A cross-sectional study of sensory-motor neuropsychological function among sewage plant and sewage net workers exposed to hydrogen sulphide when handling wastewater.

OBJECTIVES: Workers at sewage treatment plants are exposed to a complex mixture of toxins, including hydrogen sulphide (H2S). An issue of concern among sewage workers, is possible negative nervous system effects from low-level H2S exposure. Empirical neuropsychological evidence indicates both that low-dose exposure to H2S exposure affects the nervous system, and the contrary, that such exposure may facilitate nervous system function, since H2S is an endogenously produced central nervous system (CNS) gasotransmitter. The aim of this study is to describe a possible association between the H2S component of the total exposure and long-term effects on neuropsychological motor function among wastewater workers. METHODS: Workers (N = 138) treating wastewater in 6 sewage-treatment plants, or in the sewer net system participated in a cross-sectional study. H2S exposure was expressed in a dichotomous exposure variable defining currently H2S-exposed (N = 112) and unexposed referent workers (N = 26), and a variable defining a job-exposure matrix for long-term total typical workplace H2S exposure. The participants went through neuropsychological tests for hand coordination, reaction time (SRT), and balance, and completed questionnaires. Pearson chi-square test or independent samples t-test was used when comparing the currently H2S-exposed workers with the unexposed control group. Multiple linear regression was used to assess associations between the independent variables age, smoking and exposure variables, and the neuropsychological tests. RESULTS: The analyses indicate increased SRT in the currently H2S-exposed group compared to controls (mean [SD] = 225.8 [29.9] versus 210.7 [26.3] ms, P = 0.019), and an association between increased SRT and current H2S-exposure in the total study sample (ß = 14.7, P = 0.026, R2 = 0.06, P = 0.050). Blindfolded balance testing indicates a nonsignificant trend in the total study sample, of reduced balance in the highest versus lowest H2S total long-term exposure-index group (Sway area [mean {SD}, mm2: 702 [410] versus 581 [278]), and a significant association between total long-term H2S exposure and reduced balance among smokers (Sway area, mm2 [ß = 38.7, P = 0.039], mean sway, mm [ß = 0.3, P = 0.015]). CONCLUSION: The observed trends and associations may be due to exposure peaks in certain work operations and pinpoint the importance of minimizing and avoiding exposure peaks, also when H2S time-weighted average measurements do not exceed an occupational exposure limit of 5 ppm.

High aspect ratio nanomaterial-induced macrophage polarization is mediated by changes in miRNA levels.

Introduction: Inhalation of nanomaterials may induce inflammation in the lung which if left unresolved can manifest in pulmonary fibrosis. In these processes, alveolar macrophages have an essential role and timely modulation of the macrophage phenotype is imperative in the onset and resolution of inflammatory responses. This study aimed to investigate, the immunomodulating properties of two industrially relevant high aspect ratio nanomaterials, namely nanocellulose and multiwalled carbon nanotubes (MWCNT), in an alveolar macrophage model. Methods: MH-S alveolar macrophages were exposed at air-liquid interface to cellulose nanocrystals (CNC), cellulose nanofibers (CNF) and two MWCNT (NM-400 and NM-401). Following exposure, changes in macrophage polarization markers and secretion of inflammatory cytokines were analyzed. Furthermore, the potential contribution of epigenetic regulation in nanomaterial-induced macrophage polarization was investigated by assessing changes in epigenetic regulatory enzymes, miRNAs, and rRNA modifications. Results: Our data illustrate that the investigated nanomaterials trigger phenotypic changes in alveolar macrophages, where CNF exposure leads to enhanced M1 phenotype and MWCNT promotes M2 phenotype. Furthermore, MWCNT exposure induced more prominent epigenetic regulatory events with changes in the expression of histone modification and DNA methylation enzymes as well as in miRNA transcript levels. MWCNT-enhanced changes in the macrophage phenotype were correlated with prominent downregulation of the histone methyltransferases Kmt2a and Smyd5 and histone deacetylases Hdac4, Hdac9 and Sirt1 indicating that both histone methylation and acetylation events may be critical in the Th2 responses to MWCNT. Furthermore, MWCNT as well as CNF exposure led to altered miRNA levels, where miR-155-5p, miR-16-1-3p, miR-25-3p, and miR-27a-5p were significantly regulated by both materials. PANTHER pathway analysis of the identified miRNA targets showed that both materials affected growth factor (PDGF, EGF and FGF), Ras/MAPKs, CCKR, GnRH-R, integrin, and endothelin signaling pathways. These pathways are important in inflammation or in the activation, polarization, migration, and regulation of phagocytic capacity of macrophages. In addition, pathways involved in interleukin, WNT and TGFB signaling were highly enriched following MWCNT exposure. Conclusion: Together, these data support the importance of macrophage phenotypic changes in the onset and resolution of inflammation and identify epigenetic patterns in macrophages which may be critical in nanomaterial-induced inflammation and fibrosis.

Multiwalled Carbon Nanotubes Induce Fibrosis and Telomere Length Alterations.

Telomere shortening can result in cellular senescence and in increased level of genome instability, which are key events in numerous of cancer types. Despite this, few studies have focused on the effect of nanomaterial exposure on telomere length as a possible mechanism involved in nanomaterial-induced carcinogenesis. In this study, effects of exposure to multiwalled carbon nanotubes (MWCNT) on telomere length were investigated in mice exposed by intrapleural injection, as well as in human lung epithelial and mesothelial cell lines. In addition, cell cycle, apoptosis, and regulation of genes involved in DNA damage repair were assessed. Exposure to MWCNT led to severe fibrosis, infiltration of inflammatory cells in pleura, and mesothelial cell hyperplasia. These histological alterations were accompanied by deregulation of genes involved in fibrosis and immune cell recruitment, as well as a significant shortening of telomeres in the pleura and the lung. Assessment of key carcinogenic mechanisms in vitro confirmed that long-term exposure to the long MWCNT led to a prominent telomere shortening in epithelial cells, which coincided with G1-phase arrest and enhanced apoptosis. Altogether, our data show that telomere shortening resulting in cell cycle arrest and apoptosis may be an important mechanism in long MWCNT-induced inflammation and fibrosis.

A Cease in Shift Work Reverses Arterial Stiffness but Increases Weight and Glycosylated Hemoglobin A 5-Month Follow-Up in Industry.

BACKGROUND: Literature suggests an association between shift work and cardiovascular disease (CVD). Limited evidence is available on how a cessation of shift work affects CVD risk factors. AIM: We investigated whether a five-month plant shutdown affected CVD risk factors in 30 industrial shift workers. METHODS: We collected demographic data, self-reported data on physical activity (PA) and medical history by questionnaire. Pre- and post-plant shutdown, we measured blood pressure (BP), heart rate, lipids, glycosylated hemoglobin (HbA1c) and C-reactive protein (CRP). Additionally, we collected markers of inflammation, Matrix metalloproteinase-9 (MMP-9), Interleukin-6 (IL-6), Monocyte chemoattractant protein-1 (MCP-1), Tumor necrosis factor-alpha (TNF-α), P-selectin, Interleukin-1 beta (IL-1ß), and Interleukin-23 (IL-23). We also examined arterial stiffness (central blood pressure, augmentation pressure, and pulse wave velocity) by means of SphygmoCor® (AtCor Medical Pty Ltd., Sydney, Australia). We monitored sleep by actigraphy prior to and after plant shutdown, with additional registration of sleep quality and assessment of insomnia symptoms. RESULTS: After five months of plant shutdown, we found that HbA1c increased by 1.9 mmol/mol, weight by 1 kg and MCP-1 by 27.3 pg/mL, all unexpectedly. The other markers of inflammation did not change during shutdown, but CRP decreased close to significant levels. There were no changes in lipids during follow-up. Pulse-wave velocity (PWV) was reduced from 8.1 m/s (SD = 1.5) to 7.6 m/s (SD = 1.5), p = 0.03. The workers reported fewer signs of insomnia after shutdown. CONCLUSIONS: Our findings suggest that a five-month cessation in shift work increases weight and HbA1c, but also improves insomnia symptoms and reverses arterial stiffening.

Long-Term Exposure to Nanosized TiO2 Triggers Stress Responses and Cell Death Pathways in Pulmonary Epithelial Cells.

There is little in vitro data available on long-term effects of TiO2 exposure. Such data are important for improving the understanding of underlying mechanisms of adverse health effects of TiO2. Here, we exposed pulmonary epithelial cells to two doses (0.96 and 1.92 µg/cm2) of TiO2 for 13 weeks and effects on cell cycle and cell death mechanisms, i.e., apoptosis and autophagy were determined after 4, 8 and 13 weeks of exposure. Changes in telomere length, cellular protein levels and lipid classes were also analyzed at 13 weeks of exposure. We observed that the TiO2 exposure increased the fraction of cells in G1-phase and reduced the fraction of cells in G2-phase, which was accompanied by an increase in the fraction of late apoptotic/necrotic cells. This corresponded with an induced expression of key apoptotic proteins i.e., BAD and BAX, and an accumulation of several lipid classes involved in cellular stress and apoptosis. These findings were further supported by quantitative proteome profiling data showing an increase in proteins involved in cell stress and genomic maintenance pathways following TiO2 exposure. Altogether, we suggest that cell stress response and cell death pathways may be important molecular events in long-term health effects of TiO2.

Occupational Noise Exposure and Vestibular Schwannoma: A Case-Control Study in Sweden.

It has been suggested that the association between self-reported occupational noise exposure and vestibular schwannoma (VS), found in several studies, represents recall bias. Therefore, we aimed to study the relationship in a large case-control study using occupational noise measurements. We performed a case-control study using data from Sweden for 1,913 VS cases diagnosed in 1961-2009 and 9,566 age- and sex-matched population controls. We defined occupational history by linkage to national censuses from 1960, 1970, 1980, and 1990. We estimated occupational noise exposure for each case and control using a job-exposure matrix. There was no association between occupational noise exposure and VS. Among subjects assessed as ever exposed to occupational noise levels of ≥85 dB (214 cases and 1,142 controls), the odds ratio for VS per 5 years of exposure was 1.02 (95% confidence interval: 0.90, 1.17). Workers with noise levels of ≥85 dB for at least 15 years (5-year latency period), showed no increased risk of VS (odds ratio = 0.98, 95% confidence interval: 0.73, 1.31) compared with those who had never been exposed to noise levels of 75 dB or higher. In summary, our large study does not support an association between occupational noise exposure and VS.

Pneumoproteins in Offshore Drill Floor Workers.

The aim was to assess pneumoproteins and a certain biomarker of systemic inflammation in drill floor workers exposed to airborne contaminants generated during drilling offshore, taking into consideration serum biomarkers of smoking, such as nicotine (S-Nico) and cotinine. Blood samples of club cell protein 16 (CC-16), surfactant protein D (SP-D) and C-reactive protein (CRP) were collected before and after a 14-day work period from 65 drill floor workers and 65 referents. Air samples of oil mist, drilling mud components and elemental carbon were collected in person. The drill floor workers were exposed to a median air concentration of 0.18 mg/m³ of oil mist and 0.14 mg/m³ of airborne mud particles. There were no differences in the concentrations of CC-16 and SP-D across the 14-day work period and no difference between drill floor workers and referents at baseline after adjusting for differences in sampling time and smoking. CRP decreased across the work period. There was a strong association between the CC-16 concentrations and the time of sampling. Current smokers with S-Nico > detection limit (DL) had a statistically significantly lower CC-16 concentration, while smokers with S-Nico

Bulky DNA adducts, microRNA profiles, and lipid biomarkers in Norwegian tunnel finishing workers occupationally exposed to diesel exhaust.

OBJECTIVES: This study aimed to assess the biological impact of occupational exposure to diesel exhaust (DE) including DE particles (DEP) from heavy-duty diesel-powered equipment in Norwegian tunnel finishing workers (TFW). METHODS: TFW (n=69) and referents (n=69) were investigated for bulky DNA adducts (by 32P-postlabelling) and expression of microRNAs (miRNAs) (by small RNA sequencing) in peripheral blood mononuclear cells (PBMC), as well as circulating free arachidonic acid (AA) and eicosanoid profiles in plasma (by liquid chromatography-tandem mass spectrometry). RESULTS: PBMC from TFW showed significantly higher levels of DNA adducts compared with referents. Levels of DNA adducts were also related to smoking habits. Seventeen miRNAs were significantly deregulated in TFW. Several of these miRNAs are related to carcinogenesis, apoptosis and antioxidant effects. Analysis of putative miRNA-gene targets revealed deregulation of pathways associated with cancer, alterations in lipid molecules, steroid biosynthesis and cell cycle. Plasma profiles showed higher levels of free AA and 15-hydroxyeicosatetraenoic acid, and lower levels of prostaglandin D2 and 9-hydroxyoctadecadienoic acid in TFW compared with referents. CONCLUSION: Occupational exposure to DE/DEP is associated with biological alterations in TFW potentially affecting lung homoeostasis, carcinogenesis, inflammation status and the cardiovascular system. Of particular importance is the finding that tunnel finishing work is associated with an increased level of DNA adducts formation in PBMC.

In Vitro Transformation of Human Bronchial Epithelial Cells by Diesel Exhaust Particles: Gene Expression Profiling and Early Toxic Responses.

Occupational exposure to diesel exhaust may cause lung cancer in humans. Mechanisms include DNA-damage and inflammatory responses. Here, the potential of NIST SRM2975 diesel exhaust particles (DEP) to transform human bronchial epithelial cells (HBEC3) in vitro was investigated. Long-term exposure of HBEC3 to DEP led to increased colony growth in soft agar. Several DEP-transformed cell lines were established and based on the expression of epithelial-to-mesenchymal-transition (EMT) marker genes, one of them (T2-HBEC3) was further characterized. T2-HBEC3 showed a mesenchymal/fibroblast-like morphology, reduced expression of CDH1, and induction of CDH2 and VIM. T2-HBEC3 had reduced migration potential compared with HBEC3 and little invasion capacity. Gene expression profiling showed baseline differences between HBEC3 and T2-HBEC3 linked to lung carcinogenesis. Next, to assess differences in sensitivity to DEP between parental HBEC3 and T2-HBEC3, gene expression profiling was carried out after DEP short-term exposure. Results revealed changes in genes involved in metabolism of xenobiotics and lipids, as well as inflammation. HBEC3 displayed a higher steady state of IL1B gene expression and release of IL-1ß compared with T2-HBEC3. HBEC3 and T2-HBEC3 showed similar susceptibility towards DEP-induced genotoxic effects. Liquid-chromatography-tandem-mass-spectrometry was used to measure secretion of eicosanoids. Generally, major prostaglandin species were released in higher concentrations from T2-HBEC3 than from HBEC3 and several analytes were altered after DEP-exposure. In conclusion, long-term exposure to DEP-transformed human bronchial epithelial cells in vitro. Differences between HBEC3 and T2-HBEC3 regarding baseline levels and DEP-induced changes of particularly CYP1A1, IL-1ß, PGE2, and PGF2α may have implications for acute inflammation and carcinogenesis.

Pulmonary function and high-resolution computed tomography examinations among offshore drill floor workers.

PURPOSE: The aim of this study was to assess short-term changes in pulmonary function in drill floor workers currently exposed to airborne contaminants generated as a result of drilling offshore. We also aimed to study the prevalence of pulmonary fibrosis using high-resolution computed tomography (HRCT) scans of another group of previously exposed drill floor workers. METHODS: Pulmonary function was measured before and after a 14-day work period in a follow-up study of 65 drill floor workers and 65 referents. Additionally, 57 other drill floor workers exposed to drilling fluids during the 1980s were examined with HRCT of the lungs in a cross-sectional study. RESULTS: The drill floor workers had a statistically significant decline in forced expiratory volume in 1 s (FEV1) across the 14-day work period after adjustment for diurnal variations in pulmonary function (mean 90 mL, range 30-140 mL), while the small decline among the referents (mean 20 mL, range - 30 to 70 mL) was not of statistical significance. Larger declines in FEV1 among drill workers were associated with the fewer number of days of active drilling. There were no signs of pulmonary fibrosis related to oil mist exposure among the other previously exposed drill floor workers. CONCLUSION: After 14 days offshore, a statistically significant decline in FEV1 was observed in the drill floor workers, which may not be related to oil mist exposure. No pulmonary fibrosis related to oil mist exposure was observed.

Mechanisms of Breast Cancer in Shift Workers: DNA Methylation in Five Core Circadian Genes in Nurses Working Night Shifts.

Shift work has been suggested to be associated with breast cancer risk, and circadian disruption in shift workers is hypothesized as one of the mechanisms of increased cancer risk. There is, however, insufficient molecular evidence supporting this hypothesis. Using the quantitative methodology of pyrosequencing, epigenetic changes in 5-methyl cytosine (5mC) in five circadian genes CLOCK, BMAL1, CRY1, PER1 and PER2 in female nurses working night shift work (278 breast cancer cases, 280 controls) were analyzed. In breast cancer cases, a medium exposure to night work was associated with increased methylation levels of the CLOCK (p=0.050), BMAL1 (p=0.001) and CRY1 (p=0.040) genes, compared with controls. Within the cases, analysis of the effects of shift work on the methylation patterns showed that methylation of CRY1 was lower in those who had worked night shift and had a high exposure (p=0.006) compared with cases that had worked only days. For cases with a medium exposure to night work, an increase in BMAL1 (p=0.003) and PER1 (p=0.035) methylation was observed compared with day working (unexposed) cases. The methylation levels of the five core circadian genes were also analyzed in relation to the estrogen and progesterone receptors status of the tumors in the cases, and no correlations were observed. Furthermore, nineteen polymorphisms in the five circadian genes were assessed for their effects on the methylation levels of the respective genes, but no associations were found. In summary, our data suggest that epigenetic regulation of CLOCK, BMAL1, CRY1 and PER1 may contribute to breast cancer in shift workers.

Mechanisms of breast cancer risk in shift workers: association of telomere shortening with the duration and intensity of night work.

Occupational factors such as shiftwork and especially night work that involves disruption of the circadian rhythm may contribute to increased breast cancer risk. Circadian disruption may also affect telomere length (TL). While short TL generally is associated with increased cancer risk, its association with breast cancer risk is inconclusive. We suggest that working schedules might be an important factor in assessment of effects of TL on breast cancer risk. Moreover, telomere shortening might be a potential mechanism for night work-related breast cancer. In this study, effects of shift work on TL and its association with breast cancer risk were investigated in a nested breast cancer case-control study of Norwegian nurses. TL was assessed by qPCR in DNA from 563 breast cancer patients and 619 controls. Here, we demonstrate that TL is affected by intensive night work schedules, as work with six consecutive night for a period of more than 5 years was associated with decreased telomere lengths (-3.18, 95% CI: -6.46 to -0.58, P = 0.016). Furthermore, telomere shortening is associated with increased breast cancer risk in workers with long periods of consecutive night shifts. Thus, nurses with longer telomere lengths had a lower risk for breast cancer if they had worked more than four (OR: 0.37, 95% CI: 0.16-0.79, P = 0.014) or five (OR: 0.31, 95% CI: 0.10-0.83, P = 0.029) consecutive night shifts for a period of 5 years or more. These data suggest that telomere shortening is associated with the duration and intensity of night work and may be a contributing factor for breast cancer risk among female shift workers.

Physical activity initiated by employer induces improvements in a novel set of biomarkers of inflammation: an 8-week follow-up study.

PURPOSE: We investigated the level of pro- and anti-inflammatory biomarkers before and after 8 weeks of unsupervised physical activity (PA) initiated by employer. METHODS: During autumn 2014, background data, blood samples and self-reported exercise level were collected from 76 men and 41 women in a Norwegian road maintenance company. Monocyte chemoattractant protein-1 (MCP-1), tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), leptin, adiponectin, p-selectin and CD40 ligand (CD40L) were analyzed. [Formula: see text] was measured in a subgroup of 50 subjects. RESULTS: With reference point of exercise ≤1 time/week, we found that participants who exercised 2-3 times/week had higher [Formula: see text] values (5.6 mL kg-1 min-1; 95% CI [1.3, 9.9]). MCP-1 was lower in those who exercised ≥ 4 times/week (-81.98 pg/ml [-142.9, -21.0]). IL-6 and p-selectin levels were lower in females who exercised ≥4 times/week (-1.04 pg/ml [-2.04, -0.03] and -13.75 ng/ml [-24.03, -3.48]). Leptin was lower in participants who exercised 2-3 times/week (-0.39 µg/ml ln [-0.68, -0.09]) and ≥4 times/week (-0.69 µg/ml ln [-1.10, -0.28]). During follow-up, [Formula: see text] increased (2.9 mL kg-1 min-1 [1.5, 4.3]), while p-selectin and CD40L decreased (-2.33 ng/ml [-3.78, -0.87] and 718.14 ng/ml [-1368, -68]). MCP-1 levels decreased among men (-32.70 pg/ml [-51.21, -14.19]). A joint analysis of all biomarkers (inversed adiponectin) showed that those who exercised ≥4 times/week at baseline had lower total levels of biomarkers and that total biomarker levels decreased during follow-up. CONCLUSIONS: Exercising several times a week was associated with less inflammation compared to exercising once a week or less. During the 8-week follow-up, total levels of biomarkers of inflammation improved.

Lung function in asphalt pavers: a longitudinal study.

PURPOSE: To study longitudinal changes in lung function in asphalt pavers and a reference group of road maintenance workers, and to detect possible signs of lung disease by high-resolution computed tomography (HRCT) scans. METHODS: Seventy-five asphalt pavers and 71 road maintenance workers were followed up with questionnaires and measurements of lung function. Not every worker was tested every year, but most of them had four or more measurement points. The 75 asphalt pavers were also invited to have HRCT scans of the lungs at the end of the follow-up period. RESULTS: Mean annual decline in forced vital capacity (FVC) and forced expiratory volume in 1 s (FEV1) of the asphalt pavers was 58 and 35 ml, respectively. Adjusted for age at baseline, packyears of smoking and BMI, the asphalt pavers had a significant excess annual decline in FVC and FEV1 compared to the references. The screedmen, the most exposed group of the asphalt pavers, showed a significantly larger decline in FVC than the other asphalt pavers (P = 0.029). Fine intralobular fibrosis without evident cysts was identified with HRCT in three subjects (4 %). CONCLUSION: We conclude that our findings may indicate an excess annual decline in FVC and FEV1 related to exposure to asphalt fumes. The screedmen, who carry out their work behind and close to the paving machine, had the largest decline in lung function. The finding of adverse pulmonary effects in asphalt pavers calls for better technological solutions to prevent exposure.

Physical activity initiated by employer and its health effects; an eight week follow-up study.

BACKGROUND: While the health benefits of physical activity are well established, little is known about health effects of physical activity programs initiated by employer. METHODS: Background data and level of physical activity were collected by questionnaire among 78 men and 43 women working in road maintenance pre and post an 8-week physical activity motivational program. As a part of the program steps measured by accelerometer were registered online where team and individual performances could be continuously monitored. The physical activity levels were registered as 1) those physical active ≤1 time per week, 2) 2-3 times per week and 3) ≥4 times a week. Maximal oxygen uptake (VO2max), blood pressure, resting heart rate (RHR) and blood samples (glycosylated hemoglobin, lipids and C-reactive protein) were obtained at baseline and after eight weeks. Mixed models were applied to evaluate associations between physical activity and health parameters. RESULTS: With ≤1 time per week as reference, exercising 2-3 times per week at baseline was associated with higher levels of VO2max. During follow-up, VO2max increased with 2.8 mL ∙ kg(-1)∙ min(-1) (95 % CI = 1.4, 4.3). Women had more favorable body mass index (BMI), blood pressure, RHR and lipid profile than men. Total cholesterol, low density lipoprotein (LDL), RHR and diastolic blood pressure (dBP) were lower among participants who exercised 2-3 times per week or ≥4 times a week, compared with those with ≤1 time per week. Half of the participants reported increased daily PA during follow-up, with high intensity PA such as jogging by 8.6 min (SD 14.6) and 8.3 min (SD 18.2), among women and men, respectively. During follow-up dBP increased among men. Further, total cholesterol and LDL were reduced by 0.12 mmol/L and 0.13 mmol/L, respectively (95 % CI = -022, -0.01 and -0.22,-0.04). CONCLUSIONS: Exercise several times a week was associated with lower blood pressure and a favorable lipid status compared to lower weekly activity. During the 8-week follow-up of an employer initiated exercise program VO2max increased, while total cholesterol and LDL were reduced. TRIAL REGISTRATION: Current Controlled Trials ISRCTN13033050 . Registered 21 August 2015.

Weight development from age 13 to 30 years and adolescent socioeconomic status: The Norwegian Longitudinal Health Behaviour study.

OBJECTIVES: To describe the weight development and model change in body mass index (BMI), and to examine the association of adolescent socioeconomic status (SES) with change in BMI distribution in a cohort followed from adolescence through adulthood. METHODS: Participants (n = 924) from western Norway were surveyed seven times from age 13 to 30 (1990-2007). BMI was based on self-reported height and weight. Quantile regression analyses were used to model change in weight development and to investigate associations between SES (measured by parental education) and change in BMI distribution. The analyses were adjusted for curvilinearity in BMI development, gender and relevant health behaviours. RESULTS: Body mass index increased over time with the greatest increase in the 90th percentile. No significant associations between change in BMI and SES were observed at any of the percentiles (10th, 25th, 50th, 75th or 90th). CONCLUSIONS: Those in the upper BMI percentile gained more weight than those in the lower percentiles indicating that these might need targeted interventions. Further investigation of the association of change in BMI and SES with better quality data might be warranted.

Airway inflammation and ammonia exposure among female Palestinian hairdressers: a cross-sectional study.

OBJECTIVES: Little is known about the working conditions and airway inflammation in hairdressers in Palestine. We aimed to investigate if hairdressers in Palestine have a higher level of airway inflammation as compared to a control group. We also assessed the hairdressers' physical working conditions and exposure to ammonia gases at the hair salons. Lastly, we investigated the association between ammonia levels and inflammation markers in the airways and the blood. METHODS: Our study participants were 33 non-smoking hairdressers (aged 19-50 years) and 35 non-smoking control subjects (aged 18-49 years). Both groups answered a questionnaire on respiratory symptoms, and performed lung function and exhaled nitric oxide (eNO) tests. Blood and sputum samples were collected from all participants and air concentration levels of ammonia were measured in 13 salons. RESULTS: Hairdressers had a higher level of sputum neutrophil count (absolute numbers/mg sputum (median (25th-75th centiles)) compared to controls, 376 (183-980) and 182 (96-358), respectively. Hairdressers also had significantly elevated eNO and blood C reactive protein (CRP) levels compared to the control subjects, controlled for age and body mass index. Exposure measurements showed that the hairdressers in salons with scarce ventilation were exposed to ammonia concentration, ranging from 3 to 61 mg/m(3). CONCLUSIONS: Compared to unexposed controls, the hairdressers had signs of neutrophilic airway inflammation, higher eNO levels and higher CRP. The hairdressers were exposed to high concentrations of ammonia from hairdressing chemicals and their working conditions were unsatisfactory.

Longitudinal lung function decline among workers in a nitrate fertilizer production plant.

BACKGROUND: This study examines the possible effect of exposure to aerosols and gases on lung function in a fertilizer plant in Norway. METHODS: Dynamic lung volumes (FVC and FEV1) of 383 workers were measured in 2007 and 2010. During the follow-up period, most workers performed tasks with low exposure levels of acid aerosols and inorganic gases. The overall median inhalable and thoracic aerosol exposure levels were 1·1 and 0·21 mg/m(3), respectively. A questionnaire on respiratory symptoms was provided. RESULTS: During the follow-up period, there was an adjusted decrease of FEV1 of 18 ml/year (P<0·001). The respiratory symptoms score was low during follow-up. CONCLUSIONS: Work in this fertilizer industry may lead to an excessive lung function decline. We have, however, not been able to find any plausible exposure related explanation for the overall lung function decline.

Application of a novel hybrid study design to explore gene-environment interactions in orofacial clefts.

Orofacial clefts are common birth defects with strong evidence for both genetic and environmental causal factors. Candidate gene studies combined with exposures known to influence the outcome provide a highly targeted approach to detecting GxE interactions. We developed a new statistical approach that combines the case-control and offspring-parent triad designs into a "hybrid design" to search for GxE interactions among 334 autosomal cleft candidate genes and maternal first-trimester exposure to smoking, alcohol, coffee, folic acid supplements, dietary folate and vitamin A. The study population comprised 425 case-parent triads of isolated clefts and 562 control-parent triads derived from a nationwide study of orofacial clefts in Norway (1996-2001). A full maximum-likelihood model was used in combination with a Wald test statistic to screen for statistically significant GxE interaction between strata of exposed and unexposed mothers. In addition, we performed pathway-based analyses on 28 detoxification genes and 21 genes involved in folic acid metabolism. With the possible exception of the T-box 4 gene (TBX4) and dietary folate interaction in isolated CPO, there was little evidence overall of GxE interaction in our data. This study is the largest to date aimed at detecting interactions between orofacial clefts candidate genes and well-established risk exposures.

Long-term occupational outcomes of endotoxin exposure and the effect of exposure cessation.

OBJECTIVE: To study the possible respiratory and haematological effects of endotoxin exposure to bacterial single-cell protein (BSCP) in workers during a follow-up period of 5 years including 4 years of exposure and 1 year without exposure. METHODS: The study included 28 workers examined in 2002-2005 and 1 year after exposure termination in 2007. The arithmetic mean endotoxin exposure was 5800-11,000 EU/m(3) among the high exposure group and 390 EU/m(3) in the low exposure group. Assessment of lung function included spirometry and gas diffusion in 2003, 2004 and 2007. Rhinometry was performed in 2004 and 2007. Blood analysis included leukocyte cell count and measurement of the acute phase proteins: C-reactive protein, interleukin-6, eosinophilic cationic protein, macrophage inflammatory protein-1α, monocyte chemoattractant protein-1, chemoattractant protein RANTES, platelet-derived growth factor BB, fibrinogen and D-dimer. RESULTS: In the low exposure group, but not in the high exposure group, there were significant improvements in both forced vital capacity (FVC) (290 ml) and forced expiratory volume in 1 s (FEV(1)) (180-210 ml) (p=0.004-0.03) 1 year after the end of exposure. The number of leukocytes and eosinophilic cationic protein and D-dimer levels increased significantly with increasing endotoxin exposures and decreased significantly 1 year after exposure termination. Changes in acute phase proteins suggested exposure-related tolerance. CONCLUSIONS: An inflammatory tendency during an exposure period of 4 years seems to reverse 1 year after cessation of exposure to endotoxins from a single species. Lung function improved significantly among workers exposed to low levels of endotoxin but not among the highly exposed workers.