Systemic lupus erythematosus (SLE) is a chronic systemic autoimmune disease that disproportionately affects African American females. The causes of SLE are unknown but postulated to be a combination of genetic predisposition and environmental triggers. Vitamin D deficiency is one of the possible environmental triggers. In this study we evaluated relationships between vitamin D status, cellular aging (telomere length) and anti-telomere antibodies among African American Gullah women with SLE. The study population included African American female SLE patients and unaffected controls from the Sea Island region of South Carolina. Serum 25-hydroxyvitamin D levels were measured using a nonchromatographic radioimmunoassay. Telomere length was measured in genomic DNA of peripheral blood mononuclear cells (PBMCs) by monochrome multiplex quantitative PCR. Anti-telomere antibody levels were measured by enzyme-linked immunosorbent assay (ELISA). Patients with SLE had significantly shorter telomeres and higher anti-telomere antibody titers compared to age- and gender-matched unaffected controls. There was a positive correlation between anti-telomere antibody levels and disease activity among patients and a significant correlation of shorter telomeres with lower 25-hydroxyvitamin D levels in both patients and controls. In follow-up examination of a subset of the patients, the patients who remained vitamin D deficient tended to have shorter telomeres than those patients whose 25-hydroxyvitamin D levels were repleted. Increasing 25-hydroxyvitamin D levels in African American patients with SLE may be beneficial in maintaining telomere length and preventing cellular aging. Moreover, anti-telomere antibody levels may be a promising biomarker of SLE status and disease activity.
African Americans have a disproportionate burden of diabetes. Gullah African Americans are the most genetically homogeneous population of African descent in the US, with an estimated European Caucasian admixture of only 3.5%. This study assessed the previously unknown prevalence of periodontal disease among a sample of Gullah African Americans with diabetes and investigated the association between diabetes control and presence of periodontal disease.
Gullah African Americans with Type 2 diabetes (n=235) were included. Diabetes control was assessed by HbA1C, and divided into three categories: well controlled, <7%; moderately controlled, 7–8.5%; and poorly controlled, >8.5%. Participants were categorized as healthy, having no clinical attachment loss (CAL) or bleeding on probing (BOP); early periodontitis, having CAL ≥1 mm in ≥2 teeth; moderate periodontitis, having 3 sites with CAL ≥4 mm and at least 2 sites with probing depth (PD) ≥3 mm; and severe periodontitis, having CAL ≥6 mm in ≥2 teeth and PD ≥5 mm in ≥1 site. Observed prevalences of periodontitis were compared to rates reported for the NHANES studies.
All subjects had evidence of periodontal disease: 70.6% had moderate periodontitis and 28.5% had severe disease. Diabetes control was not associated with periodontal disease. The periodontal disease proportions were significantly higher than the reported national prevalence of 10.6% among African Americans without diabetes.
Our sample of Gullah African Americans with type 2 diabetes exhibits higher prevalence of periodontal disease than African Americans, both with and without diabetes, described in NHANES III and NHANES 1999–2000.
Type 2 diabetes; Gullah African Americans; Periodontal disease
To evaluate associations between glycaemic control and periodontitis progression among Gullah African Americans with type-2 diabetes mellitus (T2DM).
Materials and Methods
From an ongoing clinical trial among T2DM Gullah, we extracted a cohort previously in a cross-sectional study (N 5 88). Time from baseline (previous study) to follow-up (trial enrollment, before treatment interventions) ranged 1.93–4.08 years [mean 5 2.99, standard deviation (SD) = 0.36]. We evaluated tooth site-level periodontitis progression [clinical attachment loss (CAL) worsening of ≥ 2 mm, periodontal probing depth (PPD) increases of ≥ 2 mm and bleeding on probing (BOP) from none to present] by glycaemic control status (well-controlled = HbA1c < 7%, poorly-controlled = HbA1c ≥ 7%) using multivariable generalized estimating equations logistic regression, nesting tooth sites/person.
Poorly-controlled T2DM (68.18%) was more prevalent than well-controlled T2DM (31.82%). Proportions of tooth sites/person with CAL progression between baseline and follow-up ranged 0.00–0.59 (mean = 0.12, SD = 0.12), while PPD and BOP progression ranged 0.00–0.44 (mean = 0.09, SD = 0.11) and 0.00–0.96 (mean = 0.24, SD = 0.18), respectively. Site-level PPD at baseline was a significant effect modifier of associations between poorly-controlled T2DM and site-level CAL and PPD progression [adjusted odds ratios (OR) according to poorly-controlled T2DM among PPD at baseline = 3, 5 and 7 mm, respectively: CAL progression = 1.93, 2.64, and 3.62, PPD progression = 1.98, 2.76, and 3.84; p < 0.05 for all]. Odds of site-level BOP progression were increased (OR = 1.24) for poorly-controlled T2DM, yet the results were not significant (p = 0.32).
These findings from a distinct, homogenous population further support the clinical relevance of identifying patients with poor glycaemic control and periodontitis, particularly among those with disparities for both diseases.
diabetes; glycaemic control; Gullah African Americans; multivariable regression analysis; progression of periodontal disease
Systemic lupus erythematosus (SLE) is a systemic autoimmune disease that has a significantly higher prevalence, morbidity and mortality in African Americans compared with Americans of European descent. The pathogenesis of lupus is unclear but appears to be a result of environmental factors interacting with a genetically susceptible host. Despite the high disease load of SLE in African Americans, there is the perception that lupus is relatively rare in Africa. This prevalence gradient suggests that comparative studies of related cohorts from the two continents may provide insight into the genetic/environmental interactions that result in the development of lupus. To define if a lupus gradient exists, we began a study of autoimmunity prevalence utilizing two unique cohorts. The first is the Gullah population of the Sea Islands of South Carolina, who are unique in their low genetic admixture and their known ancestral heritage. The second is the population of young women served by the West Africa Fistula Foundation in Bo, Sierra Leone. Anthropologic studies indicate a direct ancestral link between the Gullah population and Sierra Leoneans. Since it is impossible to perform an epidemiologic study of lupus in Sierra Leone at this time, we assessed the prevalence of lupus serum autoantibodies, serologic evidence of specific infections and levels of serum 25-OH vitamin D in young women in the two cohorts who have no known relatives with lupus. Our results indicate similar prevalence of serum antinuclear antibodies in the two cohorts, though there was a significantly increased prevalence of antiphospholipid and anti-Sm antibodies in the Sierra Leone cohort. Seropositivity to common viral infections was significantly higher in women from Sierra Leone, while serum 25-OH vitamin D levels were markedly lower in the Gullah population. These data suggest that the prevalence of autoimmunity is similar in the two populations, but that there are significant environmental differences that may impact progression to autoimmune disease. Further studies comparing these two cohorts is likely to provide important insight into the impact of environmental factors on development of lupus.
African American; lupus; prevalence gradient; vitamin D
We previously established an 80 kb haplotype upstream of TNFSF4 as a susceptibility locus in the autoimmune disease SLE. SLE-associated alleles at this locus are associated with inflammatory disorders, including atherosclerosis and ischaemic stroke. In Europeans, the TNFSF4 causal variants have remained elusive due to strong linkage disequilibrium exhibited by alleles spanning the region. Using a trans-ancestral approach to fine-map the locus, utilising 17,900 SLE and control subjects including Amerindian/Hispanics (1348 cases, 717 controls), African-Americans (AA) (1529, 2048) and better powered cohorts of Europeans and East Asians, we find strong association of risk alleles in all ethnicities; the AA association replicates in African-American Gullah (152,122). The best evidence of association comes from two adjacent markers: rs2205960-T (P = 1.71×10−34, OR = 1.43[1.26–1.60]) and rs1234317-T (P = 1.16×10−28, OR = 1.38[1.24–1.54]). Inference of fine-scale recombination rates for all populations tested finds the 80 kb risk and non-risk haplotypes in all except African-Americans. In this population the decay of recombination equates to an 11 kb risk haplotype, anchored in the 5′ region proximal to TNFSF4 and tagged by rs2205960-T after 1000 Genomes phase 1 (v3) imputation. Conditional regression analyses delineate the 5′ risk signal to rs2205960-T and the independent non-risk signal to rs1234314-C. Our case-only and SLE-control cohorts demonstrate robust association of rs2205960-T with autoantibody production. The rs2205960-T is predicted to form part of a decameric motif which binds NF-κBp65 with increased affinity compared to rs2205960-G. ChIP-seq data also indicate NF-κB interaction with the DNA sequence at this position in LCL cells. Our research suggests association of rs2205960-T with SLE across multiple groups and an independent non-risk signal at rs1234314-C. rs2205960-T is associated with autoantibody production and lymphopenia. Our data confirm a global signal at TNFSF4 and a role for the expressed product at multiple stages of lymphocyte dysregulation during SLE pathogenesis. We confirm the validity of trans-ancestral mapping in a complex trait.
Systemic lupus erythematosus (SLE/lupus) is a complex disease in which the body's immune cells cause inflammation in one or more systems to cause the associated morbidity. Hormones, the environment and genes are all causal contributors to SLE and over the past several years the genetic component of SLE has been firmly established. Several genes which are regulators of the immune system are associated with disease risk. We have established one of these, the tumour-necrosis family superfamily member 4 (TNFSF4) gene, as a lupus susceptibility gene in Northern Europeans. A major obstacle in pinpointing the marker(s) at TNFSF4 which best explain the risk of SLE has been the strong correlation (linkage disequilibrium, LD) between adjacent markers across the TNFSF4 region in this population. To address this, we have typed polymorphisms in several populations in addition to the European groups. The mixed ancestry of these populations gives a different LD pattern than that found in Europeans, presenting a method of pinpointing the section of the TNFSF4 region which results in SLE susceptibility. The Non-European populations have allowed identification of a polymorphism likely to regulate expression of TNFSF4 to increase susceptibility to SLE.
A recent EPA-sponsored study of sediment and seafood contamination in Quincy Bay revealed elevated levels of several complex organic pollutants frequently of concern in human health assessments. A seafood consumption risk assessment was conducted using data from samples collected in Quincy Bay in the methodology developed for EPA's Office of Marine and Estuarine Protection for such assessments. Results showed estimated plausible, upperbound excess cancer risks in the 10(-5) to 10(-2) range. These results are comparable to those found in other seafood contamination risk assessments for areas where consumption advisories and fishing restrictions were implemented. Regulatory response included consumption advisories for lobster tomalley (hepatopancreas) and other types of locally caught seafood. Uncertainties inherent in seafood risk assessment in general and for the Quincy Bay case are discussed, along with implications for further action.
Associations between dental conditions and overall health have been previously reported. Investigators have also shown significant inverse relationships between serum albumin (a general health status marker) and root caries. This relationship was explored among a study population of Gullah African Americans (who have a considerably lower level of non-African genetic admixture when compared to other African American populations) with type-2 diabetes (T2DM) and self-reported history of normal kidney function (N = 280).
Root caries indices were defined as total decayed and/or filled root surfaces. The coronal caries index [total decayed, missing, and/or filled coronal surfaces (DMFS)], level of glycemic control, total number of teeth, and other covariates were also evaluated. Logistic regression models were used to evaluate the associations between these factors and hypoalbuminemia (serum albumin concentrations <4 g/dl).
Serum albumin concentrations ranged 2.4–4.5 g/dl (mean = 3.8, SD = 0.3), with 70.4% exhibiting hypoalbuminemia. Root caries totals ranged 0–38 (mean = 1.3, SD = 4.5) surfaces decayed/filled, while total teeth ranged 1–28 (mean = 19.4, SD = 6.2). DMFS totals ranged 2–116 (mean = 55.2, SD = 28.0). We failed to detect significant associations for root caries; however, the final multivariable logistic regression models showed significant associations between hypoalbuminemia and total teeth [odds ratio (OR) = 0.93, P = 0.01], poor glycemic control (OR = 2.49, P < 0.01), elevated C-reactive protein (OR = 1.57, P < 0.01), glomerular filtration rates ≥60 (OR = 0.31, P = 0.03), and age (OR = 0.97, P = 0.03).
Previously reported inverse relationships between serum albumin and root caries were not evident in our study population. We propose that these null findings are because of the considerably lower level of root caries as well as other differing characteristics (including oral health status, the chronic presence of T2DM, and predominantly younger age) within our study population compared to these previously assessed groups.
diabetes; Gullah African Americans; root caries; serum albumin
The patient’s perspective of how their health affects their function is health-related quality of life (HRQOL). HRQOL is poorer in patients with systemic lupus erythematosus (SLE). Few HRQOL studies in SLE patients have focused on African Americans despite an increased disease burden compared with Caucasians. The African American Gullah population of South Carolina has a homogeneous genetic and environmental background and a high prevalence of multi-patient families with SLE. Demographics, medical history, and Short-Form 36 (SF-36) were measured within a cohort of Gullah SLE cases and related controls. Compared with related controls (n = 37), cases (n = 89) had a lower Physical Component Summary (PCS, 41.8 vs. 52.3, p < 0.01), but not Mental Component Summary (MCS, 55.0 vs. 56.0, p = 0.70). The difference in PCS was no longer significant upon adjustment for working status, disability, and medical conditions. None of the 11 SLE American College of Rheumatology criteria, disease duration, or Systemic Lupus International Collaborating Clinics Damage Index were associated with either PCS or MCS. Cases and controls had similar MCS scores. We hypothesize that this lack of effect of SLE on MCS may be due to disease-coping mechanisms interplaying with cultural factors unique to the Gullah.
quality of life; SLE; systemic lupus erythematosus
Little is known about the genetic etiology of systemic lupus erythematosus (SLE) in individuals of African ancestry, despite its higher prevalence and greater disease severity. Overproduction of nitric oxide (NO) and reactive oxygen species are implicated in the pathogenesis and severity of SLE, making NO synthases and other reactive intermediate related genes biological candidates for disease susceptibility. This study analyzed variation in reactive intermediate genes for association with SLE in two populations with African ancestry.
A total of 244 SNPs from 53 regions were analyzed in non-Gullah African Americans (AA; 1432 cases and 1687 controls) and the genetically more homogeneous Gullah of the Sea Islands of South Carolina (133 cases and 112 controls) and. Single-marker, haplotype, and two-locus interaction tests were computed for these populations.
The glutathione reductase gene GSR (rs2253409, P=0.0014, OR [95% CI]=1.26 [1.09–1.44]) was the most significant single-SNP association in AA. In the Gullah, the NADH dehydrogenase NDUFS4 (rs381575, P=0.0065, OR [95%CI]=2.10 [1.23–3.59]) and nitric oxide synthase gene NOS1 (rs561712, P=0.0072, OR [95%CI]=0.62 [0.44–0.88]) were most strongly associated with SLE. When both populations were analyzed together, GSR remained the most significant effect (rs2253409, P=0.00072, OR [95%CI]=1.26 [1.10–1.44]). Haplotype and two-locus interaction analyses also uncovered different loci in each population.
These results suggest distinct patterns of association with SLE in African-derived populations; specific loci may be more strongly associated within select population groups.
systemic lupus erythematosus; African Americans; genetic association studies; oxygen compounds; single nucleotide polymorphism
We investigated the efficacy of plaque removal after an oral self-care demonstration among adult Gullah-speaking African Americans with diabetes. Fiftyfour adults with diabetes completed an observed, uninstructed oral self-care demonstration with their normal mode of oral self-care. Before and after the oral self-care demonstration, the plaque levels of six test teeth were assessed using the Plaque Index. The mean percentage of plaque removal after the oral self-care demonstration was 27.4%. The mandibular teeth and the lingual surface had less plaque removal compared with the maxillary teeth and buccal surfaces. Only approximately 10% of participants achieved 50% or more plaque removal after the oral self-care demonstration. Thus, the majority of the participants did not achieve an acceptable level of plaque removal. Dental health professionals should emphasize better oral home care for people with diabetes and teach them how to access the lingual surfaces, especially of the mandibular teeth.
OBJECTIVE—The Gullah-speaking African American population from the Sea Islands of South Carolina is characterized by a low degree of European admixture and high rates of type 2 diabetes and diabetic complications. Affected relative pairs with type 2 diabetes were recruited through the Sea Islands Genetic African American Registry (Project SuGAR).
RESEARCH DESIGN AND METHODS—We conducted a genome-wide linkage scan, genotyping 5,974 single nucleotide polymorphisms in 471 affected subjects and 50 unaffected relatives from 197 pedigrees. Data were analyzed using a multipoint engine for rapid likelihood inference and ordered subsets analyses (OSAs) for age at type 2 diabetes diagnosis, waist circumference, waist-to-hip ratio, and BMI. We searched for heterogeneity and interactions using a conditional logistic regression likelihood approach.
RESULTS—Linkage peaks on chromosome 14 at 123–124 cM were detected for type 2 diabetes (logarithm of odds [LOD] 2.10) and for the subset with later age at type 2 diabetes diagnosis (maximum LOD 4.05). Two linkage peaks on chromosome 7 were detected at 44–45 cM for type 2 diabetes (LOD 1.18) and at 78 cM for type 2 diabetes (LOD 1.64) and the subset with earlier age at type 2 diabetes diagnosis (maximum LOD 3.93). The chromosome 14 locus and a peak on 7p at 29.5 cM were identified as important in the multilocus model. Other regions that provided modest evidence for linkage included chromosome 1 at 167.5 cM (LOD 1.51) and chromosome 3 at 121.0 cM (LOD 1.61).
CONCLUSIONS—This study revealed a novel type 2 diabetes locus in an African American population on 14q that appears to reduce age of disease onset and confirmed two loci on chromosome 7.
Autoimmune thyroiditis is among the most prevalent of all the autoimmunities. Autoimmune thyroiditis is multifactorial with contributions from genetic and environmental factors. Much information has been published about the genetic predisposition to autoimmune thyroiditis both in experimental animals and humans. There is, in contrast, very little data on environmental agents that can serve as the trigger or autoimmunity in a genetically predisposed host. The best-established environmental factor is excess dietary iodine. Increased iodine consumption is strongly implicated as a trigger for thyroiditis, but only in genetically susceptible individuals. However, excess iodine is not the only environmental agent implicated as a trigger leading to autoimmune thyroiditis. There are a wide variety of other synthetic chemicals that affect the thyroid gland or have the ability to promote immune dysfunction in the host. These chemicals are released into the environment by design, such as in pesticides, or as a by-product of industry. Candidate pollutants include polyaromatic hydrocarbons, polybrominated biphenols, and polychlorinated biphenols, among others. Infections are also reputed to trigger autoimmunity and may act alone or in concert with environmental chemicals. We have utilized a unique animal model, the NOD.H2h4 mouse to explore the influence of iodine and other environmental factors on autoimmune thyroiditis.
Human uncoupling protein 3 (UCP3) is a mitochondrial transmembrane carrier that uncouples oxidative ATP phosphorylation. With the capacity to participate in thermogenesis and energy balance, UCP3 is an important obesity candidate gene. A missense polymorphism in exon 3 (V102I) was identified in an obese and diabetic proband. A mutation introducing a stop codon in exon 4 (R143X) and a terminal polymorphism in the splice donor junction of exon 6 were also identified in a compound heterozygote that was morbidly obese and diabetic. Allele frequencies of the exon 3 and exon 6 splice junction polymorphisms were determined and found to be similar in Gullah-speaking African Americans and the Mende tribe of Sierra Leone, but absent in Caucasians. Moreover, in exon 6-splice donor heterozygotes, basal fat oxidation rates were reduced by 50%, and the respiratory quotient was markedly increased compared with wild-type individuals, implicating a role for UCP3 in metabolic fuel partitioning.
Persistent organic pollutants, such as PCBs, HCB and DDE, have been found to elicit a broad spectrum of biologic, metabolic, and immunologic responses. The potential of these pollutants to impair immune responses and trigger autoimmune disease is of growing concern, given their structural similarity to thyroid hormones and their potential to modulate the mechanisms and interfere with the binding of these hormones. We examine the relationship of different groupings of PCBs, according to chlorination and structure, and of p,p’-DDE and HCB to anti-thyroid peroxidase antibody, a useful tool in the evaluation of thyroid dysfunction, among 115 young adults of the Akwesasne Mohawk Nation.
Overall, eighteen participants (15.4%) had TPOAb levels above the normal laboratory reference range (23% of females, 9% of males). Among participants who were breast fed (n=47), those with an elevated TPOAb level had significantly higher levels of all PCB groupings, with the exception of levels of non-persistent PCBs which did not differ significantly. Levels of p,p’-DDE were also significantly elevated, while HCB and mirex were not higher among those with elevated TPOAb. Also, after stratifying by breast feeding status, participants who were breast fed showed significant, positive relationships between TPOAb levels and all PCB groupings, except groups comprised of non-persistent PCBs, and with p,p’-DDE, HCB, and mirex. No effects were evident among non-breastfed young adults.
Further studies are necessary to elucidate the site and mechanism of action of these POPs and to establish thresholds for these effects, especially among populations with background levels of toxicant exposure.
PCBs; antithyroid peroxidase; Native American
The purpose of this study was to describe diabetes self-management practices and service utilization among Gullah families in South Carolina.
Data were obtained from 1,276 persons with type 2 diabetes through interviews using the Family Health History Questionnaire. This was a primary analysis of a project conducted in conjunction with a parent study (Project SuGar) which focused on the molecular aspects of diabetes. Descriptive statistics were used for data analysis.
Diabetes self-management behaviors were not consistent with recommendations from the American Diabetes Association. Over half (55.6%) reported exercising, but only 27.7% reported self-glucose monitoring. Service utilization was poor, less than half, (41.1%) reported referral to a diabetic class/diet, 32.8% reported making yearly visits to the ophthalmologist; 22.3% reported visiting the dentist, and only 12.8% reported visiting the podiatrist.
Although some self-management behaviors were identified, Gullah family members remain at risk for preventable diabetes complications. Education must reflect behaviors and beliefs valued by Gullah individuals. Culturally appropriate educational programs may increase use of health care services aimed at decreasing preventable complications of type 2diabetes in the Gullah population.
Background: The BP oil spill of 2010 resulted in contamination of one of the most productive fisheries in the United States by polycyclic aromatic hydrocarbons (PAHs). PAHs, which can accumulate in seafood, are known carcinogens and developmental toxicants. In response to the oil spill, the U.S. Food and Drug Administration (FDA) developed risk criteria and established thresholds for allowable levels [levels of concern (LOCs)] of PAH contaminants in Gulf Coast seafood.
Objectives: We evaluated the degree to which the FDA’s risk criteria adequately protect vulnerable Gulf Coast populations from cancer risk associated with PAHs in seafood.
Discussion: The FDA LOCs significantly underestimate risk from seafood contaminants among sensitive Gulf Coast populations by failing to a) account for the increased vulnerability of the developing fetus and child; b) use appropriate seafood consumption rates; c) include all relevant health end points; and d) incorporate health-protective estimates of exposure duration and acceptable risk. For benzo[a]pyrene and naphthalene, revised LOCs are between two and four orders of magnitude below the level set by the FDA. Comparison of measured levels of PAHs in Gulf seafood with the revised LOCs revealed that up to 53% of Gulf shrimp samples were above LOCs for pregnant women who are high-end seafood consumers.
Conclusions: FDA risk assessment methods should be updated to better reflect current risk assessment practices and to protect vulnerable populations such as pregnant women and children.
BP oil spill; children’s health; Deepwater Horizon; Food and Drug Administration; Gulf of Mexico; PAHs; polycyclic aromatic hydrocarbons; risk assessment; seafood
BACKGROUND—Recent years have seen increased levels of production and consumption of seafood, leading to more frequent reporting of allergic reactions in occupational and domestic settings. This review focuses on occupational allergy in the fishing and seafood processing industry.
REVIEW—Workers involved in either manual or automated processing of crabs, prawns, mussels, fish, and fishmeal production are commonly exposed to various constituents of seafood. Aerosolisation of seafood and cooking fluid during processing are potential occupational situations that could result in sensitisation through inhalation. There is great variability of aerosol exposure within and among various jobs with reported allergen concentrations ranging from 0.001 to 5.061(µg/m3). Occupational dermal exposure occurs as a result of unprotected handling of seafood and its byproducts. Occupational allergies have been reported in workers exposed to arthropods (crustaceans), molluscs, pisces (bony fish) and other agents derived from seafood. The prevalence of occupational asthma ranges from 7% to 36%, and for occupational protein contact dermatitis, from 3% to 11%. These health outcomes are mainly due to high molecular weight proteins in seafood causing an IgE mediated response. Cross reactivity between various species within a major seafood grouping also occurs. Limited evidence from dose-response relations indicate that development of symptoms is related to duration or intensity of exposure. The evidence for atopy as a risk factor for occupational sensitisation and asthma is supportive, whereas evidence for cigarette smoking is limited. Disruption of the intact skin barrier seems to be an important added risk factor for occupational protein contact dermatitis.
CONCLUSION—The range of allergic disease associated with occupational exposure to crab is well characterised, whereas for other seafood agents the evidence is somewhat limited. There is a need for further epidemiological studies to better characterise this risk. More detailed characterisation of specific protein antigens in aerosols and associated establishment of dose-response relations for acute and chronic exposure to seafood; the respective roles of skin contact and inhalational exposure in allergic sensitisation and cross reactivity; and the contribution of host associated factors in the development of occupational seafood allergies are important areas for future research.
Keywords: occupational seafood allergy; occupational asthma; protein contact dermatitis
This formative study sought to explore the factors that influence the consumption of fish and seafood among 4–6 year old children in the Perth metropolitan area. Focus groups were conducted with mothers of young children to gain insights into the enablers and barriers to regular seafood consumption in children, and the knowledge, attitudes and perceptions of their mothers to including seafood as a regular part of their children's diet.
Purposive sampling techniques were used to select and recruit mothers of children aged between four and six years from within the Perth metropolitan area. A total of seven focus groups were conducted. Thematic content analysis was employed to code data generated and to extract major themes.
Findings indicated that all children of study participants had tried fish and seafood products, with some being exposed to a wide variety from an early age. Across focus groups, several dominant factors were apparent in influencing the frequency and type of seafood purchased and consumed. Perceived cost, freshness, availability/accessibility, and the level of confidence to prepare a meal to suit all family members were significant determinants of whether seafood featured regularly on the household menu. The influence of others in the family (particularly the husband or partner) also tended to impact upon the likelihood of serving fish and seafood, and the types of products mothers were willing to serve.
Findings from this qualitative study indicate that interventions seeking to promote seafood (particularly fish) as an integral part of a healthy diet should address existing negative attitudes and beliefs around the storage and preparation of seafood. The influence of dominant male influences within the family unit should also be considered. Strategies directed at parents and children should include experimental 'hands-on' components to encourage experimentation, particularly focussing on ease of preparation and the variety of lower cost seafood available.
Methyl mercury is a developmental neurotoxicant. Exposure results principally from consumption by pregnant women of seafood contaminated by mercury from anthropogenic (70%) and natural (30%) sources. Throughout the 1990s, the U.S. Environmental Protection Agency (EPA) made steady progress in reducing mercury emissions from anthropogenic sources, especially from power plants, which account for 41% of anthropogenic emissions. However, the U.S. EPA recently proposed to slow this progress, citing high costs of pollution abatement. To put into perspective the costs of controlling emissions from American power plants, we have estimated the economic costs of methyl mercury toxicity attributable to mercury from these plants. We used an environmentally attributable fraction model and limited our analysis to the neurodevelopmental impacts—specifically loss of intelligence. Using national blood mercury prevalence data from the Centers for Disease Control and Prevention, we found that between 316,588 and 637,233 children each year have cord blood mercury levels > 5.8 μg/L, a level associated with loss of IQ. The resulting loss of intelligence causes diminished economic productivity that persists over the entire lifetime of these children. This lost productivity is the major cost of methyl mercury toxicity, and it amounts to $8.7 billion annually (range, $2.2–43.8 billion; all costs are in 2000 US$). Of this total, $1.3 billion (range, $0.1–6.5 billion) each year is attributable to mercury emissions from American power plants. This significant toll threatens the economic health and security of the United States and should be considered in the debate on mercury pollution controls.
children’s health; cognitive development; cord blood; electrical generation facilities; environmentally attributable fraction; fetal exposure; lost economic productivity; mercury; methyl mercury; power plants
Recommendations about risks and benefits of seafood intake during pregnancy have been published in the last decade, but the specific health effects of the different categories of seafood remain unknown. Fish and shellfish may differ according to their fatty acid content and their concentration of chemical pollutants and toxins. Not taking these particularities into account may result in underestimating of both the positive and negative effects of seafood on birth outcomes and partly explains inconsistent results on the subject.
In the PELAGIE cohort study, including 2398 pregnant women from Brittany, we fit multiple linear and logistic regression models to examine associations of fish (salt-water fish only) and shellfish intake before pregnancy with length of gestation, birthweight, and risks of preterm births, low birthweight or small-for-gestational-age (SGA) babies.
When fish and shellfish consumptions were considered simultaneously, we observed a decrease in the risk of SGA birth with increasing frequency of fish intake: OR = 0.57 (95%CI: 0.31 to 1.05) for women eating fish twice a week or more compared with those eating it less than once a month. The risk of SGA birth was significantly higher among women eating shellfish twice a week or more than among those eating it less than once a month: OR = 2.14 (95%CI: 1.13 to 4.07). Each additional monthly meal including fish was significantly related to an increase in gestational length of 0.02 week (95%CI: 0.002 to 0.035). No association was observed with birthweight or preterm birth.
These results suggest that different categories of seafood may be differently associated with birth outcomes, fish consumption with increased length of gestation and shellfish consumption with decreased fetal growth.
Prenatal exposure to organic methylmercury (MeHg) from seafood consumption has been reported to increase children’s blood pressure (BP). A report from the Faroe Islands noted significantly increased diastolic and systolic BP in 7 year old children as prenatal MeHg exposure increased. The Faroese diet includes sea mammals that contain MeHg, cadmium, and other pollutants. We examined this relationship in the Seychelles Islands to determine if it was present in a society exposed primarily to MeHg from consuming ocean fish.
We obtained BP at ages 12 and 15 years on children with known prenatal MeHg exposure enrolled in the Seychelles Child Development Study (SCDS). We examined the association between prenatal MeHg exposure and BP using longitudinal models and linear regression adjusted for relevant covariates.
Blood pressure at both ages was associated with BMI, height and maternal hypertension during pregnancy as expected. No association between prenatal MeHg exposure and BP was present in girls at either age or in either sex at age 12 years. At age 15 years diastolic BP in boys increased with increasing prenatal MeHg exposure, while systolic BP was unaffected.
It is unclear whether the association between prenatal MeHg exposure and diastolic BP seen in 15 year old boys is of biological significance or if it is a chance finding. However, the finding is intriguing and deserves further study.
Methylmercury; blood pressure; Seychelles Child Development Study; BMI
Seafood (fish and shellfish) is an excellent source of several essential nutrients for pregnant and lactating women. A short food frequency questionnaire (FFQ) that can be used to quantitatively estimate seafood consumption would be a valuable tool to assess seafood consumption in this group. Currently there is no such validated FFQ in Norway.
The objective of this study was to establish and validate a seafood index from a seafood FFQ against blood biomarkers (the omega-3 index, the omega-3 HUFA score, and serum 25OH vitamin D).
We assessed maternal seafood consumption during the 28th gestation week in healthy Norwegian women (n=54) with a seafood FFQ. A seafood index was developed to convert ordinal frequency data from the FFQ into numerical scale data. The following blood biomarkers were used as a validation method: omega-3 index, omega-3 HUFA score, and the serum 25OH vitamin D.
The reported frequency of seafood as dinner and as spread was strongly correlated with the estimated frequencies of seafood as dinner and as spread. This indicated that the seafood index is a valuable tool to aggregate reported frequencies from the seafood FFQ. The seafood index composed of the frequency of seafood consumption and intake of omega-3 supplements, termed the total seafood index, correlated positively with the omega-3 index, omega-3 HUFA score, and 25OH vitamin D.
We established and validated a seafood index from a seafood FFQ. The developed seafood index can be used when studying health effects of seafood consumption in large populations. This seafood FFQ captures seafood consumption and omega-3 supplement intake considerably well in a group of pregnant women.
seafood consumption; marine omega-3 fatty acids; 25OH vitamin D; FFQ; biomarkers; pregnancy
The ability of n-3 long chain polyunsaturated fatty acids (PUFAs) to prevent high fat diet-induced obesity in rodents is well documented. Evidence for a similar effect in humans is, however, limited. Intervention studies in humans are inconclusive and epidemiological studies are dichotomous. Our recent finding that sucrose and other high glycemic index carbohydrates abrogate the antiobesity effect of n-3 PUFAs might, at least in part, provide an explanation to the apparent discrepancy between human and rodent intervention studies, and the lack of effect in some human trials. In addition to the amount and type of carbohydrates, the levels of n-6 PUFAs, linoleic acid in particular, in the background diet might influence the antiobesogenic effect of n-3 PUFAs. Lastly, it is plausible that the quantity of persistent organic pollutants in fish oil, and seafood rich in n-3 PUFAs, might have an influence on the outcome of the trials.
PUFA; carbohydrates; fish oil; linoleic acid; obesity; persistent organic pollutants
The persistent organic pollutants (POPs) are highly lipophilic and resistant to biodegradation and found in e.g. seafood and marine mammals. Greenlandic Inuit have high intake of marine food and thus high POP burden that varies according to local conditions and dietary preference. We do for the very first time report the serum POP related non-steroidal xenohormone activity of Inuit across Greenland.
The aims were 1) to determine the integrated xenohormone bioactivities as an exposure biomarker of the actual lipophilic serum POP mixture measuring the effect on estrogen (ER) and androgen receptor (AR) transactivity in citizens from different Greenlandic districts and 2) to evaluate associations to serum POP markers (14 PCBs and 10 pesticides) and lifestyle characteristics.
Serum samples from 121 men and 119 women from Nuuk, Sisimiut and Qaanaaq were extracted using SPE-HPLC fractionation to obtain the serum POP fraction free of endogenous hormones. The serum POP fraction was used for determination of xenohormone transactivity using ER and AR reporter gene assays.
In overall, the xenohormone transactivities differed between districts as well as between the genders. Associations between the transactivities and age, n-3/n-6 and smoker years were observed. The xenoestrogenic and xenoandrogenic transactivities correlated negatively to the POPs for the combined female and male data, respectively.
The non-steroidal xenohormone transactivities can be used as an integrated biomarker of POP exposure and lifestyle characteristics. The actual serum POP mixtures antagonized the age adjusted sex hormone receptor functions. Comparison of different study populations requires in addition to age inclusion of diet and lifestyle factors.
Summary: Seafood is part of a healthful diet, but seafood consumption is not risk-free. Seafood is responsible for an important proportion of food-borne illnesses and outbreaks in the United States. Seafood-associated infections are caused by a variety of bacteria, viruses, and parasites; this diverse group of pathogens results in a wide variety of clinical syndromes, each with its own epidemiology. Some seafood commodities are inherently more risky than others, owing to many factors, including the nature of the environment from which they come, their mode of feeding, the season during which they are harvested, and how they are prepared and served. Prevention of seafood-associated infections requires an understanding not only of the etiologic agents and seafood commodities associated with illness but also of the mechanisms of contamination that are amenable to control. Defining these problem areas, which relies on surveillance of seafood-associated infections through outbreak and case reporting, can lead to targeted research and help to guide control efforts. Coordinated efforts are necessary to further reduce the risk of seafood-associated illnesses. Continued surveillance will be important to assess the effectiveness of current and future prevention strategies.