Publications

OBJECTIVE

We aimed to ascertain risk factors for acute mountain sickness (AMS) in miners exposed to chronic intermittent high altitude conditions.

METHODS

All new hires (2009-2012) for mine employment (4000 m above sea level) were followed up for 12 months after first ascent. Demographics, physiologic data, and cigarette smoking were assessed at preemployment screening. Mine site clinic care for AMS defined incident events. Cox regression analysis estimated risk of AMS associated with smoking and selected covariates.

RESULTS

There were 46 AMS cases among 569 individuals during the first 12 months of employment. Adjusted for age, sex, and altitude of permanent residence, cigarettes smoked per day before hiring were prospectively associated with AMS (hazard ratio [HR], 1.9; 95% CI, 1.1 to 3.2 per 10 cigarettes smoked). This risk was higher in the subset of workers with less demanding physical work (n=336; HR, 3.3; 95% CI, 1.7 to 6.3), whereas among those with more physically demanding jobs (n=233), smoking was not associated with increased risk (HR, 0.6; 95% CI, 0.1 to 2.3).

CONCLUSIONS

In workers newly hired to work at high altitude, smoking increases the likelihood of AMS, but this effect appears to be operative only among those with less physically demanding work duties.

PURPOSE

Accumulating evidence suggests an important role for psychosocial work factors in injury, but little is known about the interaction between psychosocial factors and previous injury experience on subsequent injury risk. We examined the relationships between psychosocial work factors and new or recurrent injury among hospital workers.

METHODS

We studied 492 hospital workers including 116 cases with baseline injury and 376 injury-free referents at baseline over follow-up. Job strain, total support, effort-reward imbalance, overcommitment, and musculoskeletal injury at baseline were examined in logistic regression models as predictors of new or recurrent injury experienced during a 2-year follow-up period.

RESULTS

The overall cumulative incidence of injury over follow-up was 35.6 % (51.7 % for re-injury among baseline injury cases; 30.6 % for new injury among referents). Significantly increased risks with baseline job strain (OR 1.26; 95 % CI 1.02-1.55) and effort-reward imbalance (OR 1.42; 95 % CI 1.12-1.81) were observed for injury only among the referents. Overcommitment was associated with increased risk of injury only among the cases (OR 1.58; 95 % CI 1.05-2.39).

CONCLUSIONS

The effects of psychosocial work factors on new or recurrent injury risk appear to differ by previous injury experience, suggesting the need for differing preventive strategies in hospital workers.

BACKGROUND

The association between occupational exposure and autoimmune disease is well recognized for silica, and suspected for other inhalants. We used a large cohort to estimate the risks of rheumatoid arthritis, systemic lupus erythematosus, systemic sclerosis, and dermatomyositis associated with silica and other occupational exposures.

METHODS

We analyzed data for male Swedish construction industry employees. Exposure was defined by a job-exposure matrix for silica and for other inorganic dusts; those with other job-exposure matrix exposures but not to either of the 2 inorganic dust categories were excluded. National hospital treatment data were linked for International Classification of Diseases, 10(th) Revision-coded diagnoses of rheumatoid arthritis (seronegative and positive), systemic lupus erythematosus, systemic sclerosis, and dermatomyositis. The 2 occupational exposures were tested as independent predictors of prospective hospital-based treatment for these diagnoses using age-adjusted Poisson multivariable regression analyses to calculate relative risk (RR).

RESULTS

We analyzed hospital-based treatment data (1997 through 2010) for 240,983 men aged 30 to 84 years. There were 713 incident cases of rheumatoid arthritis (467 seropositive, 195 seronegative, 51 not classified) and 128 cases combined for systemic lupus erythematosus, systemic sclerosis, and dermatomyositis. Adjusted for smoking and age, the 2 occupational exposures (silica and other inorganic dusts) were each associated with increased risk of rheumatoid arthritis, systemic lupus erythematosus, systemic sclerosis, and dermatomyositis combined: RR 1.39 (95% confidence interval [CI], 1.17-1.64) and RR 1.31 (95% CI, 1.11-1.53), respectively. Among ever smokers, both silica and other inorganic dust exposure were associated with increased risk of rheumatoid arthritis (RRs 1.36; 95% CI, 1.11-1.68 and 1.42; 95% CI, 1.17-1.73, respectively), while among never smokers, neither exposure was associated with statistically significant increased risk of rheumatoid arthritis.

CONCLUSION

This analysis reaffirms the link between occupational silica and a range of autoimmune diseases, while also suggesting that other inorganic dusts may also impart excess risk of such disease.

BACKGROUND

There is a well-established association between inhalational exposure to silica and autoimmune disease. We recently observed an outbreak of silica-related autoimmune disease among synthetic stone construction workers with silicosis referred for lung transplantation assessment.

AIMS

To characterize the rheumatologic complications in silicosis within these highly exposed, clinically well-characterized patients.

METHODS

We systematically reviewed data from all cases of silicosis due to synthetic stone dust referred to our pulmonary institute for lung transplant assessment, which represents the national centre for all such referrals. In addition to silicosis-specific data, we extracted data relevant to the clinical and serological manifestations of autoimmune diseases present in these patients.

RESULTS

Of 40 patients in our advanced silicosis national data, we identified nine (23%) with findings consistent with various autoimmune diseases. Among these nine, three also had findings consistent with pulmonary alveolar proteinosis. Based on an expected autoimmune disease prevalence of 3% (based on the upper-end estimate for this group of diseases in European international data), the proportion of disease in our group represents a >7-fold excess (prevalence ratio 7.5; 99% confidence interval 2.6-16.7).

CONCLUSIONS

These cases underscore the strong link between silicosis and multiple distinct syndromes of autoimmune diseases. Vigilance is warranted for the recognition of autoimmune complications in persons with known silicosis; so too is consideration of the occupational exposure history in persons presenting with manifestations of autoimmune disease.

BACKGROUND

Very rapidly progressive "acute silicosis" was observed prior to the 1930 International Labour Office Conference on silicosis, but its clinical significance and pathologic relationship to classic silica caused pneumoconiosis were not settled.

METHODS

Textual analysis of the 1930 Conference proceedings identified data relevant to rapidly progressive silicosis. Standard bibliographic searches identified relevant biomedical literature dating from before and after the Conference.

RESULTS

The 1930 Johannesburg Conference contained descriptions of acute silicosis, especially in the abrasive powders industry, but acute silica-related lung disease did not conform to a three-stage disease model in which tuberculosis supra-infection caused advanced disease, a model accepted at the Conference. Over following decades, additional reports appeared of rapidly progressive silicosis, unrelated to tuberculosis. Pulmonary alveolar proteinosis was identified only in 1958.

CONCLUSIONS

Adoption by the 1930 Johannesburg Conference of a classification scheme into which acute rapidly progressive disease unrelated to tuberculosis fitted poorly may have impeded the understanding of acute silicosis and its importance.

The fifth Jack Pepys Workshop on Asthma in the Workplace focused on the similarities and differences of work-related asthma (WRA) and non-work-related asthma (non-WRA). WRA includes occupational asthma (OA) and work-exacerbated asthma (WEA). There are few biological differences in the mechanisms of sensitization to environmental and occupational allergens. Non-WRA and OA, when due to high-molecular-weight agents, are both IgE mediated; it is uncertain whether OA due to low-molecular-weight agents is also IgE mediated. Risk factors for OA include female sex, a history of upper airway symptoms, and a history of bronchial hyperresponsiveness. Atopy is a risk factor for OA due to high-molecular-weight agents, and exposure to cleaning agents is a risk factor for both OA and non-WRA. WEA is important among workers with preexisting asthma and may overlap with irritant-induced asthma, a type of OA. Induced sputum cytology can confirm airway inflammation, but specific inhalation challenge is the reference standard diagnostic test. Inhalation challenges are relatively safe, with the most severe reactions occurring with low-molecular-weight agents. Indirect health care costs account for about 50% of total asthma costs. Workers with poor asthma control (WRA or non-WRA) are less likely to be employed. Income loss is a major contributor to the indirect costs of WRA. Overall, asthma outcomes probably are worse for adult-onset than for childhood-onset asthma but better for OA than adult-onset non-WRA. Important aspects of management of OA are rapid and proper confirmation of the diagnosis and reduction of exposure to sensitizers or irritants at work and home.

AIM

Studies of the potential association between cigarette smoking and acute mountain sickness (AMS) have reached contradictory conclusions. Our aim was to perform a meta-analysis of studies across a range of populations to ascertain better the true relationship between cigarette smoking and AMS.

MATERIALS AND METHODS

We used the PRISMA protocol to identify and screen eligible studies of smoking and AMS. Databases including Pubmed and Google Scholar were searched, using the terms "smoking" and "acute mountain sickness." We conducted a meta-analysis of the selected studies in order to evaluate causal inference, evaluate potential biases, and investigate possible sources of heterogeneity across studies.

RESULTS

We identified 3907 publications, of which 29 were eligible for inclusion by reporting smoking status and AMS. Of these, eight publications were excluded because they were duplicative or were lacking quantitative data. The 21 studies analyzed included 16 566 subjects. These fell into two groups: occupational/military (n = 8) or volunteers/trekkers/mixed (n = 13). Study heterogeneity was high (X (2) = 55.5, P < .001). Smoking was not statistically associated with increased risk of AMS: pooled OR = 0.88 (95% CI = 0.74-1.05). Stratification yielded similar risk estimates among the occupational/military studies versus all others and studies at relatively higher and lower altitudes.

CONCLUSIONS

Overall, smoking was not statistically significantly associated with AMS: there is no consistent effect of cigarette smoking acting as either a protective factor against or a risk factor for AMS.

IMPLICATIONS

This is the first quantitative assessment of published studies on smoking and AMS, which shows smoking to be neither a risk, nor protective. Studies specifically focusing on smoking as a risk factor, should guide further research on this issue. Although all smokers should be strongly advised to quit, studies on risk factors for AMS focusing on other exposures could shed light on the full range of risks for AMS.

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.