The study of gene-environment interactions enables us to further understand the pathogenesis of asthma and inflammation. The TNF-α gene has been associated with airway pathology in asthma but there is limited information in relation to pollutant exposure and the TNF-α 308G/A polymorphism.To determine the risk conferred by the TNF-α 308(G/A) polymorphism on respiratory outcome and to evaluate whether the association between exposure to ambient air pollutants such as SO2, NO2, NO, and PM10 and variation in lung function measures is modified by genotype.The sample comprised 129 African children (between 9-11 years old). A questionnaire based on guidelines from the British Medical Research Council and the American Thoracic Society was administered to all caregivers to evaluate the prevalence of respiratory symptoms. Atopy was evaluated by skin prick testing. Bihourly measures of lung function (spirometry) were collected at school five days per week over three week periods in each of four seasons (2004-2005) using digital hand-held devices. During each of the four intensive 3-week phases, gaseous air pollutant concentrations were monitored continuously. Polymerase Chain Reaction-Restriction Fragment Length Polymorphism (PCR-PFLP) analysis was used to detect the TNF-α 308 genotype and plasma TNF-α levels were measured using the human TNF-α Max Standard™ Enzyme-linked immuno-absorbent assay (ELISA) kit.The TNF-α variant A allele was common among this sample of African children (40% with an allelic frequency of 0.24). There was no significant association with the TNF-α G/A polymorphism and any respiratory linked phenotype, nor cytokine levels. However, when exposure to pollutants were analyzed with genotypic and phenotypic data, we found relatively modest interaction effects for the TNF-α 308 genotype. GEE models showed that children with the TNF-α 308 A allele had increased deterioration of lung function post pollution exposure to SO2 [β=2.62, CI:0.51-4.71, p=0.02 and pint=0.03] and NO [β=3.28, CI:0.68-5.89, p=0.01, pint=0.03].The TNF-α 308 (G/A) polymorphism may be associated with increased pollutant-associated effects on FEV1 intraday variability for both SO2 and NO. The A allele may increase susceptibility to the adverse effects of air pollutants.
BackgroundHigh levels of cadmium exposure are known to cause emphysema in occupationally exposed workers, but little has been reported to date on the association between chronic environmental cadmium exposure and pulmonary function.ObjectiveIn this study we examined the association between pulmonary function and cadmium body burden in a subcohort of the Normative Aging Study, a community-based study of aging.MethodsWe examined 96 men who had cadmium measured in single 24-hr urinary specimens collected in 1994–1995 and who had one to three tests of pulmonary function between 1994 and 2002 (a total of 222 observations). We used mixed-effect models to predict pulmonary function based on individual 24-hr urinary cadmium output, adjusted for age, height, time elapsed from the baseline, and smoking status. We assessed effect modification by smoking status.ResultsAmong all subjects, a single log-unit increase in baseline urinary cadmium was inversely associated with forced expiratory volume in 1 sec (FEV1) percent predicted [β = −7.56%; 95% confidence interval (CI) −13.59% to −1.53%]; forced vital capacity (FVC) percent predicted (β = −2.70%; 95% CI −7.39% to 1.99%), and FEV1/FVC ratio (β = −4.13%; 95% CI −7.61% to −0.66%). In models including an interaction between urinary cadmium and smoking status, there was a graded, statistically significant reduction in FEV1/FVC ratio across smoking status in association with urinary cadmium.ConclusionsThis study suggests that chronic cadmium exposure is associated with reduced pulmonary function, and cigarette smoking modifies this association. These results should be interpreted with caution because the sample size is small, and further studies are needed to confirm our findings.
Gluthathione-S-transferase (GSTM1 and GSTP1) and nicotinamide quinone oxidoreductase (NQO1) genes play an important role in cellular protection against oxidative stress, which has been linked to asthma pathogenesis. We investigated whether common, functional polymorphisms in GSTM1, GSTP1, and NQO1 infuence susceptibility to asthma among schoolchildren in South Africa. Genomic deoxyribonucleic acid (DNA) was extracted from 317 primary schoolchildren, aged 9-11 years, from the urban, underprivileged socio-economic communities of Durban. GSTM1 (null vs. present genotype), GSTP1 (Ile105Val; AA AG+GG) and the NQO1 (Pro/Ser; CC CT/TT) genotypes were determined using polymerase chain reaction. Among the children, 30% were GSTM1 null, 65% carried the G allele for GSTP1, and 36% carried the C allele for NQO1.There was a high prevalence of asthma of any severity (46.1%), with 20.4% reporting persistent asthma. The GSTP1 AG+GG polymorphic genotype was signifcantly associated with persistent asthma (adjusted OR = 3.98; CI = 1.39, 11.36, p-value = 0.01). Neither the GSTM1, nor the NQO1, genotype was a signifcant predictor of persistent asthma. Therefore, the GSTP1 A/G variant may modulate the risk of persistent asthma among our sample.
Abstract This study estimated the ratio of the tracheo-bronchial dust fraction to the fraction collected by a respirable dust sampler for a variety of job classifications found in conventional, continuous, and longwall coal mining sections. The ratios could then be applied in epidemiologic studies to existing respirable dust measurements to estimate thoracic mass concentrations for evaluation of the relative importance of the respirable and thoracic dust fractions to obstructive lung disease. Data collected include particle size distributions from four U.S. underground coal mines using eight-stage personal cascade impactors. A total of 180 samples were examined by mine, occupation and occupations grouped by proximity to the mine face, and by mining technology. Several fractions—that collected by the 10-mm nylon cyclone, the American Conference of Governmental Industrial Hygienists respirable and thoracic particulate mass fractions, and the estimated alveolar and tracheo-bronchial deposition fractions—were estimated. These were not significantly different when grouped by occupation, by proximity of work to the mine face, or by the type of mining technology in use. Distributions from one mine varied from the others, perhaps because it used diesel equipment in the haulage ways, which contributed to the fine aerosol fractions. Results suggest that although the tracheo-bronchial dust fraction may contribute to the development of obstructive lung disease, occupation-specific tracheo-bronchial dust fractions are not likely to produce stronger exposure-response estimates than the historically collected respirable dust concentrations.
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/m 3 ). 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.
ISEE-184 Introduction/Aim: A grant from the Fogarty international Center in the U.S. National Institutes of Health supports this collaborative effort between the University of Michigan and a number of universities, institutes, and governmental and non-governmental organizations in Southern Africa, to assist the further development of environmental and occupational health (EOH) infrastructure and human resources in the Southern Africa Development Community (SADC) region, with a particular emphasis on improving research training and capacities. Methods: Program direction is set by the Southern African based Review Committee, with program implementation carried out by Co-Program Managers based in Southern Africa. The program plan emphasizes: 1) capacity building in the SADC States outside of South Africa; 2) the use of regionally available resources, mostly found in South Africa, complemented by resources of the University of Michigan; 3) support for the regionally based research endeavours, with a special emphasis on intervention and control research projects; and, 4) regional consensus-building through periodic meetings of key stakeholders and actors in EOH, and, 5) close collaboration and coordination with other internationally supported programs (SADC/Swedish International Development Agency Work and Health in Southern Africa, WHO/ILO Occupational Health Program in Africa, University of Arizona Fogarty grant). Results: The grant has: 1) assisted the creation of three Centers of EOH located in Tanzania, Zambia, and Zimbabwe, 2) directly funded research projects of 10 junior to mid-level researchers, 3) assisted development of post graduate degree programs in EOH in Southern Africa including use of distance learning modalities, 4) fully supported degree programs at the University of Michigan and South African universities of two dozen students, 5) supported short-term focused training of a dozen scholars in the United States, 6) sponsored or co-sponsored a dozen short courses in Southern Africa, and, 7) sponsored four biennial conferences attended by regional and international stakeholders to address EOH issues in the region. There is a current major emphasis on collaboration and coordination with the recently launched SADC/SIDA program. Conclusion: Development programs in environmental and occupational health, which place major control and guidance of the program in the hands of regional institutions and leaders, aggressively pursue collaboration with other regional and international programs, and make use of well-established regional resources to increase program cost effectiveness, can contribute to major, sustainable regional capacity development while operating with relatively modest budgets.
ISEE-0852 Objective: To investigate associations between exposures to common ambient air pollutants and fluctuations in pulmonary function in children living in industrialized and non-industrialized areas of eThekwini municipality, adjusting for genetic modification of pollutant-outcome relationships. Methods: Grade 4 pupils (n = 423) from seven schools were selected to perform peak expiratory flow manoeuvres (PEF) four times during the school day over four three week periods over 12 months. Ambient pollutants were continuously measured over 24 hours for the 12 months at each school. Generalized estimating equations were used to examine associations between daily mean levels of ambient air pollutants and measures of pulmonary function across 4 seasons in models adjusted for genetic polymorphisms and other covariates. Results: Mean daily NO2 concentrations varied from 11 ppb in non-industrial areas to 19–24 ppb in the city and industrial areas. Average SO2 concentrations varied from 1–3 ppb in non-industrial to 12–20 ppb in industrial areas. Mean daily PM10 concentrations ranged from 41–57 μg/m3. The GSTP1 minor allele was significantly associated with known or probable persistent asthma (OR = 2.74, CI: 1.29–5.84, P = 0.00), but not with atopy or BHR (OR = 0.93, CI: 0.29–1.99, P = 0.59; and OR = 0.94, CI: 0.43–2.04, P = 0.88 respectively). GSTM1null was not associated with any outcomes, however statistically significant associations of NO2, NO, and SO2 with FEV1 and PEF outcomes in the expected direction were more frequent for individuals carrying the GSTM1null genotype. Significant decrements in pulmonary function associated with higher ambient concentrations were present for a substantial proportion of the regression models, with associations stronger and more frequent among those children with persistent asthma, compared to those without. Conclusion: Industrial and vehicular exposures to moderate levels of air pollutants were associated with short-term decrements in pulmonary function among schoolchildren in Durban, especially among those with persistent asthma and those with the GSTM1null genotype.
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