Occurrence of airway irritation among indoor swimming pool personnel was investigated. The aims of this study were to assess trichloramine exposure levels and exhaled nitric oxide in relation to the prevalence of airway symptoms in swimming pool facilities and to determine protein effects in the upper respiratory tract.
The presence of airway symptoms related to work was examined in 146 individuals working at 46 indoor swimming pool facilities. Levels of trichloramine, as well as exhaled nitric oxide, were measured in five facilities with high prevalence of airway irritation and four facilities with no airway irritation among the personnel. Nasal lavage fluid was collected, and protein profiles were determined by a proteomic approach.
17 % of the swimming pool personnel reported airway symptoms related to work. The levels of trichloramine in the swimming pool facilities ranged from 0.04 to 0.36 mg/m(3). There was no covariance between trichloramine levels, exhaled nitric oxide and prevalence of airway symptoms. Protein profiling of the nasal lavage fluid showed that the levels alpha-1-antitrypsin and lactoferrin were significantly higher, and S100-A8 was significantly lower in swimming pool personnel.
This study confirms the occurrence of airway irritation among indoor swimming pool personnel. Our results indicate altered levels of innate immunity proteins in the upper airways that may pose as potential biomarkers. However, swimming pool facilities with high prevalence of airway irritation could not be explained by higher trichloramine exposure levels. Further studies are needed to clarify the environmental factors in indoor swimming pools that cause airway problems and affect the immune system.
Some polycyclic aromatic hydrocarbons (PAH) are known carcinogens and workplace PAH exposure may increase the risk of cancer. Monitoring early cancer-related changes can indicate whether the exposure is carcinogenic. Here, we enrolled 151 chimney sweeps, 152 controls and 19 creosote-exposed male workers from Sweden. We measured urinary PAH metabolites using LC/MS/MS, the cancer-related markers telomere length (TL) and mitochondrial DNA copy number (mtDNAcn) using qPCR, and DNA methylation of lung cancer-related genes F2RL3 and AHRR using pyrosequencing. The median 1-hydroxypyrene (PAH metabolite) concentrations were highest in creosote-exposed workers (8.0 µg/g creatinine) followed by chimney sweeps (0.34 µg/g creatinine) and controls (0.05 µg/g creatinine). TL and mtDNAcn did not differ between study groups. Chimney sweeps and creosote-exposed workers had significantly lower methylation of AHRR CpG site cg05575921 (88.1 and 84.9%, respectively) than controls (90%). Creosote-exposed workers (73.3%), but not chimney sweeps (76.6%) had lower methylation of F2RL3 cg03636183 than controls (76.7%). Linear regression analyses showed that chimney sweeps had lower AHRR cg05575921 methylation (B = -2.04; P
To assess the effect of exposure to hydrogen fluoride (HF) on the airway mucosa in an industrial setting.
A cross-sectional study encompassing 33 industrial workers in a flame soldering plant and 44 assembly workers unexposed to HF was performed by means of a questionnaire on symptoms and diagnosis regarding upper and lower airways as well as through conduct of a clinical examination of the exposed group. Air concentrations of HF that were monitored in winter amounted to 1.0 mg/m(3) and in summer time to 0.15 mg/m(3).
A threefold risk for epistaxis (RR = 3.6, 95% confidence interval 1.1-11.0) was observed in the exposed group. Time from the start of exposure to HF until debut of a nose bleeding period varied from 1 month to 6 years. Mean induction (latency) time was 42 months. Mean duration of symptoms was 26 months, range 3-72 months, indicating that the exposure level in summer time was sufficient to maintain the propensity of almost daily nose bleeding.
HF is an irritating vapor, even at relatively low air concentrations. We recommend an 8 hr TLV lower than 1.0 mg/m(3).
PURPOSE: This case-control study was undertaken to elucidate the controversy concerning whether low-level, long-term exposure to non-sensitising air pollution at workplaces may cause asthma. METHODS: A case-control study of 192 adult-onset asthma cases aged 20-65 years and 323 controls was conducted in the southeast of Sweden. Cases were identified from computerised registers from the region, diagnosed 2000-2004 and diagnoses were confirmed via medical files. Referents were randomised from the population register of the region. Exposure was monitored by a 16-page questionnaire. Special attention was devoted to identifying and in the final analyses excluding subjects exposed to sensitising agents. RESULTS: Three years or more of occupational exposure to air pollution from dust, smoke, fumes or vapours before the year of diagnosis by analyses adjusting for age yielded an increased risk for asthma (OR = 2.3, 95% CI 1.2-4.2) in men, while in women, no risk was seen. In a multiple logistic regression analysis in men without allergy in childhood, a significant risk was seen (OR = 2.8, 95% CI 1.07-7.4), when subjects exposed to identified allergens were excluded. In women, no excess risk was observed from occupational air pollution. CONCLUSION: The results of this study support an association between occupational exposure to low level non-sensitising air pollution and adult-onset asthma in men.
The exposure for workers handling and recycling offshore drilling waste are previously not described, and given the potential for exposure to hazardous components, there is a need for characterizing this occupational exposure. In this study five plants recycling offshore drilling waste with different techniques were included. Measurements were conducted in both winter and summer to include seasonal exposure variations. Altogether >200 personal air-exposure measurements for oil mist, oil vapor, volatile organic compounds (VOC), hydrogen sulfide (H2S) and solvents were carried out respectively. Microorganisms related to drilling waste were identified in bulk samples and in stationary air measurements from two of the plants. The exposure to oil mist and oil vapor were below 10% of the current Norwegian occupational exposure limits (OEL) for all measured components. The plants using the Resoil or TCC method had a statistically significant higher exposure to oil vapor than the plant using complete combustion (p-value
Chlorination is a method commonly used to keep indoor swimming pool water free from pathogens. However, chlorination of swimming pools produces several potentially hazardous by-products as the chlorine reacts with nitrogen containing organic matter. Up till now, exposure assessments in indoor swimming pools have relied on stationary measurements at the poolside, used as a proxy for personal exposure. However, measurements at fixed locations are known to differ from personal exposure.
Eight public swimming pool facilities in four Swedish cities were included in this survey. Personal and stationary sampling was performed during day or evening shift. Samplers were placed at different fixed positions around the pool facilities, at ~1.5 m above the floor level and 0-1 m from the poolside. In total, 52 personal and 110 stationary samples of trichloramine and 51 personal and 109 stationary samples of trihalomethanes, were collected.
The average concentration of trichloramine for personal sampling was 71 µg m(-3), ranging from 1 to 240 µg m(-3) and for stationary samples 179 µg m(-3), ranging from 1 to 640 µg m(-3). The air concentrations of chloroform were well below the occupational exposure limit (OEL). For the linear regression analysis and prediction of personal exposure to trichloramine from stationary sampling, only data from personal that spent >50% of their workday in the pool area were included. The linear regression analysis showed a correlation coefficient (r2) of 0.693 and a significant regression coefficient ß of 0.621; (95% CI = 0.329-0.912, P = 0.001).
The trichloramine exposure levels determined in this study were well below the recommended air concentration level of 500 µg m(-3); a WHO reference value based on stationary sampling. Our regression data suggest a relation between personal exposure and area sampling of 1:2, implying an OEL of 250 µg m(-3) based on personal sampling.
Cites: Occup Environ Med. 2004 Apr;61(4):37415031401
Cites: Occup Environ Med. 2003 Jun;60(6):385-9412771389
Cites: Ann Occup Hyg. 2003 Apr;47(3):179-8512639831
To study the impact of occupational silica exposure on the incidence rates of sarcoidosis and rheumatoid arthritis (RA) in a cohort of exposed workers in Swedish iron foundries.
The prevalence of sarcoidosis and RA in a cohort of silica exposed workers was compared with the prevalence in the general Swedish population in this register study. A mixed model was used to calculate silica exposure, and individual silica exposures were used to compute dose responses.
Personnel records from 10 iron foundries were used to identify workers whose employment began before 2005 which was then linked to the national non-primary outpatient visits register.
The final cohort consisted of 2187 silica-exposed male workers who had been employed for at least 1?year and were still alive without having emigrated when the follow-up study began. The cohort's employment period covers 23 807 person-years at risk.
The presented results indicate that moderate to high levels of silica exposure increase risks for sarcoidosis and seropositive RA.
Mean levels of airborne silica dust in the foundries decreased significantly between the 1970s and 2000s. Incidence rates of sarcoidosis (3.94; 95%?CI 1.07 to 10.08) and seropositive RA (2.59; 95%?CI 1.24 to 4.76) were significantly higher among highly exposed individuals.
Our results reveal increased risks for sarcoidosis and seropositive RA among individuals with high exposure to silica dust (>0.048?mg/m3) compared with non-exposed and less-exposed groups.
Cites: Occup Environ Med. 1998 Oct;55(10):657-60 PMID 9930085
Work-related exposure to silica is a global health hazard that causes diseases such as silicosis. Some studies have also reported that silica exposure is linked to elevated cardiovascular disease mortality. However, these diagnoses have not been investigated in detail and there have been few studies on morbidity. The aim of this study is to examine morbidity and mortality from different cardiovascular diseases among silica-exposed Swedish foundry workers.
Historical and contemporary measurements (1968-2006) of respiratory silica exposure were matched to job categories, individual foundries, and 4 time periods (1968-1979, 1980-1989, 1990-1999, 2000-2006) using a mixed model. Morbidity and mortality data for the studied cohorts were matched against the General Population Registry. Statistical analyses were performed with SPSS and STATA, and the data were stratified by age, gender, and year.
Mortality from cardiovascular disease (SMR 1.3; 95% CI 1.2-1.4) and stroke (SMR 1.6, 95% CI 1.2-2.1) was significantly elevated among the studied population. The cohort also exhibited significantly elevated morbidity from stroke (SIR 1.34; 95% CI 1.2-1.5) but not myocardial infarction. The mean age at the time of first morbidity from stroke was 64 years, with 36% of the cases occurring before the age of 60.
Swedish foundry workers exposed to respirable silica exhibit elevated morbidity and mortality from stroke, but not from myocardial infarction. Our results also suggest a relationship between silica exposure and morbidity from stroke at a younger age than the general population.
Cites: J Expo Sci Environ Epidemiol. 2014 Jan-Feb;24(1):42-50 PMID 23385294