Mortality from Ischemic Heart Disease and Diabetes Mellitus (Type 2) in Four U.S. Wheat-Producing States: A Hypothesis-Generating Study

In this ecologic study I examined ischemic heart disease (IHD) and diabetes mortality in rural agricultural counties of Minnesota, Montana, North Dakota, and South Dakota, in association with environmental exposure to chlorophenoxy herbicides, using wheat acreage as a surrogate exposure. I collected data on agricultural land use and 1979–1998 mortality from the U.S. Department of Agriculture and the Centers for Disease Control and Prevention websites, respectively. Counties were grouped based on percentage of land area dedicated to wheat farming. Poisson relative risks (RR) and 95% confidence intervals (CIs), comparing high- and medium- with low-wheat counties, were obtained for IHD, the subcategories acute myocardial infarction (AMI) and coronary atherosclerosis (CAS), and diabetes, adjusting for sex, age, mortality cohort, and poverty index. Mortality from IHD was modestly increased (RR = 1.08; 95% CI, 1.04–1.12). Analyses of its two major forms were more revealing. Compared with low-wheat counties, mortality in high-wheat counties from AMI increased (RR = 1.20; 95% CI, 1.14–1.26), and mortality from CAS decreased (RR = 0.89; 95% CI, 0.83–0.96). Mortality from AMI was more pronounced for those < 65 years of age (RR = 1.31; 95% CI 1.22–1.39). Mortality from type 2 diabetes increased (RR = 1.16; 95% CI, 1.08–1.24). These results suggest that the underlying cause of mortality from AMI and type 2 diabetes increased and the underlying cause of mortality from CAS decreased in counties where a large proportion of the land area is dedicated to spring and durum wheat farming. Firm conclusions on causal inference cannot be reached until more definitive studies have been conducted

Risk factors for respiratory work disability in a cohort of pulp mill workers exposed to irritant gases

<p>Abstract</p> <p>Background</p> <p>The association between chronic respiratory diseases and work disability has been demonstrated a number of times over the past 20 years, but still little is known about work disability in occupational cohorts of workers exposed to respiratory irritants. This study investigated job or task changes due to respiratory problems as an indicator of work disability in pulp mill workers occupationally exposed to irritants.</p> <p>Methods</p> <p>Data about respiratory symptoms and disease diagnoses, socio-demographic variables, occupational exposures, gassing episodes, and reported work changes due to respiratory problems were collected using a questionnaire answered by 3226 pulp mill workers. Information about work history and departments was obtained from personnel files. Incidence and hazard ratios for respiratory work disability were calculated with 95% confidence intervals (CI).</p> <p>Results</p> <p>The incidence of respiratory work disability among these pulp mill workers was 1.6/1000 person-years. The hazard ratios for respiratory work disability were increased for workers reporting gassings (HR 5.3, 95% CI 2.7-10.5) and for those reporting physician-diagnosed asthma, chronic bronchitis, and chronic rhinitis, when analyzed in the same model.</p> <p>Conclusions</p> <p>This cohort study of pulp mill workers found that irritant peak exposure during gassing episodes was a strong predictor of changing work due to respiratory problems, even after adjustment for asthma, chronic bronchitis, and chronic rhinitis.</p

Long-term follow-up of beryllium sensitized workers from a single employer

<p>Abstract</p> <p>Background</p> <p>Up to 12% of beryllium-exposed American workers would test positive on beryllium lymphocyte proliferation test (BeLPT) screening, but the implications of sensitization remain uncertain.</p> <p>Methods</p> <p>Seventy two current and former employees of a beryllium manufacturer, including 22 with pathologic changes of chronic beryllium disease (CBD), and 50 without, with a confirmed positive test were followed-up for 7.4 +/-3.1 years.</p> <p>Results</p> <p>Beyond predicted effects of aging, flow rates and lung volumes changed little from baseline, while D_LCO dropped 17.4% of predicted on average. Despite this group decline, only 8 subjects (11.1%) demonstrated physiologic or radiologic abnormalities typical of CBD. Other than baseline status, no clinical or laboratory feature distinguished those who clinically manifested CBD at follow-up from those who did not.</p> <p>Conclusions</p> <p>The clinical outlook remains favorable for beryllium-sensitized individuals over the first 5-12 years. However, declines in D_LCO may presage further and more serious clinical manifestations in the future. These conclusions are tempered by the possibility of selection bias and other study limitations.</p

Mortality from lung cancer in workers exposed to sulfur dioxide in the pulp and paper industry.

Our objective in this study was to evaluate the mortality of workers exposed to sulfur dioxide in the pulp and paper industry. The cohort included 57,613 workers employed for at least 1 year in the pulp and paper industry in 12 countries. We assessed exposure to SO(2) at the level of mill and department, using industrial hygiene measurement data and information from company questionnaires; 40,704 workers were classified as exposed to SO(2). We conducted a standardized mortality ratio (SMR) analysis based on age-specific and calendar period-specific national mortality rates. We also conducted a Poisson regression analysis to determine the dose-response relations between SO(2) exposure and cancer mortality risks and to explore the effect of potential confounding factors. The SMR analysis showed a moderate deficit of all causes of death [SMR = 0.89; 95% confidence interval (CI), 0.87-0.96] among exposed workers. Lung cancer mortality was marginally increased among exposed workers (SMR = 1.08; 95% CI, 0.98-1.18). After adjustment for occupational coexposures, the lung cancer risk was increased compared with unexposed workers (rate ratio = 1.49; 95% CI, 1.14-1.96). There was a suggestion of a positive relationship between weighted cumulative SO(2) exposure and lung cancer mortality (p-value of test for linear trend = 0.009 among all exposed workers; p = 0.3 among workers with high exposure). Neither duration of exposure nor time since first exposure was associated with lung cancer mortality. Mortality from non-Hodgkin lymphoma and from leukemia was increased among workers with high SO(2) exposure; a dose-response relationship with cumulative SO(2) exposure was suggested for non-Hodgkin lymphoma. For the other causes of death, there was no evidence of increased mortality associated with exposure to SO(2). Although residual confounding may have occurred, our results suggest that occupational exposure to SO(2) in the pulp and paper industry may be associated with an increased risk of lung cancer

The role of γδ T cells in airway epithelial injury and bronchial responsiveness after chlorine gas exposure in mice

BACKGROUND: Acute exposure to chlorine (Cl(2)) gas causes epithelial injury and airway dysfunction. γδ T cells are present in the mucosal surface of the airways and may contribute to the injury/repair response of the epithelium. METHODS: C57Bl/6J (wild type) and TCR-δ(-/- )mice exposed to Cl(2 )(400 ppm) for 5 minutes underwent measurements of airway responses to i.v. methacholine (MCh) at 1, 3, and 5 days after exposure. Bronchoalveolar lavage was performed to determine epithelial and leukocyte counts, and protein content. Tissue repair was assessed by proliferating cell nuclear antigen (PCNA) immunoreactivity and by expression of keratinocyte growth factor (KGF) mRNA by real-time PCR. RESULTS: Wild type mice developed a greater degree of airway hyperresponsiveness to MCh at 1 day post exposure to Cl(2 )compared with TCR-δ(-/- )mice. Epithelial cell counts in BAL after Cl(2 )exposure were greater in TCR-δ(-/- )mice, but macrophages showed a later peak and granulocyte numbers were lower in TCR-δ(-/- )than in wild type mice. Both groups had increased levels of total protein content in BAL after Cl(2 )exposure that resolved after 3 and 5 days, respectively. Epithelial proliferating cell nuclear antigen staining was increased at 1 and 3 days post exposure and was similar in the two groups. KGF mRNA was constitutively expressed in both groups and did not increase significantly after Cl(2 )but expression was lower in TCR-δ(-/- )mice. CONCLUSION: The severity of airway epithelial injury after Cl(2 )is greater in TCR-δ(-/- )mice but the inflammatory response and the change in airway responsiveness to methacholine are reduced. The rates of epithelial regeneration are comparable in both groups

Dimethylthiourea protects against chlorine induced changes in airway function in a murine model of irritant induced asthma

<p>Abstract</p> <p>Background</p> <p>Exposure to chlorine (Cl₂) causes airway injury, characterized by oxidative damage, an influx of inflammatory cells and airway hyperresponsiveness. We hypothesized that Cl₂-induced airway injury may be attenuated by antioxidant treatment, even after the initial injury.</p> <p>Methods</p> <p>Balb/C mice were exposed to Cl₂gas (100 ppm) for 5 mins, an exposure that was established to alter airway function with minimal histological disruption of the epithelium. Twenty-four hours after exposure to Cl₂, airway responsiveness to aerosolized methacholine (MCh) was measured. Bronchoalveolar lavage (BAL) was performed to determine inflammatory cell profiles, total protein, and glutathione levels. Dimethylthiourea (DMTU;100 mg/kg) was administered one hour before or one hour following Cl₂exposure.</p> <p>Results</p> <p>Mice exposed to Cl₂had airway hyperresponsiveness to MCh compared to control animals pre-treated and post-treated with DMTU. Total cell counts in BAL fluid were elevated by Cl₂exposure and were not affected by DMTU treatment. However, DMTU-treated mice had lower protein levels in the BAL than the Cl₂-only treated animals. 4-Hydroxynonenal analysis showed that DMTU given pre- or post-Cl₂prevented lipid peroxidation in the lung. Following Cl₂exposure glutathione (GSH) was elevated immediately following exposure both in BAL cells and in fluid and this change was prevented by DMTU. GSSG was depleted in Cl₂exposed mice at later time points. However, the GSH/GSSG ratio remained high in chlorine exposed mice, an effect attenuated by DMTU.</p> <p>Conclusion</p> <p>Our data show that the anti-oxidant DMTU is effective in attenuating Cl₂induced increase in airway responsiveness, inflammation and biomarkers of oxidative stress.</p

High prevalence of respiratory symptoms among workers in the development section of a manually operated coal mine in a developing country: A cross sectional study

BACKGROUND: Few studies of miners have been carried out in African countries; most are from South Africa, where the working conditions are assumed to be better than in the rest of Africa. Several studies have focused on respiratory disorders among miners, but development workers responsible for creating underground road ways have not been studied explicitly. This is the first study assessing the associations between exposure to dust and quartz and respiratory symptoms among coal mine workers in a manually operated coal mine in Tanzania, focusing on development workers, as they have the highest exposure to coal dust. METHODS: A cross-sectional study was carried out among 250 production workers from a coal mine. Interviews were performed using modified standardized questionnaires to elicit information on occupational history, demographics, smoking habits and acute and chronic respiratory symptoms. The relationships between current dust exposure as well as cumulative respirable dust and quartz and symptoms were studied by group comparisons as well as logistic regression. RESULTS: Workers from the development group had the highest dust exposure, with arithmetic mean of 10.3 mg/m(3 )for current respirable dust and 1.268 mg/m(3 )for quartz. Analogous exposure results for mine workers were 0.66 mg/m(3 )and 0.03 mg/m(3), respectively; and for other development workers were 0.88 mg/m(3 )and 0.10 mg/m(3), respectively. The workers from the development section had significantly higher prevalence of the acute symptoms of dry cough (45.7%), breathlessness (34.8%) and blocked nose (23.9%). In addition, development workers had significantly more chronic symptoms of breathlessness (17.0%) than the mine workers (6.4%) and the other production workers (2.4%). The highest decile of cumulative exposure to respirable dust was significantly associated with cough (OR = 2.91, 95% CI 1.06, 7.97) as were cumulative exposure to quartz and cough (OR = 2.87, CI 1.05, 7.88), compared with the reference consisting of the group of workers with the lowest quartile of the respective cumulative exposure. CONCLUSION: The development workers in a coal mine had more acute and chronic respiratory symptoms than the mine and the other production workers. In addition, there was an association between high cumulative coal dust and respiratory symptoms

Beryllium increases the CD14^dimCD16+ subset in the lung of chronic beryllium disease

CD14dimCD16+ and CD14brightCD16+ cells, which compose a minor population of monocytes in human peripheral blood mononuclear cells (PBMC), have been implicated in several inflammatory diseases. The aim of this study was to investigate whether this phenotype was present as a subset of lung infiltrative alveolar macrophages (AMs) in the granulomatous lung disease, chronic beryllium disease (CBD). The monocytes subsets was determined from PBMC cells and bronchoalveolar lavage (BAL) cells from CBD, beryllium sensitized Non-smoker (BeS-NS) and healthy subjects (HS) using flow cytometry. The impact of smoking on the AMs cell phenotype was determined by using BAL cells from BeS smokers (BeS-S). In comparison with the other monocyte subpopulations, CD14dimCD16+ cells were at decreased frequency in PBMCs of both BeS-NS and CBD and showed higher HLA-DR expression, compared to HS. The AMs from CBD and BeS-NS demonstrated a CD14dimCD16+phenotype, while CD14brightCD16+ cells were found at increased frequency in AMs of BeS, compared to HS. Fresh AMs from BeS-NS and CBD demonstrated significantly greater CD16, CD40, CD86 and HLA-DR than HS and BeS-S. The expression of CD16 on AMs from both CBD and BeS-NS was downregulated significantly after 10μM BeSO4 stimulation. The phagocytic activity of AMs decreased after 10μM BeSO4 treatment in both BeS-NS and CBD, although was altered or reduced in HS and BeS-S. These results suggest that Be increases the CD14dimCD16+ subsets in the lung of CBD subjects. We speculate that Be-stimulates the compartmentalization of a more mature CD16+ macrophage phenotype and that in turn these macrophages are a source of Th1 cytokines and chemokines that perpetuate the Be immune response in CBD. The protective effect of cigarette smoking in BeS-S may be due to the low expression of co-stimulatory markers on AMs from smokers as well as the decreased phagocytic function

Asthma caused by occupational exposures is common – A systematic analysis of estimates of the population-attributable fraction

<p>Abstract</p> <p>Background</p> <p>The aim of this paper is to highlight emerging data on occupational attributable risk in asthma. Despite well documented outbreaks of disease and the recognition of numerous specific causal agents, occupational exposures previously had been relegated a fairly minor role relative to other causes of adult onset asthma. In recent years there has been a growing recognition of the potential importance of asthma induced by work-related exposures</p> <p>Methods</p> <p>We searched Pub Med from June 1999 through December 2007. We identified six longitudinal general population-based studies; three case-control studies and eight cross-sectional analyses from seven general population-based samples. For an integrated analysis we added ten estimates prior to 1999 included in a previous review.</p> <p>Results</p> <p>The longitudinal studies indicate that 16.3% of all adult-onset asthma is caused by occupational exposures. In an overall synthesis of all included studies the overall median PAR value was 17.6%.</p> <p>Conclusion</p> <p>Clinicians should consider the occupational history when evaluating patients in working age who have asthma. At a societal level, these findings underscore the need for further preventive action to reduce the occupational exposures to asthma-causing agents.</p