Publications

Wood processing workers are exposed to wood-associated microbiological contaminants, including fungi. Our aim was to study the potential association between sputum fungus and adverse respiratory effects in such workers. In a group of sawmill workers, we administered a respiratory questionnaire, performed lung function testing and quantified the proportions of leukocytes in spontaneously expectorated sputum samples. We identified fungal species by DNA sequencing. Of 54 sawmill workers, 19 yielded fungal positive sputum samples (mean age 42.5±10.4 years) and 35 were negative for fungus (mean age 36.9±5.2 years). The fungus was identified as sp. in all samples. Those with fungal-positive sputum, compared to others, reported more cough (26% 63%) and haemoptysis (6% 37%) (both p<0.05), manifested reduced forced midexpiratory flow rates (FEF) (82.3±4.5 69.2±9.9% predicted, p<0.001), and had higher sputum eosinophil counts (median 9.25 3.25%, p<0.01). Reduction of FEF was associated both with fungus detection in sputum (-12.7%, 95% CI-8.5- -16.9%) and sputum eosinophils (-2.1% per 1% increase in eosinophils, 95% CI -1.5- -2.8%) (both p<0.001). In sawmill workers, sp. detectable in sputum was associated with respiratory symptoms, sputum eosinophilia and reduced FEF.

In COPD, body composition studies have focused primarily on low BMI. We examined obesity (BMI ≥ 30 kg/m(2)) as a risk factor for poor function and longitudinal functional decline. Data from a longitudinal cohort of adults with COPD (n = 1096) and an age- and sex-matched comparison group collected in two in-person visits ∼49 months apart were analyzed. Two measures of functioning were examined: six-minute walk distance (6MWD) and Short Physical Performance Battery (SPPB). Multivariate regression analyses examined relationships of obesity with functioning. Secondary analyses stratified by GOLD classification (GOLD-0/1, GOLD-2, GOLD-3/4). Obesity (53% of COPD cohort) was associated cross-sectionally with 6MWD and SPPB in COPD, and only with 6MWD in the comparison group. Obesity predicted significant functional decline in 6MWD for individuals with COPD (odds ratio (OR) for decline [95% CI] 1.8 [1.1, 2.9]), but not the comparison group. Secondary analyses revealed that the risk of decline was significant only in those with more severe COPD (GOLD 3/4, OR = 2.3 [1.0, 5.4]). Obesity was highly prevalent and was associated with poor function concurrently and with subsequent decline in 6MWD in COPD. Obesity in COPD should be considered a risk not only for more co-morbidities and greater health care use, but also for functional decline.

We used meta-analysis to measure the effect of high-altitude climate therapy (HACT) on lung function outcomes in asthma, and systematically searched PubMed, Embase and www.elibrary.ru for publications appearing from 1970 to mid-2015. We included studies carried out with children or adults with an exposure of up to 12 weeks at an altitude of ≥1500 m above sea level. Changes in forced expiratory volume in 1 s (FEV), FEV/vital capacity ratio or peak expiratory flow rate as the HACT intervention outcomes were analysed. We included data for 907 participants (age range 4-58 years) from 21 studies, altogether including 28 substrata based on asthma type or severity. Only three of 21 included studies had high quality, whereas 93% of substudies reported lung function improvement with an overall pooled standardised mean difference (SMD) of 0.53 (95% CI 0.43-0.62). The measured effect of HACT was greater in adults (SMD 0.75, 95% CI 0.63-0.88, n=14) than in children (SMD 0.24, 95% CI 0.09-0.38, n=14). Studies at altitude >2000 m above sea level yielded the same effect as those at lower altitude. Based on a cut-point of a 0.50 change in SMD to define a meaningful clinical difference, HACT appears to have efficacy as an intervention. This extent of benefit appears to be limited to adults with asthma.

BACKGROUND

Silicosis is a progressive lung disease resulting from the inhalation of respirable crystalline silica. Lung transplantation is the only treatment for end-stage silicosis. The aim of this study was to analyze the survival experience following lung transplantation among patients with silicosis.

METHODS

We reviewed data for all patients who underwent lung transplantation for silicosis and a matched group undergoing lung transplantation for idiopathic pulmonary fibrosis (IPF) at a single medical center between March 2006 and the end of December 2013. Survival was followed through 2015.

RESULTS

A total of 17 lung transplantations were performed for silicosis among 342 lung transplantations (4.9%) during the study period. We observed non-statistically significant survival advantage (hazard ratio 0.6; 95%CI 0.24-1.55) for those undergoing lung transplantation for silicosis relative to IPF patients undergoing lung transplantation during the same period.

CONCLUSIONS

Within the limits of a small sample, survival in silicosis patients following lung transplantation was not reduced compared to IPF. Am. J. Ind. Med. 60:248-254, 2017. © 2017 Wiley Periodicals, Inc.

Importance

Skin cancer is the most common malignancy occurring after organ transplantation. Although previous research has reported an increased risk of skin cancer in solid organ transplant recipients (OTRs), no study has estimated the posttransplant population-based incidence in the United States.

Objective

To determine the incidence and evaluate the risk factors for posttransplant skin cancer, including squamous cell carcinoma (SCC), melanoma (MM), and Merkel cell carcinoma (MCC) in a cohort of US OTRs receiving a primary organ transplant in 2003 or 2008.

Design, Setting, and Participants

This multicenter retrospective cohort study examined 10 649 adult recipients of a primary transplant performed at 26 centers across the United States in the Transplant Skin Cancer Network during 1 of 2 calendar years (either 2003 or 2008) identified through the Organ Procurement and Transplantation Network (OPTN) database. Recipients of all organs except intestine were included, and the follow-up periods were 5 and 10 years.

Main Outcomes and Measures

Incident skin cancer was determined through detailed medical record review. Data on predictors were obtained from the OPTN database. The incidence rates for posttransplant skin cancer overall and for SCC, MM, and MCC were calculated per 100 000 person-years. Potential risk factors for posttransplant skin cancer were tested using multivariate Cox regression analysis to yield adjusted hazard ratios (HR).

Results

Overall, 10 649 organ transplant recipients (mean [SD] age, 51 [12] years; 3873 women [36%] and 6776 men [64%]) contributed 59 923 years of follow-up. The incidence rates for posttransplant skin cancer was 1437 per 100 000 person-years. Specific subtype rates for SCC, MM, and MCC were 812, 75, and 2 per 100 000 person-years, respectively. Statistically significant risk factors for posttransplant skin cancer included pretransplant skin cancer (HR, 4.69; 95% CI, 3.26-6.73), male sex (HR, 1.56; 95% CI, 1.34-1.81), white race (HR, 9.04; 95% CI, 6.20-13.18), age at transplant 50 years or older (HR, 2.77; 95% CI, 2.20-3.48), and being transplanted in 2008 vs 2003 (HR, 1.53; 95% CI, 1.22-1.94).

Conclusions and Relevance

Posttransplant skin cancer is common, with elevated risk imparted by increased age, white race, male sex, and thoracic organ transplantation. A temporal cohort effect was present. Understanding the risk factors and trends in posttransplant skin cancer is fundamental to targeted screening and prevention in this population.

BACKGROUND

In those with symptoms indicative of obstructive sleep apnea (OSA), respiratory-specific health-related quality of life (HRQL) may be an important patient-centered outcome. The aim of this study was to assess the associations between sleepiness, fatigue, and impaired general and respiratory-specific HRQL among persons with suspected OSA.

METHODS

We evaluated military veterans consecutively referred for suspected OSA with sleep studies yielding apnea-hypopnea index (AHI) values. They also completed the sleepiness (Epworth Sleepiness Scale [ESS]), and fatigue (Fatigue Severity Scale [FSS]) questionnaires, as well as two HRQL instruments (the generic Short-Form SF-12v2 yielding the Physical Component Scale [PCS] and the respiratory-specific Airways Questionnaire [AQ]-20R). Multiple linear regression tested the associations between ESS and FSS (standardized as Z scores for scaling comparability) with AQ-20R, accounting for AHI, SF-12v2-PCS and comorbid respiratory conditions other than OSA.

RESULTS

We studied 1578 veterans (median age 61.1 [IQR 16.8] years; 93.9% males). Of these, 823 (52%) met AHI criteria for moderate to severe OSA (AHI ≥15/h). The majority reported excessive daytime sleepiness (53%; median ESS 11 [IQR 9]) or fatigue (61%; median FSS 42 [IQR 23]). The median AQ-20R was 4 [IQR 1-8]. Controlling for AHI, SF-12v2-PCS, respiratory co-morbid conditions, body mass index, and demographics, both ESS and FSS were significantly associated with poorer AQ-20R: for each; ESS, 1.6 points (95% CI 1.4-1.9), and for FSS, 2.5 points (95% CI, 2.3-2.7).

CONCLUSIONS

Greater daytime sleepiness and fatigue are associated with poorer respiratory-specific HRQL, over and above the effects of OSA, respiratory comorbidity, and generic physical HRQL.

The history of the biomedical recognition manganese-caused neurotoxicity mirrors changing technologies as much as it does the ontology of parkinsonism. The initial 1837 report of manganese-induced neurologic injury was made by John Couper, a university-based physician in Scotland. He made clear that the outbreak occurred among workers at the Charles Tennant bleach manufactory in the environs of Glasgow. The relatively new technology of chlorine generation using manganese accounted for the novel exposure involved. At the time, this factory was the largest hypochlorite bleaching powder producer in the world. As the 19th century progressed, technological change in steel fabrication requiring higher manganese content greatly increased demand for the metal. Nonetheless, more than six decades elapsed before the next reports of manganese neurotoxicity emerged. Two unrelated outbreaks (both on Continental Europe) were reported within weeks of each other in 1901, one by von Jaksch and the other by Embden. All the cases were heavily exposed to manganese-containing dust. By the eve of the First World War, a total of 9 patients with manganese-caused neurologic illness had been reported in five separate Continental European publications. Meanwhile, new technology led to another exposure source. Magnetic separation techniques allowed the extraction of zinc from mixed ore also containing iron and manganese, leading to exploitation of a unique source of high manganese-content ore found in New Jersey. Not long after that technology's introduction, in 1912 Casamajor reported the first U.S. cases of manganism, detailing classic findings. Additional cases from the same cohort were reported a few years later, with continued exposure driven by First World War-driven demand for manganese to be used in armaments. The nosology of chronic manganese neurotoxicity remained in flux, with considerable emphasis on shared attributes with Wilson's disease, a syndrome only then recently described. A landmark 1924 primate study by Mella showed manganese-induced basal ganglion damage; human autopsy study data in the years following further supported the view that manganese toxicity represented a parkinsonian syndrome. As the 1937 centenary of Couper's first report approached, newer technologies (electric arc welding and battery making) were being linked to manganese-caused disease, even as mineral extraction was expanding as a global source of exposure.