Institutional review board challenges related to community-based participatory research on human exposure to environmental toxins: A case study

<p>Abstract</p> <p>Background</p> <p>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.</p> <p>Methods</p> <p>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.</p> <p>Results</p> <p>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.</p> <p>Conclusions</p> <p>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.</p

Associations of iron metabolism genes with blood manganese levels: a population-based study with validation data from animal models

<p>Abstract</p> <p>Background</p> <p>Given mounting evidence for adverse effects from excess manganese exposure, it is critical to understand host factors, such as genetics, that affect manganese metabolism.</p> <p>Methods</p> <p>Archived blood samples, collected from 332 Mexican women at delivery, were analyzed for manganese. We evaluated associations of manganese with functional variants in three candidate iron metabolism genes: <it>HFE </it>[hemochromatosis], <it>TF </it>[transferrin], and <it>ALAD </it>[δ-aminolevulinic acid dehydratase]. We used a knockout mouse model to parallel our significant results as a novel method of validating the observed associations between genotype and blood manganese in our epidemiologic data.</p> <p>Results</p> <p>Percentage of participants carrying at least one copy of <it>HFE C282Y</it>, <it>HFE H63D</it>, <it>TF P570S</it>, and <it>ALAD K59N </it>variant alleles was 2.4%, 17.7%, 20.1%, and 6.4%, respectively. Percentage carrying at least one copy of either <it>C282Y </it>or <it>H63D </it>allele in <it>HFE </it>gene was 19.6%. Geometric mean (geometric standard deviation) manganese concentrations were 17.0 (1.5) μg/l. Women with any <it>HFE </it>variant allele had 12% lower blood manganese concentrations than women with no variant alleles (β = -0.12 [95% CI = -0.23 to -0.01]). <it>TF </it>and <it>ALAD </it>variants were not significant predictors of blood manganese. In animal models, <it>Hfe</it>^-/-mice displayed a significant reduction in blood manganese compared with <it>Hfe</it>^+/+mice, replicating the altered manganese metabolism found in our human research.</p> <p>Conclusions</p> <p>Our study suggests that genetic variants in iron metabolism genes may contribute to variability in manganese exposure by affecting manganese absorption, distribution, or excretion. Genetic background may be critical to consider in studies that rely on environmental manganese measurements.</p

Social disparities in exposures to bisphenol A and polyfluoroalkyl chemicals: a cross-sectional study within NHANES 2003-2006

<p>Abstract</p> <p>Background</p> <p>Bisphenol A (BPA) and polyfluoroalkyl chemicals (PFCs) are suspected endocrine disrupting compounds known to be ubiquitous in people's bodies. Population disparities in exposure to these chemicals have not been fully characterized.</p> <p>Methods</p> <p>We analyzed data from the 2003-2006 National Health and Nutrition Examination Survey. Using multivariable linear regression we examined the association between urinary concentrations of BPA, serum concentrations of four PFCs, and multiple measures of socioeconomic position (SEP): family income, education, occupation, and food security. We also examined associations with race/ethnicity.</p> <p>Results</p> <p>All four PFCs were positively associated with family income, whereas BPA was inversely associated with family income. BPA concentrations were higher in people who reported very low food security and received emergency food assistance than in those who did not. This association was particularly strong in children: 6-11 year-olds whose families received emergency food had BPA levels 54% higher (95% CI, 13 to 112%) than children of families who did not. For BPA and PFCs we saw smaller and less consistent associations with education and occupation. Mexican Americans had the lowest concentrations of any racial/ethnic group of both types of chemicals; for PFCs, Mexican Americans not born in the U.S. had much lower levels than those born in the U.S.</p> <p>Conclusions</p> <p>People with lower incomes had higher body burdens of BPA; the reverse was true for PFCs. Family income with adjustment for family size was the strongest predictor of chemical concentrations among the different measures of SEP we studied. Income, education, occupation, and food security appear to capture different aspects of SEP that may be related to exposure to BPA and PFCs and are not necessarily interchangeable as measures of SEP in environmental epidemiology studies. Differences by race/ethnicity were independent of SEP.</p