threatened science itself. This book makes the case for the importance of science, knowledge, and data that are produced by and for ordinary people living with environmental risks and hazards. The international, interdisciplinary contributions range from grassroots environmental justice struggles in American hog country and contaminated indigenous communities, to local environmental controversies in Spain and China, to questions about “knowledge justice,” citizenship, participation, and data in citizen science surrounding toxicity. The book features inspiring studies of community-based participatory environmental health and justice research; different ways of sensing, witnessing, and interpreting environmental injustice; political strategies for seeking environmental justice; and ways of expanding the concepts and forms of engagement of citizen science around the world. While the book will be of critical interest to specialists in social and environmental sciences, it will also be accessible to graduate and postgraduate audiences. More broadly, the book will appeal to members of the public interested in social justice issues, as well as community members who are thinking about participating in citizen science and activism. Toxic Truths includes distinguished contributing authors in the field of environmental justice, alongside cutting-edge research from emerging scholars and community activists.
... My hometown of Buffalo, NY's first mayoral candidate identifying as a Black woman whose campaign has gained national attention, India Walton, pointed out in a newsletter that the word "radical" derives from radix, the Latin word for "root" as she seeks to address the roots of social problems (Walton 2021 Summarized in Figure 1.5, these principles go hand in hand with those laid out by scholars and activists working on civic science and community-based research projects, approaches that I describe in this section (Carroll et al. 2020 Communities living near oil and gas facilities across the US have been confronting their burden of proving environmental harm by measuring VOCs using EPA-approved protocols and tools such as bucket samplers 19 and SUMMA canisters 20 to publish white papers (Villa et al. 2017a), work with academics to produce peer-reviewed publications (Macey et al. 2014), and build collective efficacy. This work occurs in the framework of community-based participatory research (CBPR), which incorporates lay perspectives into environmental monitoring, research, and policymaking (Shepard 2002;B. Allen 2003;Ottinger 2010b;Commodore et al. 2017). ...
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Karnes County, Texas, is in the Eagle Ford Shale Play, which is one of the largest shale plays in the US where oil and gas are extracted then processed and transported, emitting toxicants along the way that damage environmental and human health. This dissertation tells the story of how residents in Karnes living adjacent to oil and gas facilities who have organized as Karnes Area Residents for the Environment (KARE), activists, scientists, and I collaborated in a civic science air monitoring study guided by a community-based participatory research approach and Indigenous principles of CARE- collective benefit, authority to control, responsibility, and ethics- to monitor their air for toxicants, specifically volatile organic compounds (VOCs) emitted throughout oil and gas production. As many residents have reported health symptoms characteristic of VOC exposure such as dizziness, asthma, allergies, and nosebleeds, they seek to hold the state and industry accountable for regulatory inattention and fugitive emissions. This dissertation therefore addresses the following community concerns: 1) how the state, both federally and in Texas, controls the visibility of institutionally marginalized communities and their perspectives in support of the oil and gas industry; 2) the absence of key health-based setback regulations in Texas, which would regulate the distance between facilities and homes or businesses in Karnes; 3) the inappropriate siting of a state air monitor and inability for it to represent fenceline residents’ exposures to emissions from oil and gas development. Through civic science, we created experimental systems that challenged infrastructures of knowledge production built and maintained by the state that push aside community voices and are not centered on community needs, which I refer to as “civic validation.” By reflecting on our experiences working with what I call an “ecosystem of tools,” including multiple air sensors and digital tools used in our air monitoring study, and analyzing data to address the study aims, I identify components and outcomes of civic validation, which I propose can fit within the theoretical framework of environmental data justice (EDJ) at the convergence of the data justice and environmental justice movements and scholarship. Throughout, I draw from scholarship that informs EDJ, including but not limited to Black feminism, feminist philosophy of science, Indigenous studies, critical environmental justice, and local community knowledge to explore how extraction has shaped Karnes’ landscape, environmental exposures, and even the environmental data that can further understandings of the environmental harms and risks community members face daily.
... Our multi-state air quality monitoring study uses a community-based, participatory research (CBPR) design to explore conditions near UOG operations [42]. Its sampling protocol is based not on access to a well pad, data needs conditioned by an existing averaging standard, or regional policy concerns. ...
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Shale deposits exist in many parts of the world and contain relatively large amounts of natural gas and oil. Recent technological developments in the process of horizontal hydraulic fracturing (hydrofracturing or fracking) have suddenly made it economically feasible to extract natural gas from shale. While natural gas is a much cleaner burning fuel than coal, there are a number of significant threats to human health from the extraction process as currently practiced. There are immediate threats to health resulting from air pollution from volatile organic compounds, which contain carcinogens such as benzene and ethyl-benzene, and which have adverse neurologic and respiratory effects. Hydrogen sulfide, a component of natural gas, is a potent neuro- and respiratory toxin. In addition, levels of formaldehyde are elevated around fracking sites due to truck traffic and conversion of methane to formaldehyde by sunlight. There are major concerns about water contamination because the chemicals used can get into both ground and surface water. Much of the produced water (up to 40% of what is injected) comes back out of the gas well with significant radioactivity because radium in subsurface rock is relatively water soluble. There are significant long-term threats beyond cancer, including exacerbation of climate change due to the release of methane into the atmosphere, and increased earthquake activity due to disruption of subsurface tectonic plates. While fracking for natural gas has significant economic benefits, and while natural gas is theoretically a better fossil fuel as compared to coal and oil, current fracking practices pose significant adverse health effects to workers and near-by residents. The health of the public should not be compromized simply for the economic benefits to the industry.
... The research on environmental protection and health has called the attention to the close relationship among environmental pollution and low socio-economical state, from the turn-of-the-century. Several – mainly American – authors exactly proved that ecologically hazardous sites and facilities (toxic waste dumps, landfills, large emitters, etc.) are disproportionally located and concentrated in the neighbourhood of disadvantaged populations[1] [2]. It means, lower social state determines lower quality of the available environment as well. ...
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The author calls the attention to the need of historical approach in human environmental studies – especially on inequities and environmental injustices – in Central and Eastern Europe. Different confounders should be considered reflecting the specific historical background of the present environmental and public health situation of the region. No deep analysis can be performed without studying the situation of ethnic and national minorities. These minorities are often subjects of environmental injusticies as well. The author demonstrates examples from the scientific literature to improper conclusions as consequences of neglecting geographic and historical facts. References to articles written in small languages may be another confounder due to the risk of mistranslations. From the disproportional environmental exposures (caused by historical or political hostilities) via the lack of availability of health care in mother tongue to the possible genetic differences of minorities can have significant impact at all levels of environment–health interactions that should be considered in the European public health studies.
... Our multi-state air quality monitoring study uses a community-based, participatory research (CBPR) design to explore conditions near UOG operations [42]. Its sampling protocol is based not on access to a well pad, data needs conditioned by an existing averaging standard, or regional policy concerns. ...
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Background: Horizontal drilling, hydraulic fracturing, and other drilling and well stimulation technologies are now used widely in the United States and increasingly in other countries. They enable increases in oil and gas production, but there has been inadequate attention to human health impacts. Air quality near oil and gas operations is an underexplored human health concern for five reasons: (1) prior focus on threats to water quality; (2) an evolving understanding of contributions of certain oil and gas production processes to air quality; (3) limited state air quality monitoring networks; (4) significant variability in air emissions and concentrations; and (5) air quality research that misses impacts important to residents. Preliminary research suggests that volatile compounds, including hazardous air pollutants, are of potential concern. This study differs from prior research in its use of a community-based process to identify sampling locations. Through this approach, we determine concentrations of volatile compounds in air near operations that reflect community concerns and point to the need for more fine-grained and frequent monitoring at points along the production life cycle. Methods: Grab and passive air samples were collected by trained volunteers at locations identified through systematic observation of industrial operations and air impacts over the course of resident daily routines. A total of 75 volatile organics were measured using EPA Method TO-15 or TO-3 by gas chromatography/mass spectrometry. Formaldehyde levels were determined using UMEx 100 Passive Samplers. Results: Levels of eight volatile chemicals exceeded federal guidelines under several operational circumstances. Benzene, formaldehyde, and hydrogen sulfide were the most common compounds to exceed acute and other health-based risk levels. Conclusions: Air concentrations of potentially dangerous compounds and chemical mixtures are frequently present near oil and gas production sites. Community-based research can provide an important supplement to state air quality monitoring programs.
... The representatives of community-based anti-poverty organizations that comprised the focus group suggested addressing issues of procedural environmental justice, which concern a neighborhood's capacity to influence the environmental policies (e.g., zoning ordinances, neighborhood improvements, and the siting of industrial facilities) that impact their lives. Participants also requested community-based action research (Bacon, deVuonoPowell, Frampton, LoPresti, & Pannu, 2013;Shepard, 2002), and suggested measuring community assets, assessing social isolation, and documenting forms of civic engagement in follow-up work. ...
Article
Inequalities in the exposure to environmental burdens and access to environmental benefits are an environmental justice concern for urban and regional environmental planning. Recent studies have assessed the exposure of different populations to a combination of environmental hazards through GIS-based Cumulative Environmental Impact Assessments (CEIA). The contribution of this study is the development of a CEIA, which incorporates the distance-based impact of transportation, the cumulative impact of environmental hazards, and access to environmental benefits for Santa Clara County (SCC), a highly diverse and rapidly developing region also known as ‘Silicon Valley’. Our results show that social vulnerability, cumulative environmental hazards, and environmental benefits exhibit distinct spatial patterns in SCC. High environmental hazard values are found along freeway and railroad corridors with substantial industrial legacies, while environmental benefit scores are generally higher in the suburban periphery. Correlations indicate that socially vulnerable populations in SCC are predominantly hispanic and are more likely to be exposed to environmental hazards, while white and wealthier populations are more likely to have access to environmental benefits. The results from this study may serve to develop community-based initiatives for neighborhood improvement and environmental-justice-based regional planning and public health policy reform.
... Community engagement has been promoted as a strategy to integrate communities' knowledge into research on environmental exposures, as well as to build community capacity to address environmental health problems. 19,20,21,22,23,24,25 Community engagement is particularly important for research on cumulative environmental risks because communities have unique knowledge about exposures experienced by residents. Also, communities can play crucial roles in planning, advocating for, and implementing the strategies to reduce exposures. ...
Article
Objectives: We systematically reviewed the Environmental Protection Agency, National Center for Environmental Research's (NCER's) requests for applications (RFAs) and identified strategies that NCER and other funders can take to bolster community engagement. Methods: We queried NCER's publically available online archive of funding opportunities from fiscal years 1997 to 2013. From an initial list of 211 RFAs that met our inclusion criteria, 33 discussed or incorporated elements of community engagement. We examined these RFAs along 6 dimensions and the degree of alignments between them. Results: We found changes over time in the number of RFAs that included community engagement, variations in how community engagement is defined and expected, inconsistencies between application requirements and peer review criteria, and the inclusion of mechanisms supporting community engagement in research. Conclusions: The results inform a systematic approach to developing RFAs that support community engagement in research. (Am J Public Health. Published online ahead of print October 15, 2015: e1-e9. doi:10.2105/AJPH.2015.302811).
... Community engagement has been promoted as a strategy to integrate communities' knowledge into research on environmental exposures, as well as to build community capacity to address environmental health problems. 19,20,21,22,23,24,25 Community engagement is particularly important for research on cumulative environmental risks because communities have unique knowledge about exposures experienced by residents. Also, communities can play crucial roles in planning, advocating for, and implementing the strategies to reduce exposures. ...
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Studies have documented cumulative health effects of chemical and nonchemical exposures, particularly chronic environmental and social stressors. Environmental justice groups have advocated for community participation in research that assesses how these interactions contribute to health disparities experienced by low-income and communities of color. In 2009, the U.S. Environmental Protection Agency issued a request for research applications (RFA), "Understanding the Role of Nonchemical Stressors and Developing Analytic Methods for Cumulative Risk Assessments." Seven research projects were funded to help address this knowledge gap. Each engaged with communities in different ways. We describe the community engagement approaches of the seven research projects, which ranged from outreach through shared leadership/participatory. We then assess the experiences of these programs with respect to the community engagement goals of the RFA. We present insights from these community engagement efforts, including how the grants helped to build or enhance the capacity of community organizations in addition to contributing to the research projects. Our analysis of project proposals, annual grantee reports, and participant observation of these seven projects suggests guidelines for the development of future funding mechanisms and for conducting community-engaged research on cumulative risk involving environmental and social stressors including: 1) providing for flexibility in the mode of community engagement; 2) addressing conflict between research timing and engagement needs, 3) developing approaches for communicating about the uniquely sensitive issues of nonchemical stressors and social risks; and 4) encouraging the evaluation of community engagement efforts.
... community-based participatory research is a process that involves community members or recipients of interventions in all phases of the research process, including (a) identifying the health 4 issues of concern to the community; (b) developing assessment tools; (c) collecting, analyzing, and interpreting data; (d) determining how data can be used to inform actions to improve community health; (e) creating the research designs; (f) designing, implementing, and evaluating interventions; and (g) disseminating findings. (unpaginated) Shepard et al. (2002) ...
Article
Racial and cultural diversity issues have been a source of some interest amongst outdoor and environmental educators. Early research was framed in terms of the "under-participation" of people of colour, which led to the development of ethnocentric and methodologically problematical "marginal- ity" and "ethnicity" theories. There is, however, a growing body of research, educational and otherwise, which focuses on people of colour, and which privileges culture as being central to the research process. I argue that there are currently (at least) three interrelated "culturally sensitive research approaches" in use to differing extents in environmental education in its widest sense: "ethnic modeling in qualitative research;" "culturing" environ- mental education; and community based participatory research. I conclude by making a plea for "culturally sensitive research approaches" to become inherent in all environmental education research. Résumé Les questions de diversité raciale et culturelle ont constitué une certaine source d'intérêt pour les éducateurs environnementaux et de plein air. Les premiers travaux de recherche se sont articulés sous le signe d'une « sous- participation » des personnes de couleur, phénomène ayant donné lieu à l'élaboration de théories ethnocentristes de la « marginalité » et de l'« eth- nicité » qui sont méthodologiquement problématiques. Il est toutefois une masse grandissante de recherches, éducationnelles et autres, consacrées aux personnes de couleur et qui privilégient la culture à titre d'élément central du processus de recherche. J'avance qu'il existe présentement (au moins) trois « approches culturo-sensibles en recherche » étroitement liées et que ces approches sont employées pour repousser les limites de l'ERE dans son sens le plus large : la « modélisation ethnique en recherche qualitative », la « culturalisation » de l'ERE et la recherche participative axée sur la commu- nauté. Je conclus en préconisant l'adoption d'« approches culturo-sensibles en recherche » dans tous les travaux de recherche qui s'effectuent dans le domaine de l'ERE.
... Increasingly, community organizations and residents are calling for a greater role in scientific research and decision-making that impacts their lives, as well as tools to document such exposures. Environmental justice organizations, that is, groups organizing to address the disparate burden of environmental hazards in working poor communities of color, are using research tools to collect and interpret their own data, offering opportunities to democratize the research paradigm [21][22][23][24][25]. ...
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Air pollution in Southern California does not impact all communities equally; communities of color are disproportionately burdened by poor air quality and more likely to live near industrial facilities and freeways. Government regulatory monitors do not have the spatial resolution to provide air quality information at the neighborhood or personal scale. We describe the A Day in the Life program, an approach to participatory air monitoring that engages youth in collecting data that they can then analyze and use to take action. Academics partnered with Los Angeles-based youth environmental justice organizations to combine personal air monitoring, participatory science, and digital storytelling to build capacity to address local air quality issues. Eighteen youth participants from four different neighborhoods wore portable personal PM2.5 (fine particles <2.5 µm in diameter) monitors for a day in each of their respective communities, documenting and mapping their exposure to PM2.5 during their daily routine. Air monitoring was coupled with photography and videos to document what they experienced over the course of their day. The PM2.5 exposure during the day for participants averaged 10.7 µg/m3, although the range stretched from <1 to 180 µg/m3. One-third of all measurements were taken <300 m from a freeway. Overall, we demonstrate a method to increase local youth-centered understanding of personal exposures, pollution sources, and vulnerability to air quality.
... Too often, EJ involves 'helicopter science,' in which scientists enter a community, take samples, and leave; the information is then used for scientific papers and environmental assessments about communities. A different approachone more aligned with EDJis to replace extractive data practices with community-based participatory research and community science projects (Shepard, 2002), in which participants are empowered as fellow researchers and take part in designing the study, collecting data, and analyzing it with an emphasis on co-learning (Minkler & Wallerstein, 2008). For example, the Louisiana Bucket Brigade developed inexpensive buckets to enable community members to sample air around polluting facilities (http://www. ...
Article
Environmental data justice (EDJ) emerges from conversations between data justice and environmental justice while identifying the limits and tensions of these lenses. Through a reflexive process of querying our entanglement in non-innocent relations, this paper develops and engages EDJ by examining how it informs the work of the Environmental Data & Governance Initiative (EDGI), a distributed, consensus-based organization that formed in response to the 2016 US presidential election. Through grassroots archiving of data sets, monitoring federal environmental and energy agency websites, and writing rapid-response reports about how federal agencies are being undermined, EDGI mobilizes EDJ to challenge the ‘extractive logic’ of current federal environmental policy and data infrastructures. ‘Extractive logic’ disconnects data from provenance, privileges the matrix of domination, and whitewashes data to generate uncertainty. We use the dynamic EDJ framework to reflect on EDGI’s public comment advising against the US Environmental Protection Agency’s proposed rule for Transparent Science. Through EDJ, EDGI aspires to create new environmental data infrastructures and practices that are participatory and embody equitable, transparent data care.
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Brazilian immigration to Massachusetts and other states in the US grew significantly in the last two decades. There is a lack of data about the working conditions and health and safety hazards faced by Brazilian immigrant workers. We surveyed over 500 workers in Eastern Massachusetts through a community-based participatory research project to explore occupational and immigration factors that may represent a risk to the health of Brazilian immigrant workers, who mostly work in the construction, housecleaning, and food services segments of the state labor force. Our pilot study suggests that Brazilian immigrant workers are exposed to chemical, ergonomic, physical, and psychosocial job hazards and have experienced a variety of health symptoms that may be associated with these work environment exposures. Since most Brazilian workers have not received proper training to recognize the hazards, there is an urgent need for the implementation of culturally adequate training programs and enforcement of safety and health regulations to prevent occupational injuries and fatalities.
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We conducted a cross sectional study, involving 145 children randomly selected from three different socioeconomic locations. We selected social, environment and health indicators and measured the prevalence and prevalence odds ratios. Children from the brick producing site (segregation index 5), are exposed to high levels of multiple toxic agents, and showed the highest morbidity rates and malnutrition, anemia, dental fluorosis, and the lowest IQ, followed by children from municipal garbage dump (segregation index 4), where we detected the highest prevalence of dermatological and enteric diseases. Children from the Central Zone (segregation index 2) showed the lowest rates of malnutrition and higher IQ than the other two groups. A unified vision of social, health and environmental indicators opens the possibility of novel intervention programs and a legal framework that specifically protect children against environmental exposures.
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We implemented and evaluated multiple interventions to increase walking activity at a multicultural public housing site. A community-based participatory research partnership and community action teams assessed assets and barriers related to walking and developed multiple interventions to promote walking activity. Interventions included sponsoring walking groups, improving walking routes, providing information about walking options, and advocating for pedestrian safety. A pre-post study design was used to assess the changes in walking activity. Self-reported walking activity increased among walking group participants from 65 to 109 minutes per day (P = .001). The proportion that reported being at least moderately active for at least 150 minutes per week increased from 62% to 81% (P = .018). A multicomponent intervention developed through participatory research methods that emphasized walking groups and included additional strategies to change the built and social environments increased walking activity at a public housing site in Seattle.
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While it is well understood that multiple and cumulative environmental stressors negatively impact health at the community level, existing ethical research review procedures are designed to protect individual research participants but not communities. Increasing concerns regarding the ethical conduct of research in general and environmental and genetic research in particular underscore the need to expand the scope of current human participant research regulations and ethical guidelines to include protections for communities. In an effort to address this issue, West Harlem Environmental Action (WE ACT), a nonprofit, community-based environmental justice organization in New York City that has been involved in community-academic partnerships for the past decade, used qualitative interview data to develop a pilot model for community review of environmental health science research.
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Among the first tasks in a collaboration between Tufts University and community organizations in Somerville, MA, was designing an interview instrument to assess occupational health needs among immigrant workers. Human subjects protections was a critical issue, but community partners were not well informed about the need for such protections or the role of the institutional review board (IRB). During research meetings, members of the team from Tufts trained community collaborators to work with research participants and organized a presentation by a key university IRB administrator. We present findings from the process evaluation of this project and suggest ways to (1) assess community partners' understanding about working with research volunteers, (2) train collaborators, and (3) involve IRBs.
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In 1994, the National Institute of Environmental Health Sciences (NIEHS) initiated a program to address communication gaps between community residents, researchers and health care providers in the context of disproportionate environmental exposures. Over 13 years, together with the Environmental Protection Agency and National Institute for Occupational Health and Safety, NIEHS funded 54 environmental justice projects. Here we examine the methods used and outcomes produced based on data gathered from summaries submitted for annual grantees' meetings. Data highlight how projects fulfilled program objectives of improving community awareness and capacity and the positive public health and public policy outcomes achieved. Our findings underscore the importance of community participation in developing effective, culturally sensitive interventions and emphasize the importance of systematic program planning and evaluation.
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Several US universities have initiated community-engaged environmental justice research in the community and the workplace.1 I focus here on projects implemented by the University of Massachusetts Lowell (UML) since the mid-1990s. The pioneer settlement fund Work Environment Justice Fund (WEJF) built on efforts to address immigrant communities' exposures to hazardous chemicals in Massachusetts. After the WEJF university faculty and staff engaged in community-based partnerships with Southeast Asian, Brazilian, and Hispanic communities in the Merrimack Valley and the Boston Metro area.2 Brief descriptions of a few of these will illustrate the university's commitment to improving the work environment conditions of immigrant populations in the state.
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The signaling pathways leading to cellular protection or cell death following exposure to heavy metals have not been fully clarified. Mitogen-activated protein kinases (MAPKs), i.e., extracellular signal-regulated protein kinase (ERK), c-Jun NH(2)-terminal kinase (JNK) and p38 MAPK transmit extracellular signals into the nucleus, and have been shown to participate in a diverse array of cellular functions such as cell growth, differentiation and apoptosis. Treatment with cadmium, inorganic mercury or tributyltin can activate ERK, JNK and p38 MAPK, and induces the expression of c-fos and c-jun genes prior to the development of apoptosis. However, the members of the MAPK family appear to be differentially activated depending on the heavy metal and the cell type exposed. Consequently, various cellular responses may be caused by the distinct pattern of MAPKs activation. MAPKs may be one of the important cellular signal transduction pathways affected by various environmental pollutants, including heavy metals.
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We conducted a multimethod case study analysis of a community-based participatory research partnership in West Oakland, California, and its efforts to study and address the neighborhood's disproportionate exposure to diesel air pollution. We employed 10 interviews with partners and policymakers, participant observation, and a review of documents. Results of the partnership's truck count and truck idling studies suggested substantial exposure to diesel pollution and were used by the partners and their allies to make the case for a truck route ordinance. Despite weak enforcement, the partnership's increased political visibility helped change the policy environment, with the community partner now heavily engaged in environmental decision-making on the local and regional levels. Finally, we discussed implications for research, policy, and practice.
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Over the last decade, a growing number of social scientists have turned their attention to the study of activism around health issues. Health social movements (HSMs) have pressed the institution of medicine to change in dramatic ways, embracing new modes of healthcare delivery and organization. Health activists have also pushed medicine to evolve by connecting their health concerns to other substantive issues such as social and environmental justice, poverty, and occupational or environmentally induced diseases. HSMs therefore serve as an important bridge, connecting the institution of medicine to other social institutions. In similar fashion, the study of HSMs has motivated medical sociology to develop new tools and theoretical perspectives to understand these alterations in the medical landscape. Medical sociologists stand to learn a great deal about the institution of medicine by observing it as it comes into conflict with patients and activists around issues of health care delivery, science and policy, and regulatory action. This broad sweep of interests must be systematized, which is our project here.
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Possible interactions of the historical-political events and environmental hygienic circumstances can outline the central subject of a novel -- history based -- interdisciplinary environmental health. The author cites several examples from the human history when both the environment and the human health were impacted by wars, revolutions, occupations, territorial changes, etc. The examples taken predominantly from the European history of the 20th century indicate the importance of the new attitude. Performing research on relations of the environment and human health a dilemma has often arisen: development of diseases is (also) determined by social factors beside biotic and abiotic environmental ones. This issue is studied by social medicine, ab ovo. But social medicine is not focused on how historical-political events affect human health via changes of environment, in not sensu stricto topographic[1] meaning. What events of the past can be recognized in the background of the recent environmental situations and how can they define the present international and intergovernmental relations? However, these basically historical problems often appear in the present attitudes of certain countries to the common natural environment. Two basic questions markedly indicate the subject of a new conception of history based interdisciplinary Environmental Health (Varga 2009): – How can environmental health or hygienic factors impact the human history or can they determine it? – Are there any effects of historical events on the environmental hygienic circumstances? Several, partly independent topics can be considered in this field, for example the environmental (esp. physical and chemical) pollution that is not a typically contemporary challenge. Biological factors should be mentioned studying correlations among communicable or non-communicable diseases, and wars or other military, political events (revolutions, territorial changes). Genetics can play role in the long-term evolution of history, as well. Let us see some distinct examples of world history to prove these statements. Infectious diseases and susceptibility of populations Why was the European “white man” so successful in certain historical periods and was not other time and elsewhere? Outbreaks initiated by the colonizers could play crucial role in conquests of the Caucasian race. Prehistoric spread of mankind encountered basically geographical barriers allowing only few individuals to get across. Beside the consequential decrease in genetic diversity, these individuals did not carry the majority of characteristic pathogens and parasites of the species, either. It was sometimes fatal to the particular populations. Their offsprings had been living through several generations in a pathogen-free environment and because of high susceptibility they became the victims of epidemics initiated by the colonizers[2]. That is, European colonizers conquered each continent in military sense, while biological prevalence (habitat) of the Caucasian race is much more moderate. In America, the conquerors were aware of the specific situation and they applied this knowledge. Sometimes, however, the tactics backfired, e.g. during the war of independence in Haiti, where the French army faced to the more resistant population of African origin to yellow fever (Rózsa 2005). Later, the pathogens and parasites determined the outcome of revolutions and wars. During the Russian revolution, there was an outbreak of typhus (transmitted by lice) so severe that Lenin remarked: "Either socialism will defeat the louse, or the louse will defeat socialism." (HistoryHouse 2010). If the ectoparasites had won that time, mankind could have saved much more human sacrifices later. In 1848-49, one of European revolutions, the Hungarian revolution and war of independence was beaten by the Habsburgs, with help of the Russian tsar. But Hungary did not only yield to superior number of the Russian army, but also to cholera came from Russia with the 200 000 soldiers (Varga 2009). But it is unnecessary to go back to the 19th century. The history of the modern wars is simultaneously the history of outbreaks, inasmuch as, up to the WWII mortality of communicable diseases has been higher than mortality of direct military actions (Molnár 2009).
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Chlorophenols are a class of chemicals commonly used in preservatives, disinfectants, algaecides, herbicides and pesticides. However, there is a growing evidence that these compounds are a threat to human health. This is alarming as many chlorophenols are common pollutants found in the global environment at potentially biohazardous levels. Despite chlorophenols being abundant, widely used and poisonous, we know relatively little about their mechanism of toxicity in eukaryotes. Thus, we performed genome-wide growth screens using Saccharomyces cerevisiae to understand the molecular basis of chlorophenol toxicity. Of ∼4850 single gene knockout strains tested, 393 mutants showed growth sensitivity to treatment with 4-chlorophenol (4-CP), 2,4-dichlorophenol (2,4-DCP) or pentachlorophenol (PCP). Only eight mutants showed growth hypersensitivity to all the three treatments and harboured deletions in genes important for aromatic amino acid biosynthesis (ARO1, ARO7) or mitochondrial protein synthesis and respiration (ATP5, ISA1, RML2, GET2, SLS1, MRPL38).
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Community-based participatory research (CBPR) increasingly is seen as a potent tool for studying and addressing urban environmental health problems by linking place-based work with efforts to help effect policy-level change. This paper explores a successful CBPR and organizing effort, the Toxic Free Neighborhoods Campaign, in Old Town National City (OTNC), CA, United States, and its contributions to both local policy outcomes and changes in the broader policy environment, laying the groundwork for a Specific Plan to address a host of interlocking community concerns. After briefly describing the broader research of which the OTNC case study was a part, we provide background on the Environmental Health Coalition (EHC) partnership and the setting in which it took place, including the problems posed for residents in this light industrial/residential neighborhood. EHC's strong in-house research, and its training and active engagement of promotoras de salud (lay health promoters) as co-researchers and policy change advocates, are described. We explore in particular the translation of research findings as part of a policy advocacy campaign, interweaving challenges faced and success factors and multi-level outcomes to which these efforts contributed. The EHC partnership's experience then is compared with that of other policy-focused CBPR efforts in urban environmental health, emphasizing common success factors and challenges faced, as these may assist other partnerships wishing to pursue CBPR in urban communities.
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We report on the challenges of obtaining Institutional Review Board (IRB) coverage for a community-based participatory research (CBPR) environmental justice project, which involved reporting biomonitoring and household exposure results to participants, and included lay participation in research. We draw on our experiences guiding a multi-partner CBPR project through university and state Institutional Review Board reviews, and other CBPR colleagues' written accounts and conference presentations and discussions. We also interviewed academics involved in CBPR to learn of their challenges with Institutional Review Boards. We found that Institutional Review Boards are generally unfamiliar with CBPR, reluctant to oversee community partners, and resistant to ongoing researcher-participant interaction. Institutional Review Boards sometimes unintentionally violate the very principles of beneficence and justice which they are supposed to uphold. For example, some Institutional Review Boards refuse to allow report-back of individual data to participants, which contradicts the CBPR principles that guide a growing number of projects. This causes significant delays and may divert research and dissemination efforts. Our extensive education of our university Institutional Review Board convinced them to provide human subjects protection coverage for two community-based organizations in our partnership. IRBs and funders should develop clear, routine review guidelines that respect the unique qualities of CBPR, while researchers and community partners can educate IRB staff and board members about the objectives, ethical frameworks, and research methods of CBPR. These strategies can better protect research participants from the harm of unnecessary delays and exclusion from the research process, while facilitating the ethical communication of study results to participants and communities.
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Despite indoor home environments being where people spend most time, involving residents in testing those environments has been very limited, especially in marginalized communities. We piloted participatory testing and reporting that combined relatively simple tests with actionable reporting to empower residents in Main South/Piedmont neighborhoods of Worcester, Massachusetts. We answered: 1) How do we design and implement the approach for neighborhood and household environments using participatory methods? 2) What do pilot tests reveal? 3) How does our experience inform testing practice? The approach was designed and implemented with community partners using community-based participatory research. Residents and researchers tested fourteen homes for: lead in dust indoors, soil outdoors, paint indoors and drinking water; radon in basement air; PM2.5 in indoor air; mold spores in indoor/outdoor air; and drinking water quality. Monitoring of neighborhood particulates by residents and researchers used real-time data to stimulate dialogue. Given the newness of our partnership and unforeseen conflicts, we achieved moderate-high success overall based on process and outcome criteria: methods, test results, reporting, lessons learned. The conflict burden we experienced may be attributable less to generic university-community differences in interests/culture, and more to territoriality and interpersonal issues. Lead-in-paint touch-swab results were poor proxies for lead-in-dust. Of eight units tested in summer, three had very high lead-in-dust (>1000 microg/ft2), six exceeded at least one USEPA standard for lead-in-dust and/or soil. Tap water tests showed no significant exposures. Monitoring of neighborhood particulates raised awareness of environmental health risks, especially asthma. Timely reporting back home-toxics' results to residents is ethical but it must be empowering. Future work should fund the active participation of a few motivated residents as representatives of the target population. Although difficult and demanding in time and effort, the approach can educate residents and inform exposure assessment. It should be considered as a core ingredient of comprehensive household toxics' testing, and has potential to improve participant retention and the overall positive impact of long-term environmental health research efforts.
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In order to select priority hotspots for environment and health research in Flanders (Belgium), an open procedure was organized. Environment and health hotspots are strong polluting point sources with possible health effects for residents living in the vicinity of the hot spot. The selection procedure was part of the work of the Flemish Centre of Expertise for Environment and Health, which investigates the relation between environmental pollution and human health. The project is funded and steered by the Flemish government. The involvement of other actors than merely experts is inspired by the 'analytical-deliberative' approach of the National Research Council in the United States and the extended peer community approach. These approaches stress the importance of involving different expert- and social perspectives in order to increase the knowledge base on complex issues. In the procedure used in the project a combination of expert and stakeholder input was essential. The final decision was supported by a multi-criteria analysis of expert assessment and stakeholder advice. The endeavour was challenging from the start because of the complicated ambition of including a diversity of actors, potential hotspots, concerns and assessment criteria, but nevertheless the procedure proved its value in both structuring and informing the decision-making process. Moreover the process gained the support of most actors participating in the process, even though the final selection could not satisfy all preferences. Opening the research agenda exemplifies the value of inter- and transdisciplinary cooperation as well as the need for a well-structured and negotiated procedure that combines relevant factors and actors with pragmatism. The value of such a process also needs to prove itself in practice after the procedure has been completed: the tension between an ambition of openness on the one hand and a more closed attitude amongst experts on the other will continue to play a role even after closure.
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Several strains of Sphingobium chlorophenolicum have been isolated from soil that was heavily contaminated with pentachlorophenol (PCP), a toxic pesticide introduced in the 1930s. S. chlorophenolicum appears to have assembled a poorly functioning pathway for degradation of PCP by patching enzymes recruited via two independent horizontal gene transfer events into an existing metabolic pathway. Flux through the pathway is limited by PCP hydroxylase. PCP hydroxylase is a dimeric protein that belongs to the family of flavin-dependent phenol hydroxylases. In the presence of NADPH, PCP hydroxylase converts PCP to tetrachlorobenzoquinone (TCBQ). The k(cat) for PCP (0.024 s(-1)) is very low, suggesting that the enzyme is not well evolved for turnover of this substrate. Structure-activity studies reveal that substrate binding and activity are enhanced by a low pK(a) for the phenolic proton, increased hydrophobicity, and the presence of a substituent ortho to the hydroxyl group of the phenol. PCP hydroxylase exhibits substantial uncoupling; the C4a-hydroxyflavin intermediate, instead of hydroxylating the substrate, can decompose to produce H(2)O(2) in a futile cycle that consumes NADPH. The extent of uncoupling varies from 0 to 100% with different substrates. The extent of uncoupling is increased by the presence of bulky substituents at position 3, 4, or 5 and decreased by the presence of a chlorine in the ortho position. The effectiveness of PCP hydroxylase is additionally hindered by its promiscuous activity with tetrachlorohydroquinone (TCHQ), a downstream metabolite in the degradation pathway. The conversion of TCHQ to TCBQ reverses flux through the pathway. Substantial uncoupling also occurs during the reaction with TCHQ.
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Pentachlorophenol (PCP) represents a critical concern worldwide due to its toxicity and recalcitrance to degradation. The capacity of Mucor plumbeus to transform PCP into several detoxification metabolites, including tetrachlorohydroquinone and several phase II conjugates, was observed by LC-HRMS. The data obtained support the degradation pathway proposed previously. PCP effects in M. plumbeus, an unsequenced species, were investigated using a proteomics approach (bidimensional gel electrophoresis followed by MALDI TOF/TOF analyses). The mycelial proteins identified in the differentially accumulated spots allowed the identification of PCP responsive proteins. The presence of PCP increased the energy demand, altered the cell wall architecture and cytoskeleton and induced a significant stress response. The latter was emphasised by the up-accumulation of protein species associated with defence mechanims (e.g. HSP70 and cytochrome c peroxidase). Overall the data produced corroborate the capability of PCP to uncouple oxidative-phosphorylation in mitochondria. Importantly, one of the identified mycelial protein species, a NAD- and Zn- dependent ADH, is likely to be involved in PCP degradation. Amongst the fungal secretome analysed, no putative PCP degradative enzymes were detected. This work constitutes the first toxicoproteomic study involving a Zygomycota fungus and the very first concerning the effect of PCP in a fungal proteome.
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Brownfields have been a powerful force attempting to advance both sustainability and economic development. The author, principally using U.S. examples, advances the belief that the true benefits potentially offered by Brownfields can only be fully realized by using tools such as found in the application of Community Benefit Agreements. In a similar way use of Community-Based Participatory Research frameworks holds out similar promise. The proof of this promise will only be found in the implementation of these models.
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Conventional, positivist science is not well suited for addressing the contemporary risk landscape. To address high-uncertainty, high-stakes risks, Funtowicz and Ravetz have called for a postnormal science. Two key characteristics of postnormal science are the involvement of an extended peer community and the deliberation of extended facts. The health research community has responded to the shortcomings of normal science with approaches to field research, known collectively as community-based participatory research (CBPR). A review of case literature shows that although CBPR is not inherently postnormal, it can be friendly to a postnormal approach. A postnormal CBPR practice would rely more heavily on a deliberative process, which engages a broad range of expertise, including experts in normal science, in decisions about data collection, analysis, and actions.
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Residents of pollution hotspots often take on projects in ‘citizen science’, or popularepidemiology, in an effort to marshal the data that can prove their experience of the pollution to the relevant authorities. Sometimes these tactics, such as pollution logs or bucket brigades, take advantage of residents’ spatially ordered and finely honed experiential and sensory knowledge of the places they inhabit. But putting that knowledge into conversation with law requires them to mobilize a new, ‘foreign’ set of tools, primarily oriented to the observation, measurement and sampling of pollution according to conventional scientific standards. Here, I employ qualitative empirical methods in two case studies of communities ‘downwind’ of Canada’s contested tar sands region to demonstrate that the knowledge that is crucial to these citizen science strategies is not only local, situated and experiential in origin but also collectively generated and held. I draw on the notion of transcorporeality, emanating from feminist theory of the body, to demonstrate that the knowledge offered to law through these efforts often represents a fluid merger of experiential and conventional ways of knowing, posing a productive challenge to the strictly positive notions of science and evidence dominant in legal proceedings.
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Scientists are participating in more visible and vocal forms of political action. In this essay, I sketch key moments in this shift, with the hope of generating new research questions and lines of sociological inquiry. Specifically, I ponder whether this is a new wave of science activism, and if so, how is it different from past forms of science activism? I also ask whether and in what form we, as sociologists, should “stand up for science”?
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To address society’s complex challenges, campus-community partnerships are increasingly being undertaken by academia. As a result, questions of how to ensure that these partnerships succeed have taken on a new urgency. This urgency has led to an emphasis on the creation of ‘how to’ guides focused on the mechanics of building effective partnerships. This article argues that this focus is premature and attention instead needs to be directed to the neglected but ultimately more fundamental question of who is ‘allowed’ to initiate the partnerships. It is argued here that the seemingly simple and straightforward issue of who initiates the partnership leads us into the complex problems of choice, power and perspective which bedevil campus-community partnerships. Until these problems are fully addressed, the partnership approach is unlikely to achieve its status as a central means by which community-university engagement can be realised in academia. Keywords: campus-community partnerships, community engagement, partnership initiation, research, knowledge creation, reciprocity.
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Advocates for civil rights, environmental justice, and movements promoting social justice require data and may lack trust in public authorities, turning instead to academic scientists to help address their questions. Assessing historical exposure to toxic chemicals, especially in situations of a specific industrial source of pollution affecting a community, is critical for informing appropriate public health and policy responses. We describe a community-driven approach to integrate retrospective environmental hazard exposure assessment with community organizing to address concerns about the extent of exposure to toxic metals in a predominantly working-class, Latinx community living near a now-closed lead–acid battery smelter facility. Named the “Truth Fairy Project” by leaders of the community organization East Yard Communities for Environmental Justice, this community–university partnership aimed to assess prenatal and early-life exposures to toxic metals through biomarkers of exposure in baby/deciduous teeth. This partnership integrated community mobilization with empirical research, informing residents about toxic metal exposures and improving the community’s capacity to respond to a public health crisis.
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Pentachlorophenol (PCP) has been used extensively as a biocide and a wood preservative and has been reported to be immunosuppressive in rodents and humans. Tetrachlorohydroquinone (TCHQ) is a major metabolite of PCP. TCHQ has been identified as the main cause of PCP-induced genotoxicity due to reactive oxidant stress (ROS). However, the precise mechanisms associated with the immunotoxic effects of PCP and TCHQ remain unclear. The aim of this study was to examine the effects of PCP and TCHQ on the induction of ROS and injury to primary mouse splenocytes. Our results shown that TCHQ was more toxic than PCP and that a high dose of TCHQ led to necrotic cell death of the splenocytes through induction of massive and sudden ROS and prolonged ROS-triggered ERK activation. Inhibition of ROS production by N-acetyl-cysteine (NAC) partially restored the mitochondrial membrane potential, inhibited ERK activity, elevated caspase-3 activity and PARP cleavage, and, eventually, switched the TCHQ-induced necrosis to apoptosis. We suggest that prolonged ERK activation is essential for TCHQ-induced necrosis, and that ROS play a pivotal role in the different TCHQ-induced cell death mechanisms.
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This essay examines the problem of scientist activism as a specialized form of environmental struggle. Following research on “state-society synergy,” the author argues that this framework encourages a broader view of scientist environmental activism and its socially embedded character “in between” states and civil society. Environmental research and advocacy networks crisscross the public–private divide, linking scientists to one another, to state actors, and to environmental justice groups. These collective structures are important sites for examining the opportunities and constraints to scientist environmental activism. The synergy perspective is also useful for identifying the various forms that scientist activism can take, and for assessing the consequences of scientists' collective responses to the degradation of ecosystems and human communities.
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Determined to learn the extent to which a local contaminated site was impacting community health, the Native American community of Akwesasne reached out to a research university, eventually partnering on the first large-scale environmental health community based participatory research project (CBPR). Based on interviews with scientists, community fieldworkers, and study participants, this article examines the ways in which collaborating on these studies was beneficial for all parties-especially in the context of citizen science goals of education and capacity building-as well as the challenges they faced, including communicating the limits of what scientific studies could accomplish for the community.
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Background: Environmental contaminants are often located in areas heavily populated by African Americans, Hispanics/Latinos, and the poor. In many communities, the discovery of environmental hazards occurs following concern and investigation by its constituents. The residents of Fresno, Texas, which is a predominantly minority community located near Houston, Texas, have long-standing undocumented concerns related to potential environmental exposures and associated health effects. To begin to document the concerns of the members of the Fresno community, we used focus group methodology to examine the resident's perceptions of the environment in the Fresno community, potential routes and sources of environmental exposures, and how Fresno residents perceived that these environmental hazards could affect their health. Methods: Focus group methodology was used to assess the Fresno communities' perceptions of environmental exposure, perceived routes of exposure, and perceived adverse health affects. Nineteen Fresno residents took part in four focus group discussions that were recorded, transcribed, and analyzed using content analysis. Results: The residential participants overwhelmingly described poor water quality in the Fresno community. While some residents perceived that the air quality was good or clear, others described the air as poor or potentially dangerous. Some residents identified the local chemical companies, a landfill, chlorination, and a lack of public water supply as potential sources of contamination in the Fresno community. The residents perceived that environmental exposures could potentially affect their health status, in particular the drinking water. Conclusions: The findings of our study convey the concerns of the members of the Fresno community. Potential environmental exposures were identified along with sources of environmental hazards. Although there were differing perceptions of air quality, the perceptions of water quality and sources of contamination were consistent. These findings should be used in developing a larger-scale environmental health assessment in the Fresno community to examine self-reported health status and measure contaminant levels in the residential drinking water.
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Health social movements address several issues: (a) access to, or provision of, health care services; (b) disease, illness experience, disability and contested illness; and/or (c) health inequality and inequity based on race, ethnicity, gender, class and/or sexuality. These movements have challenged a variety of authority structures in society, resulting in massive changes in the health care system. While many other social movements challenge medical authority, a rapidly growing type of health social movement, “embodied health movements” (EHMs), challenge both medical and scientific authority. Embodied health movements do this in three ways: (1) they make the body central to social movements, especially with regard to the embodied experience of people with the disease; (2) they typically include challenges to existing medical/scientific knowledge and practice; and (3) they often involve activists collaborating with scientists and health professionals in pursuing treatment, prevention, research, and expanded funding. We present a conceptual framework for understanding embodied health movements as simultaneously challenging authority structures and allying with them, and offer the environmental breast cancer movement as an exemplar case.
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Doctors, patients, and public health professionals widely recognize that certain physical environments are more conducive to the emergence and spread of Lyme disease. However, ecological solutions to the spread of the disease are rarely pursued. Drawing on interviews with Lyme activists, politicians, and state and local administrators dealing with Lyme disease related issues as well as an analysis of Lyme disease legislation in the state of Virginia, we examine why solutions to Lyme disease most often focus on expanding individual choices for diagnosis and treatment over changing the environments that enhance the risk of Lyme disease. We argue that the emergence of Lyme disease in a neoliberal society pushed debates on how to best deal with the disease away from its underpinning environmental causes and into individual human bodies.
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Participatory action research (PAR) is widely recognized for its potential to improve environmental problem solving. However, PAR proponents and observers have paid relatively little attention to the ways in which lay participation complicates the research process. In this article, I examine the challenges presented by lay participation in the case of the Drift Catcher, a participatory air monitoring program in which community residents in the United States work with scientists from an environmental nongovernmental organization (NGO) to sample their own air for pesticides and then to use those data to press for social change. My findings suggest the need for a more nuanced understanding of “participation,” one that accounts for the technical complexity of a PAR project, other challenges, and the participants' organizational capacity. Successfully executing a participatory research project, especially one that produces politically controversial data, may require substantial capacity building to weather the political and technical challenges that arise.
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summary Research is needed on environmental health risks to children in disadvantaged, minority communities to improve environmental health policy and environmental justice. Multiple health effects in children have already been associated with environmental pollution, and minority communities tend to be both disproportionately exposed to pollutants and disproportionately affected by environmentally-related disease. Identifying environmental risks in these populations will lead to prevention of serious diseases including childhood asthma, developmental disorders, and cancer. Translation to policy requires the communication of scientific results to the health policy context. Effective community-academic partnerships to translate scientific data into public health policy are essential and will ensure major benefits to children's environmental health and greater environmental justice.
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Although various governmental entities in the USA are required to consider environmental justice (EJ) impacts of their actions during decision-making, socially vulnerable groups continue to be disproportionately exposed to environmental hazards. Tools and programs to quantify and mitigate environmental injustices are limited by existing data, which may not capture the full range of health disparities exacerbated by the complex interactions between environmental exposures and social stressors. In this study, we analyzed how the scientific literature approaches EJ issues in the USA. We searched PubMed for journal articles discussing at least one sociodemographic or environmental variable in the context of cumulative impacts and analyzed the relative frequency with which various EJ topics were studied. Our findings indicate that demographic variables are commonly used in epidemiologic studies, though some areas (e.g., age) are better studied than others. Similarly, occupational exposure and ambient air pollution were more studied than other types of exposures. Word frequency analyses revealed which toxicants and health outcomes are the most frequently studied. In addition, temporality analyses showed that the rate of occupational publications rose rapidly in the 1970–1980s and has since plateaued, while other publication rates increased two decades later and are still on the rise. Cumulative impacts are considered in a relatively small portion of journal articles across all topics; nevertheless, they have seen an exponential climb in the last decade. A more equitable distribution of scientific efforts might be needed for a better distribution of funding, policy-making efforts, and other resources to socially and environmentally vulnerable communities.
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The West End Revitalization Association (WERA), a community-based organization (CBO) in Mebane, North Carolina, was awarded a Collaborative Problem-Solving (CPS) grant from the U.S. Environmental Protection Agency's Office of Environmental Justice (EPA OEJ). The purpose of this paper is to highlight WERA's efforts to bring stakeholders in three low-income African-American communities where environmental hazards created public health risks together for collaboration rather than litigation. WERA's board and staff organized nine working groups with specific areas of expertise that would facilitate research, identify lack of basic amenities, and encourage funding for corrective action and participation in progress reporting workshops. WERA used consensus building, dispute resolution, and resource mobilization as part of the CPS model to address noncompliance with environmental laws, including the Clean Air Act, Clean Water Act, Safe Drinking Water Act, Toxic Substances Control Act, and Solid Waste Disposal Act. WERA's CPS "Right to Basic Amenities" project produced a framework for (1) grassroots management and ownership of a collaborative problem-solving process; (2) bringing stakeholders together with diverse and conflicting viewpoints; (3) implementation of an innovative community-owned and managed (COMR) research model; and (4) leveraging millions of dollars to fund installation of first-time municipal water/sewer services, street paving, and relocation of the 119-bypass to advance environmental health solutions. The structure and successes of WERA's Right to Basic Amenities project have been discussed at demonstration and training sessions to help others replicate the model in comparable low-income communities of color in North Carolina and across the United States.
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Immune parameters were examined in 188 patients who were exposed for more than 6 mo to pentachlorophenol-containing pesticides. Blood levels of pentachlorophenol, lymphocyte subpopulations, in-vitro responses to mitogenic and allogeneic stimulation, plasma neopterin levels, and plasma cytokine and cytokine receptor levels were determined. Impaired in-vitro lymphocyte stimulation responses were impaired in 65% of the patients. The likelihood of impaired lymphocyte stimulation increased significantly with levels of pentachlorophenol that exceeded 10 microliters/l (p < .05). Patients who had high blood levels of pentachlorophenol and abnormal lymphocyte stimulation also had increased proportions of blood monocytes in blood (p < .05), as well as increased IL-8 serum levels (p < .02). Eleven patients who had abnormal mitogen stimulation experienced decreased CD4/CD8 ratios of < 1.0; 5 of these patients had decreased CD4+ lymphocyte counts of < 500/microliters, and 3 patients had increased plasma neopterin of > 15 nmol/l. These results indicate that increased levels of pentachlorophenol in blood can lead to severe T lymphocyte dysfunction.
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The compound U0126 (1,4-diamino-2,3-dicyano-1, 4-bis[2-aminophenylthio]butadiene) was identified as an inhibitor of AP-1 transactivation in a cell-based reporter assay. U0126 was also shown to inhibit endogenous promoters containing AP-1 response elements but did not affect genes lacking an AP-1 response element in their promoters. These effects of U0126 result from direct inhibition of the mitogen-activated protein kinase kinase family members, MEK-1 and MEK-2. Inhibition is selective for MEK-1 and -2, as U0126 shows little, if any, effect on the kinase activities of protein kinase C, Abl, Raf, MEKK, ERK, JNK, MKK-3, MKK-4/SEK, MKK-6, Cdk2, or Cdk4. Comparative kinetic analysis of U0126 and the MEK inhibitor PD098059 (Dudley, D. T., Pang, L., Decker, S. J., Bridges, A. J., and Saltiel, A. R. (1995) Proc. Natl. Acad. Sci U. S. A. 92, 7686-7689) demonstrates that U0126 and PD098059 are noncompetitive inhibitors with respect to both MEK substrates, ATP and ERK. We further demonstrate that the two compounds bind to deltaN3-S218E/S222D MEK in a mutually exclusive fashion, suggesting that they may share a common or overlapping binding site(s). Quantitative evaluation of the steady state kinetics of MEK inhibition by these compounds reveals that U0126 has approximately 100-fold higher affinity for deltaN3-S218E/S222D MEK than does PD098059. We further tested the effects of these compounds on the activity of wild type MEK isolated after activation from stimulated cells. Surprisingly, we observe a significant diminution in affinity of both compounds for wild type MEK as compared with the deltaN3-S218E/S222D mutant enzyme. These results suggest that the affinity of both compounds is mediated by subtle conformational differences between the two activated MEK forms. The MEK affinity of U0126, its selectivity for MEK over other kinases, and its cellular efficacy suggest that this compound will serve as a powerful tool for in vitro and cellular investigations of mitogen-activated protein kinase-mediated signal transduction.
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2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a common environmental pollutant causing public concern. Its toxic effects include disruption of the immune, endocrine, and reproductive systems, impairment of fetal development, carcinogenicity, and lethality in rodents. Here, we report that TCDD induces apoptosis in two cultured human leukemic lymphoblastic T cell lines. This cell death was found not to be dependent on an aryl hydrocarbon receptor and to be inhibited by the inhibitor of tyrosine kinases and caspases. Apoptosis-linked c-Jun N-terminal kinase is rapidly activated in these cells by the treatment with TCDD. A dominant-negative mutant of c-Jun N-terminal kinase prevented cell death in the treatment with TCDD. Furthermore, TCDD decreases the Bcl-2 protein level in these cell lines. These findings will help in the understanding of the molecular mechanism underlying TCDD-mediated immunotoxicity.
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The high prevalence of childhood asthma in low-income, inner-city populations is not fully understood but has been at least partly attributed to the disproportionate exposures associated with socioeconomic disadvantage. The contribution of indoor allergens to asthma is well documented, but links between socioeconomic disadvantage and indoor allergen levels are not clear. We investigated levels of cockroach allergens (Bla g 2) in a sample of 132 Dominican or African American low-income households with young children in northern Manhattan in New York City (40% were receiving public assistance) to determine whether the distribution of allergens is a function of housing deterioration. Deterioration was measured by the presence and number of physical housing problems (holes in the ceilings and walls, water damage, etc.). More than 50% of the sample had two or more types of housing dilapidation, and 67% of the sample reported cockroach sightings in their homes. Samples of dust were collected from kitchen and bedroom surfaces. We hypothesized that the greater the dilapidation, the higher the allergen levels, independent of income, sociocultural factors, and pest-control methods. In addition, we hypothesized that the homes of families characterized by frequent moves (23.5%) would have higher allergen levels than more stable families. Results showed significant positive associations between housing deterioration and allergen levels in kitchens, after adjusting for income and ethnicity, with independent effects of residential stability (p< 0.05). Bedroom allergen levels were associated with housing instability (p < 0.01) and ethnicity (p< 0.01). Findings demonstrated that indoor household allergen levels are related to degree of household disrepair, after adjusting for individual family attributes, suggesting that social-structural aspects of housing may be appropriate targets for public health interventions designed to reduce allergen exposure.
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Activists in the environmental justice movement are challenging expert-driven scientific research by taking the research process into their own hands and speaking for themselves by defining, analyzing, and prescribing solutions for the environmental health hazards confronting communities of the poor and people of color. I highlight the work of El Puente and The Watchperson Project--two community-based organizations in the Greenpoint/Williamsburg neighborhood in Brooklyn, New York, that have engaged in community-based participatory research (CBPR) to address asthma and risks from subsistence-fish diets. The CBPR process aims to engage community members as equal partners alongside scientists in problem definition, information collection, and data analysis--all geared toward locally relevant action for social change. In the first case I highlight how El Puente has organized residents to conduct a series of asthma health surveys and tapped into local knowledge of the Latino population to understand potential asthma triggers and to devise culturally relevant health interventions. In a second case I follow The Watchperson Project and their work surveying subsistence anglers and note how the community-gathered information contributed key data inputs for the U.S. Environmental Protection Agency Cumulative Exposure Project in the neighborhood. In each case I review the processes each organization used to conduct CBPR, some of their findings, and the local knowledge they gathered, all of which were crucial for understanding and addressing local environmental health issues. I conclude with some observations about the benefits and limits of CBPR for helping scientists and communities pursue environmental justice.
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Lead poisoning prevention requires knowledge of lead sources and of appropriate residential lead standards. Data are severely lacking on lead sources for Native American children, many of whom live in rural areas. Further, the relation of mining waste to blood lead concentrations (BPbs) of rural children is controversial. In collaboration with the eight tribes of northeastern Oklahoma, we assessed lead sources and their effects on BPbs for rural Native American and White children living in a former mining region. Venous blood lead, residential environmental (soil, dust, paint, water), and caregiver interview (e.g., hand-to-mouth behaviors, socioeconomic conditions) data were obtained from a representative sample of 245 children 1-6 years of age. BPbs ranged from 1 to 24 mug/dL. There were no ethnic differences in BPbs (p = 0.48) nor any patterns of excess lead sources for Native American or White children. Multiple linear regression analyses indicated that mean soil lead, mean floor lead loading, mouthing behaviors, caregivers' education, and residence in former mining towns were all strongly associated with BPbs. Logistic regression results showed mean floor dust lead loading >10.1 pg/ft(2) (odds ratio [OR], 11.4; 95% confidence interval [0], 3.5-37.3), and yard soil lead >165.3 mg/kg (OR, 4.1; CI, 1.3-12.4) were independently associated with BPbs greater than or equal to10 mug/dL. We also found strong interactions between soil lead and poverty (p = 0.005), and dust and soil sources (p = 0.02). Our findings indicate that soil and dust lead derived largely from mining waste pose a health hazard to Native American and White children, and that current residential dust lead standards are insufficient to adequately protect children. Moreover, our finding that poor children are especially vulnerable to lead exposures suggests that residential standards should consider interactions among socioeconomic conditions and lead sources if environmental justice is to be achieved.
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Although allergic diseases such as asthma and hay fever are a major cause of morbidity in industrialized countries, most studies have focused on patterns of prevalence among children and adolescents, with relatively few studies on variations in prevalence by race/ethnicity and socioeconomic position among adults. Our study examined racial/ethnic and socioeconomic patterns in the prevalence of asthma overall, asthma with hay fever, asthma without hay fever, and hay fever overall, in a population of 173,859 women and men in a large prepaid health plan in northern California. Using education as a measure of socioeconomic position, we found evidence of a positive gradient for asthma with hay fever with increasing level of education but an inverse gradient for asthma without hay fever. Hay fever was also strongly associated with education. Compared with their White counterparts, Black women and men were more likely to report asthma without hay fever, and Black women were less likely to have asthma with hay fever. Asian men were also more likely to report asthma with hay fever, and Asian women and men were much more likely to have hay fever. Racial/ethnic disparities in prevalence of allergic diseases were largely independent of education. We discuss implications for understanding these social inequalities in allergic disease risk in relation to possible differences in exposure to allergens and determinants of immunologic susceptibility and suggest directions for future research.
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The recent growth and restructuring of the swine industry in the state of Mississippi has raised various environmental and socioeconomic concerns. We spatially examined the location and attributes of 67 industrial hog operations to determine if African American and low-income communities have a high prevalence of industrial hog operations located near their neighborhoods at the census block group level. We used spatial data and cross-classification analysis to compare the prevalence of industrial hog operations in neighborhoods that are primarily African American and low income with the prevalence in neighborhoods that are African American and affluent. We also used logistic regression to evaluate the relationship between the environmental justice variables and the location of the industrial hog operations. The block group characterization showed a high prevalence of hog operations in the four highest quintiles compared with the lowest quintile for percentage African American and percentage poverty. At increasing levels of percentage African Americans and percentage of persons in poverty, there are 2.4-3.6 times more operations compared with the referent group; additionally, scale adjustment to only the hog counties reduces this to 1.8-3.1 more operations compared with the referent group. The inequitable distribution of hog-confined agricultural feeding operations in these communities may have adverse environmental impacts associated with industrial hog production, such as increased health risks and quality of life degradation, as have occurred in other areas having similar facilities.
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We report on the research conducted by the Community Action Against Asthma (CAAA) in Detroit, Michigan, to evaluate personal and community-level exposures to particulate matter (PM) among children with asthma living in an urban environment. CAAA is a community-based participatory research collaboration among academia, health agencies, and community-based organizations. CAAA investigates the effects of environmental exposures on the residents of Detroit through a participatory process that engages participants from the affected communities in all aspects of the design and conduct of the research; disseminates the results to all parties involved; and uses the research results to design, in collaboration with all partners, interventions to reduce the identified environmental exposures. The CAAA PM exposure assessment includes four seasonal measurement campaigns each year that are conducted for a 2-week duration each season. In each seasonal measurement period, daily ambient measurements of PM2.5 and PM10 (particulate matter with a mass median aerodynamic diameter less than 2.5 microm and 10 microm, respectively) are collected at two elementary schools in the eastside and southwest communities of Detroit. Concurrently, indoor measurements of PM2.5 and PM10 are made at the schools as well as inside the homes of a subset of 20 children with asthma. Daily personal exposure measurements of PM10 are also collected for these 20 children with asthma. Results from the first five seasonal assessment periods reveal that mean personal PM10 (68.4 39.2 microg/m(3)) and indoor home PM10 (52.2 30.6 microg/m(3)) exposures are significantly greater (p < 0.05) than the outdoor PM10 concentrations (25.8 11.8 microg/m(3)). The same was also found for PM2.5 (indoor PM2.5 = 34.4 21.7 microg/m(3); outdoor PM2.5 = 15.6 8.2 microg/m(3)). In addition, significant differences (p < 0.05) in community-level exposure to both PM10 and PM2.5 are observed between the two Detroit communities (southwest PM10 = 28.9 14.4 microg/m(3)), PM2.5 = 17.0 9.3 microg/m(3); eastside PM10 = 23.8 12.1 microg/m(3), PM2.5 = 15.5 9.0 microg/m(3). The increased levels in the southwest Detroit community are likely due to the proximity to heavy industrial pollutant point sources and interstate motorways. Trace element characterization of filter samples collected over the 2-year period will allow a more complete assessment of the PM components. When combined with other project measures, including concurrent seasonal twice-daily peak expiratory flow and forced expiratory volume at 1 sec and daily asthma symptom and medication dairies for 300 children with asthma living in the two Detroit communities, these data will allow not only investigations into the sources of PM in the Detroit airshed with regard to PM exposure assessment but also the role of air pollutants in exacerbation of childhood asthma.
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Glutathione (GSH) conjugate formation with tetrachlorohydroquione (TCHQ) and the GSH content in vivo were measured by capillary zone electrophoresis. A more than 60% depletion of GSH content was found in liver tissue of mice treated with TCHQ. In addition, p53 protein accumulation and DNA fragmentation was induced by TCHQ. A two-stage model of chemical transformation of mouse embryonic fibroblasts was used to elucidate the transformation activity of TCHQ in vitro, and a 33% foci formation efficiency was found at the concentration of 5 μM. GSH depletion caused by TCHQ could abolish the protective ability of the cell against reactive oxygen species provided by GSH. When DNA was damaged, p53 protein accumulated in the nucleus and, in the case of severe damage, initiated apoptosis. TCHQ's ability to cause GSH depletion and DNA damage may play a role in the cytotoxic and genotoxic properties of its metabolic precursor, PCP.
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Ultrastructural changes in mitochondrial morphology were observed in amoebae exposed to the uncoupling agents dinitrophernol (DNP), pentachlorophenol (PCP), and m-chlorocarbonyl cyanide phenylhydrazone (CCCP). These alterations occurred with rapidity and were present before whole-cell activity changes could be detected. They included changes in profile shape and overall dimensions, matrix density changes, and alterations to the cristal membranes, so that distinction between control Type I and Type II conformations was eliminated and a form with intermediate characters generated. It is proposed that, in producing these altered forms, the uncoupling agents are acting by suppressing the control functional states of the mitochondria. At the end of the uncoupler treatment all alterations were shown to be reversible, i.e. in cells transferred back to normal culture medium, mitochondrial profiles identical to those in control cells were again evident with time. These effects on the mitochondria could be produced whether the uncoupler was introduced externally by total cell exposure, or to the inside of the cell by microinjection. The importance of precisely defining conditions for treatments and at disrupting cell activity was evident. Thus, an uncoupler, which is a weak acid, proved to be more effective in whole cell treatments if applied at a pH near to it pKa - so ensuring its penetration across the outer cell membrane.
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Electron-capture-gas chromatographic (EC-GC) methods for the determination of chlorinated phenol metabolites of hexachlorobenzene (HCB) and pentachlorophenol (PCP) in urine are presented. After extraction the sample was reacted with diazomethane to produce the methyl ether of each metabolite prior to determination by EC-GC. An acid alumina column was used for cleanup and separation of methylated phenols into groups. Average recoveries of greater than 80% were obtained from urine fortified with known amounts of the phenol metabolites under investigation. A level of 1 ppb1 was established as minimum detection limit for each phenol metabolite. Previously unreported urinary metabolites of HCB and PCP were found as a result of a rat feeding study. Levels of chlorinated phenol residues from (a) human general population and (b) a worker occupationally exposed to PCP are also included.
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To investigate the potential effects of technical pentachlorophenol (PCP-T, contaminated with polychlorinated dioxins and furans) and of analytical grade pentachlorophenol (PCP-A) on the human immune system, in vitro assays with freshly prepared human peripheral blood lymphocytes were used as an alternative to experimental animals. Both cell-mediated and humoral immune functions were examined after direct lymphocyte exposure to PCP-T or PCP-A at concentrations ranging from 0-200 microM. In each case the viability of the treated cells remained within the control value range. T lymphocyte blastogenesis after 3 days incubation with PCP was measured using both optimal and suboptimal mitogen (PHA) concentration. Interleukin-2 activity of 24.5-h supernatants of lymphocytes in response to PHA, pretreated with PCP for 20-24 h, was examined in a bioassay using the mouse IL-2-dependent CTLL-6 cell line. The synthesis of immunoglobulins was determined after stimulation with T-dependent (PWM) and T-independent (KlebsM) polyclonal B cell activators. In the proliferation assay the effects of PCP-T became more evident after suboptimal mitogen stimulation. Whereas after optimal mitogen stimulation blastogenesis was affected only at the highest concentration of 200 microM PCP-T, cell reactivity after suboptimal PHA stimulation was altered by all PCP-T doses. In the lower concentration range PCP-T caused enhanced proliferative responses, but at the two highest PCP-T concentrations cell reactivity was significantly suppressed as compared to the medium controls. Significant differences between the effects of PCP-T and PCP-A could be demonstrated only after optimal mitogen stimulation at the highest PCP concentration (200 microM). In contrast, lymphokine production as well as Ig secretion showed severe dose-dependent suppression after exposure to both PCP-T and PCP-A. The humoral immune response appeared to be more suppressed when cultures were stimulated with T-dependent rather than T-independent mitogens. The two different PCP preparations caused immunosuppression of both lymphocyte functions to the same extent. To summarize, the results of our studies indicate that PCP itself is directly immunotoxic to human immunocompetent cells and the T helper cell subset appears to be especially sensitive to PCP exposure. Furthermore, the observation of a direct effect on humoral immunity is similar to previous results showing considerable alterations of antigen specific antibody production in experimental animals after in vivo exposure.
Article
Pentachlorophenol (PCP) is a substance whose widespread use, mainly in wood protection and pulp and paper mills, has led to a substantial environmental contamination. This in turn accounts for a significant exposure of the general human population, with rather high exposure levels being attained in occupational settings. Investigations on the genotoxic activity of PCP have given rise to divergent results which would seem to make an evaluation difficult. By grouping them into 3 categories a somewhat clearer picture, allowing finally an (admittedly tentative) assessment, can be obtained. PCP does seem to be at most a weak inducer of DNA damage: it produces neither DNA-strand breaks nor clear differential toxicity to bacteria in rec-assays in the absence of metabolic activation. Also in SCE induction no increase can be observed in vivo, while PCP is found marginally active in a single in vitro experiment. Metabolic activation, however, leads to prophage induction and to DNA strand breaks in human lymphocytes, presumably through the formation of oxygen radicals. A possible further exception in this area might be the positive results in the yeast recombination tests, although their inadequate reporting makes a full evaluation difficult. PCP does not seem to induce gene (point) mutations, as most bacterial assays, the Drosophila sex-linked recessive lethal test and in vitro assays with mammalian cells did not demonstrate any effects. Marginally positive results were obtained in the mammalian spot test in vivo and in one bacterial test; the positive result in the yeast assay for cycloheximide resistance is fraught somewhat with its questionable genetic basis. PCP does, however, induce chromosomal aberrations in mammalian cells in vitro and in lymphocytes of exposed persons in vivo. Those in vivo results that were unable to provide evidence of chromosomal damage are hampered either by methodological inadequacies or by too low exposure levels. The (rodent) metabolite tetrachlorohydroquinone might be a real genotoxic agent, capable of binding to DNA and producing DNA strand breaks; this activity is probably due to semiquinone radical formation and partly mediated through active oxygen species. Since this compound has not been tested in the common bacterial and mammalian mutagenicity assays, the few ancillary results on this substance cannot be used in a meaningful human risk assessment of PCP. Furthermore, this metabolite has only been produced by human liver microsomes in vitro, but has not been detected in exposed humans in vivo.(ABSTRACT TRUNCATED AT 400 WORDS)
Article
Evaluation of lymphocyte phenotype frequencies, functional responses, serum immunoglobulin levels, and autoantibodies was completed for 38 individuals (i.e., 10 families) who were exposed to pentachlorophenol (PCP) in manufacturer-treated log houses. Comparison of subjects with controls revealed that the exposed individuals had activated T-cells, autoimmunity, functional immunosuppression, and B-cell dysregulation. Autoimmunity was evidenced by elevation of TA1 phenotype frequencies and a 21% incidence of anti-smooth muscle antibody. Functional immunosuppression was evidenced by the significantly reduced responses to all mitogens tested and to allogeneic lymphocytes in the mixed lymphocyte culture test. There was a significant elevation of CD10, and an 18% increase or decrease in serum immunoglobulins was noted. A striking anomaly was the enhanced natural killer activity found in exposed females but not in males.
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It is shown that p-tetrachlorohydroquinone (TCH), the metabolite of the environmental chemical pentachlorophenol (PCP), is more toxic to cultured CHO cells than PCP, and that it causes DNA single-strand breaks and/or alkali-labile sites at concentrations of 2-10 microgram/ml as demonstrated by the alkaline elution technique.
Article
Pentachlorophenol (PCP) was given orally to three volunteers at single doses of 3.9, 4.5, 9, and 18.8 mg. Daily urinary excretion of PCP and PCP conjugated to glucuronic acid was monitored using gas chromatography with electron capture detection (GC/ECD). Based on first-order elimination kinetics an elimination half-life of 20 days was derived. To eliminate interference by the uncontrolled absorption of PCP from the environment 0.98 mg 13C-PCP was taken by one of the volunteers. PCP levels in urine and plasma were determined using mass spectrometry (GC/ MS) with negative chemical ionization. An elimination half-life of 17 days was found in both urine and blood. The collected data were used to calculate the clearance of PCP: a value of 0.07 ml/min was found. The long elimination half-life of PCP is explained by the low urinary clearance due to the high plasma protein binding (>96%) and the tubular reabsorption. The pH-dependency of the elimination of PCP was investigated, and a distinct increase in the daily excretion was observed following alkalinization by oral administration of sodium bicarbonate. In order to elucidate the role of the enterohepatic circulation as a possible pool for PCP in humans, the bile of cholelithiasis patients with postoperative T-drainage was investigated for PCP and compared with the corresponding urine and plasma levels, but no accumulation of PCP in the enterohepatic circulation could be observed. The daily elimination and plasma levels of PCP in a group of individuals without a specific exposition were found to range from 10 to 48 μg/day and 19 to 36 μg/l, respectively.
Article
The DNA-damaging potential of pentachlorophenol (PCP) and its metabolite tetrachlorohydroquinone (TCH) was investigated. TCH was found to bind covalently to calf-thymus DNA and to cause single-strand breaks in PM2 DNA. No DNA-damaging effects were observed for PCP. Exposure of human fibroblasts to PCP and TCH showed that TCH is more toxic, when colony-forming ability after exposure to the agent is used as a measure of toxicity. In the evaluation of the mutagenic and carcinogenic potential of PCP the metabolite TCH should be taken into consideration.
Article
Excretion of pentachlorophenol-14C in the urine of rats and mice after oral and intraperitoneal administration (10 to 25 mg/kg) was studied. 41 to 43% of the excretion activity was found to be present as unchanged pentachlorophenol. By means of gas chromatography-mass spectrometry, one metabolite was identified as tetrachlorohydroquinone, representing 5 and 24% of the excreted activity in rats and mice, respectively. Conjugation with glucuronic acid could not be demonstrated by enzymatic hydrolysis since tetrachlorohydroquinone was found to be a potent inhibitor of β-glucuronidase, the I50 being 1.6 to 2.0×10−6 M. Boiling the urine with hydrochloric acid was shown to convert all of the excreted activity to pentachlorophenol and tetrachlorohydroquinone, the latter representing 43 and 46% in rats and mice, respectively. Tetrachlorohydroquinone was found in the urine of workers occupationally exposed to pentachlorophenol.
Article
Chromosome analyses were carried out on peripheral lymphocytes from 22 male workers employed at a pentachlorophenol (PCP) producing factory. As compared with a group of 22 matched controls a small, but significant, increase in the frequency of dicentrics and acentrics was observed. There was no significant increase of sister-chromatid exchange (SCEs) in smoking PCP workers, as compared with smoking controls. Within the control group, smokers had a higher incidence of SCEs than non-smokers.
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A class of pyridinyl imidazoles inhibit the MAP kinase homologue, termed here reactivating kinase (RK) [Lee et al. (1994) Nature 372, 739-746]. We now show that one of these compounds (SB 203580) inhibits RK in vitro (IC50 = 0.6 microM), suppresses the activation of MAPKAP kinase-2 and prevents the phosphorylation of heat shock protein (HSP) 27 in response to interleukin-1, cellular stresses and bacterial endotoxin in vivo. These results establish that MAPKAP kinase-2 is a physiological RK substrate, and that HSP27 is phosphorylated by MAPKAP kinase-2 in vivo. The specificity of SB 203580 was indicated by its failure to inhibit 12 other protein kinases in vitro, and by its lack of effect on the activation of RK kinase and other MAP kinase cascades in vivo. We suggest that SB 203580 will be useful for identifying other physiological roles and targets of RK and MAPKAP kinase-2.
Article
Incubation of the pentachlorophenol (PCP) metabolites, tetrachloro-p-benzoquinone (chloranil, TCpBQ), tetrachloro-p-hydroquinone (TCpHQ) and tetrachloro-p-benzoquinone (TCoBQ) with V79 Chinese hamster cells led to a significant enhancement of the amount of 8-hydroxydeoxyguanosine (8-OH-dG) in DNA. With PCP itself and the metabolite tetrachloro-o-hydroquinone (TCoHQ) no distinct induction of this lesion could be observed. The average yields of 8-OH-dG were about 2-2.5 times above background levels. In addition, TCpBQ and TCpHQ were able to generate DNA single-strand breaks, while PCP, TCoHQ and TCoBQ failed to induce this lesion. All incubations were performed for 1 h without exogenous metabolic activation and concentrations were 25 microM of the respective agent. It is concluded that these metabolites may contribute to the carcinogenicity of PCP observed in mice, by generating reactive oxygen species (ROS) through their redox cycling properties.
Article
Nearly all cell surface receptors utilize one or more of the mitogen-activated protein kinase cascades in their repertoire of signal transduction mechanisms. Recent advances in the study of such cascades include the cloning of genes encoding novel members of the cascades, further definition of the roles of the cascades in responses to extracellular signals, and examination of cross-talk between different cascades.
Article
After more than a year had elapsed since a single oral exposure to 2 and 4 μg 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)/kg, there was an apparent dose-related increased incidence of significant endocervical squamous metaplasia in a group of cynomolgus macaques (Scottet al.,1998). In the present experiments we investigated the mechanisms by which chemicals like TCDD could induce epithelial cell transdifferentiation in the primate endocervix. One focus of investigation was epidermal growth factor receptor (EGFR) and the key cytosolic signaling kinases, c-Src and protein tyrosine kinase (PTK), whose responses to TCDD are well characterized. A second focus was the distal kinase Erk2 that transduces the cytosolic signal into a nuclear signal, and which in combination with nuclear casein kinase II (CKII), can lead to activation of p53. Finally, we studied three key target proteins of activated p53 (wafl/p21, Cdc2 p34, and Cdk4), whose modulation could produce cell cycle effects.
Article
The effects of co-treatment of C3H10T1/2 (10T1/2) cells with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and 12-O-tetradecanoylphorbol-13-acetate (TPA) on the expression of the novel cytochrome P4501B1 (CYP1B1) were investigated. As monitored by CYP1B1-catalyzed 7,12-dimethylbenzanthracene (DMBA) metabolism, TPA suppressed basal and TCDD-induced DMBA metabolism in a concentration-dependent manner, with a maximum inhibitory concentration of 100 nM. The suppression of CYP1B1 catalytic activity occurred at two time points during which protein kinase C (PKC) was activated and down-regulated in these cells as judged by analyses of cellular PKC content and PKC-inhibitor (chelerythrine chloride)-influenced suppression of CYP1B1 catalytic activity. Experiments in which TCDD and benzanthracene (BA)-induced DMBA metabolism were monitored in PKCbeta1-overexpressing 10T1/2 cells revealed that the suppression of CYP1B1 activity is a consequence of cellular PKC elevation. This suppression phenomenon could be accounted for by PKC-mediated suppression of TCDD-induced CYP1B1 mRNA and apoprotein and of nuclear translocation of the Ah-receptor. In contrast, the mitogen-activated protein kinase (MAPK) proteins ERKs 1 and 2 were stimulated by TCDD under conditions in which PKC was activated. Collectively, our results suggest that PKC participates in the regulation of CYP1B1 in 10T1/2 cells, positively by directly suppressing the Ah-receptor signaling pathway, followed by an indirect or negative activation of the MAPK signaling pathway.
Article
Macrocyclic nonaketide compounds, radicicol and its two analogues, 87-250904-F1 and LL-Z1640-2, have various biological activities. Here we show that these compounds inhibit signal-dependent transcriptional activation with different specificity with distinct mechanism. Although all three compounds inhibited PMA-induced AP-1 transcriptional activity in cell-based reporter assay, these compounds exhibited differential effects in separate transcriptional reporter assays for NF-kappaB and glucocorticoid receptor. Next we found that one of these compounds, LL-Z1640-2, was a signal-specific inhibitor of the JNK/p38 pathways. In contrast to LL-Z1640-2, radicicol and 87-250904-F1 did not inhibit JNK/p38 activation. Recently, radicicol was reported as an inhibitor of activated-Ras-induced ERK activation. These results indicated that radicicol and LL-Z1640-2 showed distinct specificity to various MAP kinase pathways despite their structural similarity. Furthermore, LL-Z-1640-2 inhibited anisomycin-induced but not TNF-induced JNK/p38 activation, indicating that the inhibition mechanism is signal-specific.
Article
Polychlorinated biphenyls (PCBs) are environmental contaminants that induce release of insulin in rat insulinoma cells, RINm5F (Fischer et al., Life Sci. (1996) 59, 2041-2049). In the present study the mechanisms of this effect were investigated using noncytotoxic concentrations (10 microg/ml) of a PCB mixture, Aroclor-1254, and the pure PCB congeners 2,2',4,4'-tetrachlorobiphenyl and 2,2',4,4',5, 5'-hexachlorobiphenyl. Treatment of RINm5F cells with each of these agents resulted in a rapid increase in intracellular free calcium. The presence of extracellular calcium was required for PCB-induced insulin release because removal of calcium from the medium attenuated the effect. In addition, pretreatment of RINm5F cells with the calcium channel blocker verapamil also blocked PCB-induced insulin release. To determine whether PCB-related insulin release could be associated with the enzyme, calcium/calmodulin-dependent kinase II (CaM kinase II), RINm5F cells were pretreated with the CaM kinase II inhibitor KN-93. PCB-induced insulin release was completely blocked by KN-93. Under similar treatment conditions, PCBs also induced the activity of mitogen-activated protein kinases (MAPK) 1 and 2. However, inhibition of MAPK activation by a specific inhibitor, PD-98059 (10.0 microM) did not prevent insulin release induced by PCBs. The results of the present investigation suggest a role for calcium and CaM kinase II in PCB-induced insulin release. Furthermore, the results suggest that insulin release by PCBs is independent of the activation of MAPKs.
Article
Exposure to environmental contaminants, such as polychlorinated biphenyls (PCBs), may severely compromise normal function of vascular endothelial cells (EC). We have previously shown that PCB 77 (3,3',4,4'-tetrachlorobiphenyl), an arylhydrocarbon receptor (AhR) agonist, can induce oxidative stress in cultured EC. We now show that PCB 77 can activate EC and induce a cellular stress response that is reflected by the activation of c-Jun N-terminal/stress-activated protein kinases (JNK/SAPK). Our data also suggest that this PCB 77-mediated stress response can be modulated by the intracellular glutathione content. EC treated with buthionine-sulphoximine (BSO), an inhibitor of glutathione synthesis, further enhanced PCB-induced JNK/SAPK activity. This stress response was sustained only in the presence of BSO plus PCB 77. Media supplementation with the glutathione precursor N-acetyl-cysteine (NAC) reduced PCB 77-induced JNK/SAPK. Intracellular glutathione also may be implicated in PCB-induced EC apoptosis. Individual treatment with PCB, BSO, or linoleic acid induced activation of caspase 3. Compared to PCB 77 alone, annexin V activity was further amplified during combined treatment with BSO and PCB 77. DNA fragmentation was mostly observed when cells were treated with both BSO and PCB 77. The caspase 3-specific inhibitor DEVD-CHO protected cells against PCB 77/BSO-mediated apoptosis and inhibited the caspase activity without affecting JNK/SAPK activation or cellular glutathione levels. These results suggest that AhR ligands, such as PCB 77, cause vascular EC dysfunction by modulating intracellular glutathione, which subsequently leads to activation of stress-specific kinases. Furthermore, inhibition of glutathione synthesis by BSO can further potentiate the PCB 77-induced stress response and ultimately lead to apoptotic cell death.
Article
Effects of tributyltin chloride (TBT) and other organotin compounds on mitogen-activated protein kinases (MAPKs) were examined in CCRF-CEM human T lymphoblastoid cells. In response to the incubation with 0.25-2 microM TBT for 1 h, the levels of the phosphorylated form of extracellular signal-regulated protein kinase (ERK), c-Jun NH(2)-terminal kinase (JNK), and p38 MAPK increased in a dose-dependent manner. The phosphorylation was observed after 15 min and lasted for 4 h following exposure to 1 microM TBT, while the cell viability was not lowered significantly within 6 h. On the other hand, no clear changes were found in the total protein levels of ERK, JNK, and p38 MAPK. The in vitro activities of MAPKs also increased in response to TBT exposure. The potentials of MAPKs phosphorylation and of cellular damage were TBT > dibutyltin dichloride (DBT) > monobutyltin trichloride (MBT). When compared to other triorganotin compounds such as trimethyltin chloride (TMT), triphenyltin chloride (TPT), and triethyltin bromide (TET), TBT exposure induced the most marked phosphorylation of MAPKs. Chelation of intracellular Ca(2+) suppressed TBT-induced MAPKs phosphorylation almost completely, but removal of external Ca(2+) did not. The present results showed that tributyltin is a potent activator of ERK, JNK, and p38 MAPK pathways, and Ca(2+) mobilized from intracellular stores plays an important role for the phosphorylation of MAPKs in this human T cell line.
Article
Pentachlorophenol (PCP) and its salt are used extensively as biocide and wood preservative. Due to improper disposal, PCP has become an environmental pollutant and is now considered to be ubiquitos. Metabolic studies carried out in rodents or human liver homogenate have indicated that PCP undergoes oxidative dechlorination to form tetrachlorohydroquinone (TCHQ). The cytotoxicity, cell death mechanisms and gene expression of PCP and TCHQ are investigated in human liver and bladder cells and show that TCHQ induces apoptosis and DNA genomic fragmentation in bladder cells but not liver cells. No apoptotic features could be induced by treatment of PCP in both cell lines. The concentrations of PCP required to cause 50% cell death in T-24 and Chang liver cells were 5-10-fold greater than the concentrations of TCHQ. Several gene products are important in controlling the apoptotic and necrotic processes. Of these, hsp 70, CAS, bcl-2 and bax were studied. The expression of the hsp70 gene increased significantly (2-3-fold) in cells treated with TCHQ. However, no significant change was found in the cells treated with PCP. The expression of CAS gene decreased significantly in T-24 cells treated with both TCHQ and PCP. Whereas, no significant change was found in Chang liver cells with the same treatment. In addition, the expression of the bcl-2/bax protein decreased significantly in these two cell lines treated with TCHQ but not PCP.
Article
Exposure of HgCl2 to CCRF-CEM human lymphoblastoid cells induced phosphorylation of mitogen-activated protein kinases (MAPKs); extracellular signal-regulated protein kinase (ERK), c-Jun N-terminal kinase (JNK) and p38. LL-Z1640-2, a macrocyclic nonaketide, inhibited HgCl2-induced JNK phosphorylation at 5-100 ng/ml. It also inhibited phosphorylation of ERK and p38 but only at 100 ng/ml. The same doses of radicicol did not suppress MAPKs activation. LL-Z1640-2 (at 100 ng/ml) inhibited HgCl2-induced JNK phosphorylation in NIH 3T3 fibroblasts but not in LLC-PK(1) renal epithelial cells. Thus, LL-Z1640-2 is a potent inhibitor of HgCl2-induced MAPKs activation, especially that of JNK, in CCRF-CEM cells.
Article
When CCRF-CEM cells were incubated with 5-40 microM CdCl(2,) apoptosis was observed most clearly at 10 microM. Prior to the development of apoptosis, mitogen-activated protein kinases (MAPKs), i.e. extracellular signal-regulated protein kinase (ERK), c-Jun N-terminal kinase (JNK), and p38 MAPK, were activated with different sensitivity to CdCl(2) exposure. ERK and p38 MAPK were phosphorylated with incubation of 1 microM CdCl(2,) but higher than 20 microM CdCl(2) was required for the clear phosphorylation of JNK. In the time-course study, ERK and p38 MAPK were phosphorylated earlier than JNK after CdCl(2) exposure. The in vitro activities of MAPKs also increased in response to CdCl(2) exposure. Pretreatment with an intracellular Ca(2+) chelator, 1, 2-bis(o-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid tetra(acetoxymethyl) ester (BAPTA/AM), suppressed almost completely CdCl(2)-induced phosphorylation of JNK and p38 MAPK, but not ERK phosphorylation, indicating that the activation of JNK and p38 MAPK depends on the intracellular Ca(2+) but that of ERK does not. On the other hand, treatment with a MAPK/ERK kinase (MEK) inhibitor, U0126 (1,4-diamino-2,3-dicyano-1,4-bis[2-aminophenylthio]butadiene ), suppressed CdCl(2)-induced ERK activation and the apoptosis as well. The inhibition of p38 MAPK activity with SB203580 (4-[4-fluorophenyl]-2-[4-methylsulfinylphenyl]-5-[4-pyridyl]1H- imidaz ole) did not protect cells from apoptosis. The present results showed that the activation of ERK, JNK, and p38 MAPK is differently regulated in CCRF-CEM cells exposed to CdCl(2,) and that the ERK pathway seems to be responsible for the induction of apoptosis by CdCl(2) exposure in this human T cell line.
Article
The oncogene erbB-2 codes for a receptor tyrosine kinase that functions as a key mitotic signal in a variety of cell types. Amplification or overexpression of erbB-2 occurs in many forms of cancer, such as of the breast, colon, and prostate, and is an indicator of poor prognosis in those diseases. In the human prostate cancer cell lines LNCaP and PC-3, erbB-2 kinase was activated by pesticides of different chemical classes: (1) the organochlorine insecticides beta-hexa-chlorocyclohexane (beta-HCH), o,p'-dichlorodiphenyltrichloroethane (o,p'-DDT), and heptachlor epoxide; (2) the pyrethroid insecticide trans-permethrin, and (3) the fungicide chlorothalonil. o,p'-DDT also causes phosphorylation of mitogen-activated protein kinase (MAPK) and cellular proliferation of the androgen-dependent LNCaP line. However, no proliferative effect was observed in the androgen-independent PC-3 line. The proliferative effect of o,p'-DDT in LNCaP could not be blocked by the androgen receptor antagonist p,p'-dichlorodiphenyldichloroethene (p,p'-DDE), indicating that this effect of o,p'-DDT does not occur through direct interaction with the androgen receptor. Together these data demonstrate a putative mechanism for the action of certain pesticides in hormonal carcinogenesis.
Article
It has long been suspected that pentachlorophenol (PCP) exerts a damaging influence on the immune system. In this study, the possible relationship between blood levels of PCP and immune function was studied in 190 patients who had been exposed for more than 6 mo to PCP-containing pesticides. The patients suffered from frequent respiratory infections and general fatigue. Lymphocyte subpopulations, in-vitro responses to mitogens, allogeneic stimulator cells, plasma neopterin, cytokines, soluble cytokine receptors, soluble adhesion molecules, and immunoglobulin autoantibodies were determined. A dose-response relationship between blood levels of PCP and cellular and humoral immune parameters was established. Blood levels of PCP were associated negatively with (a) total lymphocyte counts (p = .0002), CD4/CD8 ratios (p = .0015), and absolute counts of CD3+ (p < .0001), CD4+ (p < .0001), CD16+ (p < .0001), CD25+ (p = .0003), DR+ (p < .0001), CD8+/56+ (p = .020), and CD19+ cells (p = .092); (b) plasma levels of interleukin-2 (IL-2) (p < .0001), soluble IL-2R (p < .0001), IL-6 (p < .0001), IL-10 (p = .0039), interferon-gamma (IFN-gamma) (p < .0001), tumor necrosis factor-alpha (TNF-alpha) (p < .0001), transforming-growth factor-beta2 (p = .023), soluble IL-1 receptor antagonist (sIL-1 RA) (p < .0001), soluble intercellular adhesion molecule-1 (p = .0003); and (c) immunoglobulin (Ig) M-anti-Fab type autoantibodies (p = .0353). PCP levels were associated positively with (a) number of impaired stimulation assays per patient (p = .041); (b) number of circulating CD11b+ monocytes (p = .0015); and (c) plasma levels of neopterin (p < .0001), IL-4 (p = .020), and sIL-6R (p = .020). Compared with patients who had PCP plasma levels that were less than or equal to 10 microg/l, patients with blood levels of PCP that exceeded 10 microg/l experienced the following more often: low numbers of total blood lymphocytes (p = .054), CD3+ (p = .0014), CD4+ (p = .0001), DR+ (p = .0003), CD16+ (p = .0033), and CD25+ cells (p = .0033). In addition, the same aforementioned patients experienced the following more frequently: undetectable plasma levels of IL-2 (p = .0057), IL-6 (p = .042), IL-8 (p = .038), IL-10 (p = .0001), TNF-alpha (p = .0062), and IFN-gamma (p = .016); and impaired in-vitro responses of lymphocytes (p = .071). The authors concluded that increased blood levels of PCP were associated significantly with cellular and humoral immunodeficiencies. Recurrent respiratory infections and general fatigue could originate from PCP-associated immunosuppression.
Article
Farmworkers in the United States constitute a population at risk for serious environmental and occupational illness and injury as well as health disparities typically associated with poverty. Pesticides are a major source of occupational injury and illness to which farmworkers are exposed. Efforts to provide safety training for farmworkers have not been fully evaluated. Based on the Health Belief Model, this analysis examines how safety information affects perceived pesticide safety risk and control among farmworkers and how perceived risk and control affect farmworker knowledge and safety behavior. Data are based on interviews conducted in 1999 with 293 farmworkers in eastern North Carolina as part of the Preventing Agricultural Chemical Exposure in North Carolina Farmworkers' Project. Perceived pesticide risk and perceived pesticide control scales were developed from interview items. Analysis of the items and scales showed that farmworkers had fairly high levels of perceived risk from pesticides and perceived control of pesticide safety. Receiving information about pesticide safety (e.g., warning signs) reduced perceived risk and increased perceived control. Pesticide exposure knowledge was strongly related to perceived risk. However, perceived risk had a limited relationship to safety knowledge and was not related to safety behavior. Perceived control was not related to pesticide exposure knowledge, but was strongly related to safety knowledge and safety behavior. A key tenet of environmental justice is that communities must have control over their environment. These results argue that for pesticide safety education to be effective, it must address issues of farmworker control in implementing workplace pesticide safety.
Article
The past two decades have witnessed a rapid proliferation of community-based participatory research (CBPR) projects. CBPR methodology presents an alternative to traditional population-based biomedical research practices by encouraging active and equal partnerships between community members and academic investigators. The National Institute of Environmental Health Sciences (NIEHS), the premier biomedical research facility for environmental health, is a leader in promoting the use of CBPR in instances where community-university partnerships serve to advance our understanding of environmentally related disease. In this article, the authors highlight six key principles of CBPR and describe how these principles are met within specific NIEHS-supported research investigations. These projects demonstrate that community-based participatory research can be an effective tool to enhance our knowledge of the causes and mechanisms of disorders having an environmental etiology, reduce adverse health outcomes through innovative intervention strategies and policy change, and address the environmental health concerns of community residents.
Article
The National Bioethics Advisory Commission has proposed that regulatory oversight for research with human subjects be extended beyond the protection of individual research participants to include the protection of social groups. To accomplish this, the commission recommends that investigators and ethics review boards a) work directly with community representatives to develop study methods that minimize potential group harms, b) discuss group implications as part of the informed consent process, and c) consider group harms in reporting research results. We examine the utility of these recommendations in the context of research with American Indian and Alaska Native communities. Because much attention has been given to the question of how best to consult with members of these communities in the design and conduct of research, we believe it behooves investigators to consider the lessons to be learned from research involving American Indians and Alaska Natives. After describing several difficulties surrounding the application of the commission's approach to these research contexts, we propose a research agenda to develop best practices for working with local communities in the ethical assessment of epidemiologic and environmental health research.
Environmental injustice and the Mississippi hog industry Environmental Justice @BULLET Shepard et al. 140 VOLUME 110 | SUPPLEMENT 2
  • Sm Wilson
  • F Howell
  • S Wing
  • Sobsey
Wilson SM, Howell F, Wing S, Sobsey M. Environmental injustice and the Mississippi hog industry. Environ Health Perspect 110(suppl 2):195–201 (2002). Environmental Justice @BULLET Shepard et al. 140 VOLUME 110 | SUPPLEMENT 2 | April 2002 @BULLET Environmental Health Perspectives