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The US Environmental protection agency (EPA) has published guidance that includes test procedures for evaluating indoor exposure to chemicals from products. One of the test procedures represents the migration test for evaluating potential dermal exposure from home furniture. Such an evaluation involves the chemical measurement of the sweat which is currently unavailable in the literature. The objective of this project was to develop and validate an analytical method for quantification of migration of 4,4'-methylenediphenyl diisocyanate (MDI), 2,6-toluene diisocyanate (2,6-TDI) and 2,4-toluene diisocyanate (2,4-TDI) from a polyurethane (PU) flexible foam to artificial sweat that meets the recommendations of the EPA test protocol. Following the EPA protocol, six synthetic sweat solutions were prepared and used in evaluation of isocyanate recovery performance. The migration tests were conducted using five foam types that were chosen and supplied by PU foam manufacturers to represent the types most commonly found in commercial products, and with formulations anticipated to have the highest potential residual TDI or MDI. Migration tests were conducted using glass fiber filters (GFF) coated with 1-(2-methoxyphenyl)piperazine (1,2-MP) and analyzed using HPLC equipped with a UV detector for quantification and a MS detector to qualify peaks. The detection limits of the method were 0.002 µg/mL for 2,6-TDI, 0.011 µg/mL for 2,4-TDI, and 0.003 µg/mL for MDI. Quantification limits were 0.006 µg/mL, 0.037 µg/mL, and 0.010 µg/mL, respectively. The recovery tests on a Teflon surface for 5 of the 6 EPA-recommended synthetic sweat solutions indicate the recovery percentage was approximately 80% for diisocyanates. Recovery for the sixth sweat solution was low, approximately 30%. TDI and MDI migration was not observed when testing was conducted on foam samples., Competing Interests: Declaration of Competing Interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: The authors wish to thank the Institut de recherche Robert-Sauvé en santé et en sécurité du travail (IRSST) for providing instrument support and the International Isocyanate Institute, Inc. for their financial support. The research reported herein was performed under an agreement with the International Isocyanate Institute, Inc. Any conclusions are those of the authors and not necessarily of the Institute., (Copyright © 2020 The Authors. Published by Elsevier B.V. All rights reserved.)

Background: Byssinosis is an occupational lung disease observed among workers exposed to cotton, flax, and hemp dust. The severity and extent of Byssinosis are well recognised in the high-income countries and control measures have been implemented to prevent the disease. In India, there are conflicting evidence on burden estimation of the disease, followed by inadequate prevention and control of Byssinosis., Design/methods: We did a cross-sectional study to assess the prevalence of Byssinosis in "home-based" power-loom workers in Mominpura, an administrative ward of Burhanpur Municipality with 2800 population in the state of Madhya Pradesh, India. 290 adults working from "home-based" power loom units were randomly selected, profiled and screened for Byssinosis like symptoms with the help of a semi-structured questionnaire and simple hand-held peak expiratory flow monitor. For epidemiological purposes the symptoms were classified based on Schilling's classification. Chest x-rays were done for selected subjects. Sputum smear microscopy for detecting TB was done for those who had Byssinosis like symptoms., Results: Prevalence of Byssinosis among "home based" powerloom workers was found to be 98% [n = 283, 95 CI (95.65-98.96)]. Peak expiratory flow rate (PEFR) was reduced in 44% (n = 124), of which 81 (29%) had more than 50% PEFR reduction, and of these, 69 (29%) were in early stage of Byssinosis (Grade 0.5). 11% of study participants who had Byssinosis like symptoms, also had TB., Conclusions: Byssinosis is highly prevalent in "home-based" power loom units in Madhya Pradesh. Adequate advocacy on awareness and prevention; prompt diagnosis and linkages to treatment services in "home-based" power loom units are urgently required to address Byssinosis at an early disease stage., (Copyright © 2019 Tuberculosis Association of India. Published by Elsevier B.V. All rights reserved.)

This study aimed to identify sensitive and not-invasive biomarkers of early genotoxic/oxidative effect for exposure to styrene in the fibreglass reinforced plastic manufacture. We studied 11 workers of a plastic manufacture using open molding process (A), 16 workers of a manufacture using closed process (B) and 12 controls. We evaluated geno/cytotoxic effects on buccal cells by Buccal Micronucleus Cytome (BMCyt) assay and genotoxic/oxidative effects on lymphocytes by Fpg-comet test. On A workers we also evaluated urinary 8oxoGua, 8oxodGuo and 8oxoGuo to investigate oxidative stress. Personal inhalation exposure to styrene was monitored by passive air sampling and GC/MS. Biological monitoring included urinary metabolites mandelic acid (MA) and phenylglyoxylic acid (PGA). The findings show higher styrene exposure, urinary MA + PGA levels and micronucleus frequency in manufacture A. Higher buccal karyolytic cell frequency vs controls were found in both exposed populations. We found in exposed workers, no induction of direct DNA damage but oxidative DNA damage. Fpg-comet assay and urinary oxidized guanine seem to be sensitive biomarkers of oxidative stress and BMCyt assay a good-not invasive biomarker of cyto-genotoxicity at target organ. The study, although limited by the small number of studied subjects, shows the usefulness of used biomarkers in risk assessment of styrene-exposed workers., (Copyright © 2018 Elsevier B.V. All rights reserved.)

Naphthalene occurs together with polycyclic aromatic hydrocarbons (PAHs) at industrial workplaces and is ubiquitous in the environment. For biological monitoring of naphthalene exposures, up to now mainly 1- and 2-naphthol in urine have been used. Recently, we proposed 1,2-dihydroxynaphthalene (1,2-DHN) and the 1- and 2-naphthylmercapturic acid (1- and 2-NMA) as new urinary biomarkers to characterise a naphthalene exposure. In this study, in a collective of nine occupationally exposed workers handling with creosote the naphthalene metabolites 1,2-DHN, 1- and 2-NMA as well as 1- and 2-naphthol were analysed in order to evaluate the suitability of the different parameters for their application in biomonitoring studies. Additionally, air sampling was conducted to characterise the exposure in task related exposure situations at different workplaces. In the analysed 51 urine samples, 1,2-DHN was the main metabolite with concentrations ranging from 2.3 to 886 μg/g creatinine (crea) (median 34 μg/g crea). For the sum of 1- and 2-naphthol, concentrations in the range of 2.6-174 μg/g crea (median 15 μg/g crea) were observed. 1-NMA concentrations were in the range of < LOD-2.4 μg/g crea (61% > LOD), while 2-NMA was not detected in the analysed urine samples. The biomarkers 1,2-DHN, 1- and 2-naphthol as well as 1-NMA showed significant correlations, which pointed out to naphthalene as the common exposure source. The poor correlations between naphthalene in the air and the biomarkers in urine may be a result of the varying exposure situations and may indicate not solely inhalative, but additional dermal uptake. 1,2-DHN was the most sensitive and, together with 1-NMA, the most specific parameter of the biological monitoring of naphthalene exposure at workplaces. Further studies with this parameter are needed for individuals at different workplaces as well as for persons of the general population without occupational PAH exposure to characterise 1,2-DHN levels as well as to establish their relationship with the naphthalene exposure., (Copyright © 2018 Elsevier B.V. All rights reserved.)

Background: Previously healthy firefighters with World Trade Center (WTC) dust exposure developed airway disease. Risk factors for irritant-associated asthma/COPD overlap are poorly defined., Methods: This study included 2,137 WTC-exposed firefighters who underwent a clinically indicated bronchodilator pulmonary function test (BD-PFT) between 9/11/2001 and 9/10/2017. A post-BD FEV 1 increase of > 12% and 200 mL from baseline defined asthma, and a post-BD FEV 1 /FVC ratio < 0.7 identified COPD cases. Participants who met both criteria had asthma/COPD overlap. Eosinophil levels were measured on screening blood tests performed shortly after 9/11/2001 and prior to BD-PFT; a subgroup of participants also had serum IgE and 21 cytokines measured (n = 215). Marginal Cox regression models for multiple events assessed the associations of eosinophil levels or serum biomarkers with subsequent diagnosis, with age, race, smoking, WTC exposure, first post-9/11 FEV 1 /FVC ratio, and BMI included as covariates., Results: BD-PFT diagnosed asthma/COPD overlap in 99 subjects (4.6%), isolated-asthma in 202 (9.5%), and isolated-COPD in 215 (10.1%). Eosinophil concentration ≥ 300 cells/μL was associated with increased risk of asthma/COPD overlap (hazard ratio [HR], 1.85; 95% CI, 1.16-2.95) but not with isolated-asthma or isolated-COPD. Serum IL-4 also predicted asthma/COPD overlap (HR, 1.51 per doubling of cytokine concentration; 95% CI, 1.17-1.95). Greater IL-21 concentration was associated with both isolated-asthma and isolated-COPD (HRs of 1.73 [95% CI, 1.27-2.35] and 2.06 [95% CI, 1.31-3.23], respectively)., Conclusions: In WTC-exposed firefighters, elevated blood eosinophil and IL-4 levels are associated with subsequent asthma/COPD overlap. Disease-specific T-helper cell type 2 biomarkers present years before diagnosis suggest patient-intrinsic predisposition to irritant-associated asthma/COPD overlap., (Copyright © 2018 American College of Chest Physicians. Published by Elsevier Inc. All rights reserved.)

Studies suggest that leukocyte telomere length is an index of systemic ageing. Here, we discuss telomere length as a marker of biological ageing in relation to residential landscape (greenness), residential air pollution and work-related exposures. Telomere lengths are memories of cumulative oxidative and inflammatory stress, and show to have inverse associations with the risk of non-communicable diseases. For this reason, telomeres are considered as markers of biological ageing. Studies at birth, in children, young adulthood, and elderly show that residential green space, lower traffic exposure and long-term lower exposure to particulate air pollution are associated with longer telomeres. Work-related exposures including exposure to toxic metals, polycyclic aromatic hydrocarbons and particulate matter are associated with shorter telomeres for a given age. In contrast to chronic exposures, evidence is present of the observation that recent exposure is associated with longer telomeres. Our overview shows that the magnitude of residential and work-related environmental factors on telomere length are often as important as many classical lifestyle factors., (Copyright © 2018 Elsevier B.V. All rights reserved.)

Objectives: We performed a cross-sectional study with the main aim of evaluating occupational exposure to polycyclic aromatic hydrocarbons (PAHs) in workers involved in the pavement construction of a new highway in Northern Italy, where modified bitumen was used as binder for Hot Mix Asphalt., Methods: We applied a combined approach of air and biological monitoring. Both the aerosol and vapour phases of bitumen were collected applying the NIOSH 5506 method. The 16 PAHs listed as high priority by EPA were determined by HPLC-UV. End-of-shift urine samples were collected from 144 workers to determine 1-hydroxypyrene (1-OHP) and 2-naphthol (2-NAP) concentrations after enzyme digestion and HPLC-UV analysis. Socio-demographic and lifestyle information was collected by a questionnaire., Results: Paving workers were actually exposed to PAHs, including carcinogenic compounds, that were measurable only in the aerosol phase. Higher exposure as well as dose levels were measured for the paver group. Biological monitoring confirmed that 1-OHP was less affected by smoking habits as compared to 2-NAP and showed a higher association with occupational exposure., Conclusion: Carcinogenic PAH compounds were detectable only in the aerosol phase and this must be taken into account in the adoption of preventive measures. Biomonitoring supported the superiority of 1-OHP as compared to 2-NAP in assessing the internal dose in such workers., (Copyright © 2018 Elsevier B.V. All rights reserved.)

Exhaled breath condensate (EBC) is a non-invasive biological matrix that allows easy access to the lung epithelial lining fluid. It can provide, for instance, useful biochemical information in workers following inhalatory exposure. Recently, nuclear magnetic resonance (NMR)-based metabolomics has been applied to EBC profiling to identify metabolic phenotypes ("metabotypes") of relevance in respiratory medicine. We aimed at verifying if NMR-based metabolomics of EBC, combined with statistical analysis, could find differences in metabolomic profiles between groups of subjects occupationally exposed to levels of airborne inhalable dust, phenol, formaldehyde and volatile organic compounds (VOCs) below regulatory limits. Samples were collected from 20 blue-collar workers without wearing a mask (therefore "exposed" to ambient air) and after wearing a mask ("not exposed"). This procedure was only allowed after the standard air quality tests had shown levels of airborne xenobiotics below the occupational exposure limit or even below the LOD. Ten white-collar controls were also included. After partial least squares discriminant analysis, the exposed to the controlled plant environment and the not exposed groups were clearly separated, and discrimination was due to alteration of fatty acids and alcohols, whose statistical significance was also evaluated. Our results show that NMR-based metabolomics of EBC is a useful tool that has the potential to be successfully used in occupational health to distinguish between subjects exposed and non-exposed to very low airborne levels of chemicals., (Copyright © 2018 Elsevier B.V. All rights reserved.)

Introduction: High styrene exposures are still experienced in various occupational settings, requesting regular exposure assessments. The aims of this study were to study occupational exposures in various industrial sectors and to determine factors influencing styrene urinary metabolites levels., Methods: Biomonitoring was conducted in 141 workers from fiberglass-reinforced plastic (FRP) manufacture, thermoplastic polymers production, vehicle repair shops and cured-in-place pipe lining (CIPP). Urinary styrene (StyU) as well as Mandelic (MA) / Phenyglyoxylic Acids (PGA) were quantified at the beginning and at the end of week, and multivariate linear regression models were used., Results: StyU levels revealed very low, rarely exceeding 3 μg.L -1 . Highest concentrations of MA + PGA were observed in FRP sector, with levels reaching up to 1100 mg.g -1 of creatinine. Factors influencing end-of-week MA + PGA concentrations were levels at the beginning of week, open molding processes, proximity to the emission source, respiratory protection, styrene content in raw materials. Elevated levels were also observed during CIPP process, whereas thermoplastic injection and vehicle repair shop workers exhibited much lower exposures., Conclusions: Intervention on process (decreasing styrene proportion, using closed molding), protective equipment (local exhaust ventilation, respiratory protection) and individual practices (stringent safety rules) are expected to decrease occupational exposures. Urinary MA + PGA remain the most appropriate biomarkers for occupational biomonitoring., (Copyright © 2018 Elsevier B.V. All rights reserved.)

The aim of the study was to investigate the effect of various factors that modulate the metabolism of benzene, including smoking habits, metabolic genotype of GST and co-exposure to toluene, on the levels of three biomarkers, i.e. urinary benzene (UB), S-phenylmercapturic acid (SPMA) and t,t-muconic acid (t,t-MA), in 146 refinery workers exposed to low levels of air benzene (AB) in the range <1.5-529.2 μg/m 3 (mean value 32.6 μg/m 3 ). The study confirmed the validity of SPMA as a good biomarker of benzene exposure even at low levels of exposure. It was also confirmed that cigarette smoking is the main confounding factor when assessing biological monitoring data of occupational exposure to AB. Our data indicate that the GSTT1, but not the GSTM1 genotype, significantly increases the urinary levels of SPMA, even at low levels of exposure. It is not known, though, whether subjects with a GSTT1 "null" genotype may be more susceptible to the effects of benzene. Finally, environmental toluene appears to inhibit the metabolism of benzene to SPMA even at low concentrations, also resulting in an underestimation by SPMA levels of the actual exposure of workers to benzene., (Copyright © 2018 Elsevier B.V. All rights reserved.)

The assessment of dermal exposure to volatile organic compounds (VOCs) is becoming increasingly important in industrial settings. The study aimed to evaluate the overall exposure (inhalation and dermal) of workers to VOCs, and to assess the suitability of activated charcoal cloth (ACC) patches for the evaluation of the contribution of dermal exposure (vs. inhalation exposure) to the whole body burden, as reflected by human biomonitoring. Inhalation exposure to toluene, acetone and styrene (passive 3 M organic vapour monitors, OVMs) and dermal exposure (ACC patches on the index finger, thumb and neck) were measured simultaneously in 37 subjects performing different tasks in a factory of thermoplastic panels. Systemic exposure was assessed in urine by quantification of mandelic acid (MA) and phenyl glyoxylic acid (PGA), as biomarkers for styrene, as well as acetone and hippuric acid (HA) as biomarkers for acetone and toluene, respectively. High styrene (range 30.66-302 mg/m 3 ) and acetone (range 11-644 mg/m 3 ) concentrations were found in the air of the workplace, while toluene was less abundantly present (range 0.05-2.6 mg/m 3 ). On the ACC patches, considerable amounts of these VOCs were found. For employees manually handling styrene, dermal exposure on the index finger and thumb were substantially higher compared to the neck ACC patch. A good correlation between air and urinary levels of acetone exposure was found. MA and PGA levels in urine, markers for styrene exposure, were correlated with both air and dermal exposure. These data suggest that there is a substantial benefit from assessing dermal exposure in the work place in addition to the more conventional air monitoring and urinary biomonitoring., (Copyright © 2018 Elsevier B.V. All rights reserved.)

Lead is an environmental hazard with great public health concern and has been known to inhibit delta-aminolevulinate dehydratase (ALAD) activity involved in the heme biosynthetic pathway. The study aimed to investigate the influence of ALAD polymorphism (G177C) on retention of Pb-B levels and ALAD activity on occupationally exposed lead workers. In the present study, we enrolled 561 lead exposed and 317 non-occupationally exposed subjects and performed a comprehensive analysis of Pb-B levels along with ALAD activity and genotyping. The frequency of ALAD variants observed in the total subjects (n = 878) was 70.04% for ALAD 1-1, 27.44% for heterozygous ALAD 1-2 and 2.5% for homozygous mutant ALAD 2-2. Our study revealed that ALAD 1-2 carriers presented higher Pb-B levels compared to wild type ALAD 1-1 carriers. Further, a significant difference was observed in the activity of ALAD between ALAD 1-2/ 2-2 and ALAD 1-1 carriers of non-occupationally exposed group indicating that the polymorphic nature of the enzyme may contribute to altered activity of ALAD irrespective of lead exposure. Hence, ALAD 2 allele might contribute to increased susceptibility to high Pb-B retention, and genotyping of ALAD in lead exposed subjects might be used as a prediction marker to impede tissue/organ damage due to lead toxicity., (Copyright © 2018. Published by Elsevier B.V.)

In 2016, the American Conference of Governmental Industrial Hygienists (ACGIH) lowered the 8-hr Threshold Limit Value - time-weighted average (TLV-TWA) for toluene diisocyanate (TDI) from 5 ppb to 1 ppb, and the 15-min short-term exposure limit (STEL) from 20 ppb to 5 ppb. We evaluated ACGIH's basis for lowering these values. It is our opinion that the ACGIH's evaluation of the evidence for occupational asthma and respiratory effects from TDI exposure does not fully integrate the results of all the available human and animal studies. We found that some studies reported occupational asthma cases at TWAs less than 5 ppb, but these cases were likely caused by peak exposures above 20 ppb. Advances in industrial hygiene have reduced peak exposures and the incidence of upset conditions, such as spills and accidents, in modern TDI facilities. Taken together, the human evidence indicates that adherence to the previous 8-hr TLV-TWA and 15-min STEL (5 ppb and 20 ppb, respectively) prevents most, if not all, cases of occupational asthma, and eliminates or reduces the risk of lung function decrements and other respiratory effects. While limited, the animal literature supports the human evidence and indicates that TDI-induced asthma is a threshold phenomenon. We conclude that ACGIH's decision to lower the TLV-TWA and STEL values for TDI is not adequately supported., (Copyright © 2018 Gradco LLC dba Gradient. Published by Elsevier Inc. All rights reserved.)

The respiratory tract is the main target organ of the inhaled hexavalent chromium (Cr-VI) and nickel (Ni) contained in stainless steel (SS) welding fumes (WFs). The aim of this study was to investigate the Cr and Ni content of the exhaled breath condensate (EBC) of SS tungsten inert gas (TIG) welders, and relate their concentrations with oxidative stress and inflammatory biomarkers. EBC and urine from 100 SS TIG welders were collected pre-(T 0 ) and post-shift (T 1 ) on a Friday, and pre-shift (T 2 ) on the following Monday morning. Both EBC and urinary Cr concentrations were higher at T 1 (0.08 μg/L and 0.71 μg/g creatinine) and T 0 (0.06 μg/L and 0.74 μg/g creatinine) than at T 2 (below the limit of detection [LOD] and 0.59 μg/g creatinine), and EBC Ni concentrations generally remained 2 O 2 ) concentration increased from 0.18 μM at T 0 to 0.25 μM at T 1 , but had decreased to 0.16 μM by T 2 . EBC malondialdehyde (MDA) concentrations were higher at T 0 (2.79 nM) and T 1 (2.98 nM) than at T 2 (2.43 nM), and EBC 4-hydroxy-nonenal (HNE) concentrations were higher at T 0 (0.53 nM) than at T 2 (0.51 nM). These findings confirm that, unlike Ni-EBC, Cr-EBC is a reliable biomarker of exposure even at very low environmental concentrations. However, given the weak relationship between the biomarkers and effects of exposure, we speculate that other substances generated during SS TIG welding also play a role in generating lung oxidative stress., (Copyright © 2018 Elsevier B.V. All rights reserved.)

Sensory irritation of eyes and upper airways is an important endpoint for setting occupational exposure limits (OELs) and indoor air guidelines. Sensory irritants cause a painful burning, stinging and itching sensation. Controlled chamber studies are the "golden standard" for evaluations. Well conducted workplace studies offer another possibility. For generalization, the number of participants and their age, smoking, gender, and prior exposure, experience and mood has to be considered. Exposure assessments have to be reliable and exposure duration sufficiently long to establish time-response relationships. A potential confounding by odour has to be assessed. For workplace exposures, mixed exposure and healthy worker effects have to be evaluated. The "Alarie test" is the only validated animal bioassay for prediction of sensory irritation in humans. The mouse bioassay uses the trigeminal reflex-induced decrease in the respiratory rate. The 50% decrease (RD 50 ) has been correlated with OELs set for sensory irritants; predicted OELs for sensory irritants are 0.03xRD 50 . Evaluation of the bioassay comprises the number of mice and the strain, the reliability of the exposure concentrations and exposure-response relationships, and the similar mode-of-action in mice and humans. These approaches can be used for quality assurance of reported data to set air quality guidelines., (Copyright © 2017 The Authors. Published by Elsevier Inc. All rights reserved.)

Data on the genotoxic and mutagenic effects of occupational exposure to the most frequently used volatile anesthetics are limited and controversial. The current study is the first to evaluate genomic instability, cell death and proliferative index in exfoliated buccal cells (EBC) from anesthesiologists. We also evaluated DNA damage and determined the concentrations of the anesthetic gases most commonly used in operating rooms. This study was conducted on physicians who were allocated into two groups: the exposed group, which consisted of anesthesiologists who had been exposed to waste anesthetic gases (isoflurane, sevoflurane, desflurane and nitrous oxide - N 2 O) for at least two years; and the control group, which consisted of non-exposed physicians matched for age, sex and lifestyle with the exposed group. Venous blood and EBC samples were collected from all participants. Basal DNA damage was evaluated in lymphocytes by the comet assay, whereas the buccal micronucleus (MN) cytome (BMCyt) assay was applied to evaluate genotoxic and cytotoxic effects. The concentrations of N 2 O and anesthetics were measured via a portable infrared spectrophotometer. The average concentration of waste gases was greater than 5 parts per million (ppm) for all of the halogenated anesthetics and was more than 170ppm for N 2 O, expressed as a time-weighted average. There was no significant difference between the groups in relation to lymphocyte DNA damage. The exposed group had higher frequencies of MN, karyorrhexis and pyknosis, and a lower frequency of basal cells compared with the control group. In conclusion, exposure to modern waste anesthetic gases did not induce systemic DNA damage, but it did result in genomic instability, cytotoxicity and proliferative changes, which were detected in the EBC of anesthesiologists. Thus, these professionals can be considered at risk for developing genetic alterations resulting from occupational exposure to these gases, suggesting the need to minimize this exposure., (Copyright © 2016 Elsevier B.V. All rights reserved.)

Objectives: To evaluate how exposure to deep-frying oils, repeated frying oil (RFO) and restaurant waste oil (RWO) affects emission of polycyclic aromatic hydrocarbons (PAHs) and oxidative stress in male restaurant workers., Methods: The study participants included 236 male restaurant workers in 12 restaurants in Shenzhen. Airborne particulate PAHs were measured over 12h on each of two consecutive work days. Urinary 1-hydroxypyrene (1-OHP) measurements were used to indicate cooking oil fumes (COF) exposure, and urinary malondialdehyde (MDA) and 8-hydroxy-2'-deoxyguanosine (8-OHdG) were adopted as oxidative stress markers., Results: The production and emission rates of ultrafine particles (UFPs) and PM2.5 were higher in the exposed groups than in the control group. The concentrations of summed PAHs were in the order of RFO-frying group>RWO-frying group>deep-frying group>unexposed control group. Urinary 1-OHP was found to be a significant predictor of elevated urinary MDA and 8-OHdG concentrations (all, P<0.05). UFPs were a significant predictor of elevated urinary 8-OHdG for restaurant workers (P<0.05). The RFO- and RWO-frying groups had higher mean urinary concentrations of 1-OHP, MDA and 8-OHdG than the control group (P<0.05). RFO exposure was found to be a significant risk factor for elevated urinary 8-OHdG and RWO exposure was found to be a significant risk factor for elevated urinary MDA (both, P<0.001)., Conclusions: Concentrations of urinary 1-OHP, MDA and 8-OHdG reflect occupational exposure to PAHs from COFs and oxidative stress in restaurants workers. Exposure to RFO may cause increased oxidative DNA damage, and exposure to RWO might cause increased lipid peroxidation., (Copyright © 2016 Elsevier Ireland Ltd. All rights reserved.)

An inhalation unit risk factor (URF) was developed for cadmium. The URF is based on excess lung cancer mortality in a key epidemiological study of cadmium smelter workers (Park et al., 2012). The Park et al. (2012) study is an update of the Thun et al. (1985) cohort that was previously used to derive a URF in USEPA (1985). Park et al. re-analyzed the cadmium smelter worker population (near Denver, CO) using more detailed work history information, a revised cadmium exposure matrix, a detailed retrospective exposure assessment for arsenic (potential confounder), and updated mortality data (through 2002). Grouped observed and expected number of lung cancer mortalities along with cumulative cadmium exposures were used in the current study to obtain the maximum likelihood estimate and asymptotic variance of the slope (β) for the linear multiplicative relative risk model using Poisson regression modeling. Life-table analyses were used to derive the final URF for cadmium of 4.9E-04 per μg Cd/m(3). The corresponding lifetime air concentration at the 1 in 100,000 no significant excess risk level is 0.020 μg Cd/m(3), which can be used to protect the general public in Texas against the potential carcinogenic effects from chronic exposure to cadmium and cadmium compounds., (Copyright © 2016 Elsevier Inc. All rights reserved.)

Photocopiers emit high levels of nanoparticles (PM0.1). To-date little is known of physicochemical composition of PM0.1 in real workplace settings. Here we perform a comprehensive physicochemical and morphological characterization of PM0.1 and raw materials (toners and paper) at eight commercial photocopy centers that use color and monochrome photocopiers over the course of a full week. We document high PM0.1 exposures with complex composition and several ENM in toners and PM0.1. Daily geometric mean PM0.1 concentrations ranged from 3700 to 34000 particles/cubic-centimeter (particles/cm(3)) (GSD 1.4-3.3), up to 12 times greater than background, with transient peaks >1.4 million particles/cm(3). PM0.1 contained 6-63% organic carbon, <1% elemental carbon, and 2-8% metals, including iron, zinc, titania, chromium, nickel and manganese, typically in the <0.01-1% range, and in agreement with toner composition. These findings document widespread ENM in toner formulations and high nanoparticle exposures are an industry-wide phenomenon. It further calls attention to the need to substantially redesign the interface of this technology with workers and consumers., (Copyright © 2015 Elsevier B.V. All rights reserved.)

Background: Although active tobacco smoking is the main risk factor for COPD, COPD is not uncommon also among never-smokers. Different study locations along with different spirometric definitions of COPD have historically yielded different prevalence estimates of the disease., Aim: To study current prevalence and risk factors of COPD among never-smokers in two areas of Sweden., Methods: Data collected in 2008-2012 within the West Sweden Asthma Study and Obstructive Lung Disease in Northern Sweden Studies was pooled. The study population consisted of 1839 subjects who participated in spirometry and interviews. COPD was defined as post-bronchodilator a) FEV(1)/(F)VC < 0.7, b) FEV(1)/FVC < 0.7 and c) FEV(1)/FVC < lower limit of normal., Results: Of the 1839 subjects, 967 (52.6%) were never-smokers. Among the never-smoking subjects, the prevalence of COPD according to definitions a-c was 7.7%, 4.9% and 3.0%, respectively. The corresponding prevalence of GOLD grade ≥2 was 2.0%, 1.4% and 1.3%. No significant difference in prevalence between the two study areas was observed. In never-smokers, occupational exposure to gas, dust or fumes (GDF) was significantly associated with both COPD (OR 1.85, 95% CI 1.03-3.33), and GOLD ≥2 (OR 4.51, 1.72-11.9) according to definition a), after adjusting for age, educational level and exposure to passive smoking at work., Conclusion: Depending on definition, prevalence of COPD among never-smokers was 3.0-7.7%, whereas GOLD ≥2 was present in 1.3-2.0%. Occupational exposure to GDF remained independently and significantly associated with COPD regardless of spirometric definition of the disease., (Copyright © 2015 Elsevier Ltd. All rights reserved.)

Agriculture industry workers are at a higher risk for chronic bronchitis and obstructive pulmonary diseases, and current therapeutics are not entirely effective. We previously found that the specialized proresolving lipid mediator maresin-1 (MaR1) reduced proinflammatory cytokine release and intracellular adhesion molecule-1 (ICAM-1) expression in bronchial epithelial cells exposed to extracts of organic dust (DE) derived from swine confinement facilities in vitro. The objective of this study was to determine whether MaR1 is effective at limiting lung inflammation associated with acute and repetitive exposures to DE in an established murine model of inhalant dust exposures. C57Bl/6 mice were treated with MaR1 or vehicle control and intranasally instilled with DE once or daily for 3 weeks. Bronchioalveolar lavage fluid was analyzed for total and differential cell counts and proinflammatory cytokine levels, and lung tissues were assessed for histopathology and ICAM-1 expression. In both single and repetitive DE exposure studies, MaR1 significantly decreased bronchoalveolar lavage neutrophil infiltration, interleukin 6, tumor necrosis factor α, and chemokine C-X-C motif ligand 1 levels without altering repetitive DE-induced bronchioalveolar inflammation or lymphoid aggregate formation. Lung tissue ICAM-1 expression was also reduced in both single and repetitive exposure studies. These data suggest that MaR1 might contribute to an effective strategy to reduce airway inflammatory diseases induced by agricultural-related organic dust environmental exposures., (Copyright © 2015 Elsevier Inc. All rights reserved.)

Objective: The aim of the present study was to elucidate whether occupational exposure to vapors, gases, dusts, and fumes increases the mortality risk of COPD, especially among never smokers., Methods: The study population was a cohort of 354,718 male construction workers; of these, 196,329 were exposed to vapors, gases, dusts, and fumes, and 117,964 were unexposed. Exposure to inorganic dust, wood dust, vapors, fumes, gases, and irritants was based on a job-exposure matrix with a focus on exposure in the mid-1970s. The cohort was followed from 1971 to 2011. Relative risks (RRs) were obtained using Poisson regression models adjusting for age, BMI, and smoking habits., Results: There were 1,085 deaths from COPD among the exposed workers, including 49 never smokers. Workers with any occupational exposure to vapors, gases, fumes, and dust showed an increased mortality due to COPD (RR, 1.32; 95% CI, 1.18-1.47). When comparing different exposure groups, there was a significantly increased mortality due to COPD among those exposed to fumes (RR, 1.20; 95% CI, 1.07-1.36) and inorganic dust (RR, 1.19; 95% CI ,1.07-1.33). Among never smokers, there was high mortality due to COPD among workers with any occupational airborne exposure (RR, 2.11; 95% CI, 1.17-3.83). The fraction of COPD attributable to occupational exposure was 0.24 among all workers and 0.53 among never-smoking workers., Conclusions: Occupational exposure to airborne pollution increases the mortality risk for COPD, especially among never smokers.

Bisphenol A (BPA), a monomer used in the manufacture of epoxy, polycarbonate, and polystyrene resins, is a xenoestrogen present in many consumer products. We investigated the effects of 2-week exposure to BPA, either alone or in combination with X-rays, on the induction of DNA damage in somatic cells of female mice in vivo. The micronucleus and alkaline comet assays were used to evaluate genotoxicity. BPA induced DNA strand breaks in lung cells but not in bone marrow lymphocytes, liver, kidney, or spleen cells. Induction of micronuclei was observed only in polychromatic reticulocytes of peripheral blood. Levels of damage following combination exposure to ionizing radiation plus BPA depended on tissue, assay, and time., (Copyright © 2013 Elsevier B.V. All rights reserved.)

Background: Specific inhalation challenges (SICs) with occupational agents are used to establish the diagnosis and etiology of occupational asthma. The aim of this study was to assess the frequency and determinants of severe asthmatic reactions induced by various occupational agents during SICs performed using realistic methods of exposure., Methods: The SIC records of 335 consecutive subjects with a positive SIC (ie, ≥ 20% fall in FEV1) due to various occupational agents were reviewed. Asthmatic reactions were graded as moderate when requiring repeated administration of an inhaled short-acting β₂-agonist (SABA) and severe when requiring repeated SABA and systemic corticosteroids., Results: Overall, 68 of the 335 subjects (20%) required an inhaled SABA during the SICs. The multivariate logistic regression analysis showed that the need for an inhaled SABA increased when the SIC involved a low-molecular-weight agent (LMW) (OR, 2.47; 95% CI, 1.43-4.28) and marginally so when the subjects required regular treatment with an inhaled corticosteroid (OR, 1.62; 95% CI, 0.93-2.80). The severity of asthmatic reactions was graded as moderate in 12% and severe in 3% of the subjects. Of the 10 severe reactions, five developed after exposures ≤ 5 min. Multivariate logistic regression analysis showed that challenging subjects with a LMW agent was the only significant determinant for the development of moderate/severe reactions (OR, 3.05; 95% CI, 1.62-5.73)., Conclusions: Challenges with LMW agents are associated with a higher risk of an asthmatic reaction requiring pharmacologic treatment. This study may provide useful guidelines for further improving the safety of SICs.

The efficiency of a risk management tool, such as occupational exposure limits (OELs), partly depends on the responsible parties' awareness and understanding of it. The aim of this study was to measure the awareness and understanding of OELs at Swedish workplaces and to collect opinions on their use and function. Through a web-based questionnaire targeting workers that are exposed to air pollutants or chemicals, and persons working with occupational health and safety or in management at workplaces where workers are exposed to air pollutants or chemicals 1017 responses were collected. The results show that awareness and understanding of Swedish OELs is low among workers, as well as managers and occupational health and safety employees. Statistically significant, but small, differences were found depending on the size of the company and the position in the company. Based on the results, it is recommended that authorities and the social partners target this lack of awareness and understanding regarding OELs. Also, other tools to ascertain a safe working environment with regards to chemicals exposure might be useful for Swedish workplaces., (Copyright © 2013 Elsevier Inc. All rights reserved.)

Purpose: Beryllium's classification as a carcinogen is based on limited human data that show inconsistent associations with lung cancer. Therefore, a thorough examination of those data is warranted. We reanalyzed data from the largest study of occupational beryllium exposure, conducted by the National Institute of Occupational Safety and Health (NIOSH)., Methods: Data had been analyzed using stratification and standardization. We reviewed the strata in the original analysis, and reanalyzed using fewer strata. We also fit a Poisson regression, and analyzed simulated datasets that generated lung cancer cases randomly without regard to exposure., Results: The strongest association reported in the NIOSH study, a standardized rate ratio for death from lung cancer of 3.68 for the highest versus lowest category of time since first employment, is affected by sparse-data bias, stemming from stratifying 545 lung cancer cases and their associated person-time into 1792 categories. For time since first employment, the measure of beryllium exposure with the strongest reported association with lung cancer, there were no strata without zeroes in at least one of the two contrasting exposure categories. Reanalysis using fewer strata or with regression models gave substantially smaller effect estimates. Simulations confirmed that the original stratified analysis was upwardly biased. Other metrics used in the NIOSH study found weaker associations and were less affected by sparse-data bias., Conclusions: The strongest association reported in the NIOSH study seems to be biased as a result of non-overlap of data across the numerous strata. Simulation results indicate that most of the effect reported in the NIOSH paper for time since first employment is attributable to sparse-data bias., (Copyright © 2013 Elsevier Inc. All rights reserved.)

Non-mechanised sugarcane harvesting preceded by burning exposes workers and the people of neighbouring towns to high concentrations of pollutants. This study was aimed to evaluate the respiratory symptoms, lung function and oxidative stress markers in sugarcane workers and the residents of Mendonça, an agricultural town in Brazil, during the non-harvesting and harvesting periods and to assess the population and individual exposures to fine particulate matter (PM(2.5)). Sugarcane workers and healthy volunteers were evaluated with two respiratory symptom questionnaires, spirometry, urinary 1-hydroxypyrene levels, and the measurement of antioxidant enzymes and plasma malonaldehyde during the non-harvesting and harvesting periods. The environmental assessment was determined from PM(2.5) concentration. PM(2.5) level increased from 8 μg/m³ during the non-harvesting period to 23.5 μg/m³ in the town and 61 μg/m³ on the plantations during the harvesting period. Wheezing, coughing, sneezing, and breathlessness increased significantly in both groups during the harvesting period, but more markedly in workers. A decrease in lung function and antioxidant enzyme activity was observed in both populations during harvesting; this decrease was greater among the sugarcane workers. The urinary 1-hydroxypyrene levels only increased in the sugarcane workers during the harvesting period. The malonaldehyde levels were elevated in both groups, with a higher increase observed in the workers. This research demonstrates the exposure of sugarcane workers and the inhabitants of a neighbouring town to high PM(2.5) concentrations during the sugarcane harvest period. This exposure was higher among the sugarcane workers, as illustrated by both higher PM(2.5) concentrations in the sugarcane fields and higher urinary 1-hydroxypyrene levels in the volunteers in this group. The higher incidence of respiratory symptoms, greater decrease in lung function and more marked elevation of oxidative stress markers among the sugarcane workers during the harvest confirms the greater effect magnitude in this population and a dose-dependent relationship between pollution and the observed effects., (Copyright © 2012 Elsevier B.V. All rights reserved.)

Bisphenol-A (BPA) is a commonly used color developer in thermal paper. In this application, BPA is present in its free, unbound form and can be readily released, making thermal paper a potential source for human exposure. In this study, BPA was determined in 44 thermal paper samples collected in Belgium. BPA was detected in all the samples; 73% of the samples had concentrations between 0.9% and 2.1% (between 9 and 21 mg BPA/g paper), while the remaining 27% of the samples had concentrations below 0.01% (0.1mg BPA/g paper). The BPA concentrations measured in thermal paper were comparable with those reported in other international studies. Since thermal paper is a feedstock for paper recycling processes, contamination of other "BPA-free" papers can occur. An estimation of human exposure through thermal paper results in a median intake of 445 ng BPA/day for the general population, which corresponds to an exposure of 6.4 ng/kg bw/day for a person of 70 kg. The exposure of those people who come occupationally in contact with thermal paper can be much higher., (Copyright © 2012 Elsevier B.V. All rights reserved.)

Background: There is no consensus at the present time about the effect of welding on lung function decline. This study compared lung function decline between blue-collar workers exposed and not exposed to welding fumes in a French longitudinal cohort of 21,238 subjects aged 37 to 52 years at inclusion., Methods: Medical data, occupation, sector of activity, and spirometry were recorded twice by occupational physicians in 1990 and 1995. A job-exposure matrix was used to identify 503 male blue-collar workers exposed to welding fumes and 709 control subjects and to define the weekly duration of exposure to welding fumes., Results: Baseline lung function parameters were higher in workers exposed to welding fumes than in control subjects. After a 5-year follow-up, welding-fume exposure was associated with a nonsignificant decline in FVC (P = .06) and FEV(1) (P = .07) after adjustment for age, pack-years, BMI, and baseline value of the parameter. A significant accelerated decline in FEV(1) (P = .046) was also observed in never smokers exposed to welding fumes. An “exposure-response” relationship was observed between FEV(1) decline and weekly duration of exposure to welding fumes in nonsmokers but not in smokers., Conclusions: Blue-collar workers exposed to welding fumes showed accelerated decline in lung function, which, in nonsmokers, was related to weekly duration of exposure.

Occupational exposure to welding fumes (WF) is thought to cause Parkinson's disease (PD)-like neurological dysfunction. An apprehension that WF may accelerate the onset of PD also exists. Identifying reliable biomarkers of exposure and neurotoxicity are therefore critical for biomonitoring and neurological risk characterization of WF exposure. Manganese (Mn) in welding consumables is considered the causative factor for the neurological deficits seen in welders. Hence, we sought to determine if Mn accumulation in blood or nail clippings can be a marker for adverse exposure and neurotoxicity. To model this, rats were exposed by intratracheal instillation to dissolved or suspended fume components collected from gas metal arc-mild steel (GMA-MS) or manual metal arc-hard surfacing (MMA-HS) welding. Trace element analysis revealed selective Mn accumulation in dopaminergic brain areas, striatum (STR) and midbrain (MB), following exposure to the two fumes. This caused dopaminergic abnormality as evidenced by loss of striatal tyrosine hydroxylase (Th; 25-32% decrease) and Parkinson disease (autosomal recessive, early onset) 7 (Park7; 25-46% decrease) proteins. While blood Mn was not detectable, Mn levels in nails strongly correlated with the pattern of Mn accumulation in the striatum (R(2)=0.9386) and midbrain (R(2)=0.9332). Exposure to manganese chloride (MnCl(2)) caused similar Mn accumulation in STR, MB and nail. Our findings suggest that nail Mn has the potential to be a sensitive and reliable biomarker for long-term Mn exposure and associated neurotoxicity. The non-invasive means by which nail clippings can be collected, stored, and transported with relative ease, make it an attractive surrogate for biomonitoring WF exposures in occupational settings., (Published by Elsevier Ireland Ltd.)

Objectives: There is little information on the changes in the pattern of occupational asthma (OA) over time. The objective of this study was to evaluate the time trends in the incidence and causes of immunological OA in Belgium using workers' compensation data., Methods: Cases of OA were identified through a retrospective review of all claims submitted by salaried workers to the Belgian Workers' Compensation Board from 1993 to 2002. The likelihood of OA was categorized as definite, probable, or possible based upon the results of from diagnostic procedures. Time trends were evaluated using Spearman's rank correlation for crude numbers of cases and through the negative binomial regression for incidence rates of OA per industry., Results: From a total of 1852 claims, 971 were categorized as having definite, probable, or possible OA. There was a downward trend in the annual number of cases due to the main causes of OA (i.e. flour, isocyanates, woods, and enzymes) and an apparent increase in cases of latex-induced OA. The estimated average annual incidence of OA was 29.4 (95% CI: 27.6-31.3) new cases per million salaried workers during the 1993-2002 period. There was a significant decline in the overall incidence rate of OA throughout the study period from 35.5 new cases per million salaried workers in 1993 to 25.8 in 2002., Conclusions: These compensation-based data indicate that there has been a global downward trend in the incidence of OA during the nineties, although the factors that determined this reduced incidence should be further investigated., (Copyright © 2011 Elsevier Ltd. All rights reserved.)

Epidemiological studies suggest that welding, a process which generates an aerosol of inhalable gases and metal rich particulates, increases the risk for cardiovascular disease. In this study we analyzed systemic inflammation and atherosclerotic lesions following gas metal arc-stainless steel (GMA-SS) welding fume exposure. Apolipoprotein E knockout (apoE(-/-)) mice, fed a Western diet, were exposed to GMA-SS at 40mg/m(3) for 3h/day for ten days (∼8.26μg daily alveolar deposition). Mice were sacrificed two weeks after exposure and serum chemistry, serum protein profiling and aortic lesion area were determined. There were no significant changes in serum total cholesterol, triglycerides or alanine aminotransferase. Serum levels of uric acid, a potent antioxidant, were decreased perhaps suggesting a reduced capacity to combat systemic oxidative stress. Inflammatory serum proteins interleukin 1 beta (IL-1β) and monocyte chemoattractant protein 3 (MCP-3) were increased two weeks after GMA-SS exposure. Analysis of atherosclerotic plaques showed an increase in lesion area as the result of GMA-SS exposure. In conclusion, GMA-SS exposure showed evidence of systemic inflammation and increased plaque progression in apoE(-/-) mice. These results complement epidemiological and functional human studies that suggest welding may result in adverse cardiovascular effects., (Published by Elsevier Ireland Ltd.)

About 2000 tons of chrysotile is used annually to produce friction materials in Islamic Republic of Iran. Approximately, 3000 workers are exposed to the asbestos fibers in the different processes of brake and clutch manufacturing. In the current study, asbestos fiber concentrations during brake and clutch manufacture were measured. This study also evaluated the fiber size and morphology distribution according to the Asbestos International Association (AIA) for standardization analytical method for asbestos. The airborne asbestos fiber concentrations and its chemical composition of 92 personal samples were analyzed by phase contrast microscopy (PCM) and scanning electron microscope (SEM) equipped with an energy-dispersive X-ray analyzer (EDX). Personal monitoring of fiber levels demonstrated counts that ranged from 0.31 to 1.3 PCM f/ml (15.5-51.5 SEM f/ml). Geometric means of the asbestos concentrations were 1.3 PCM f/ml (51.5 SEM f/ml) and 0.86 PCM f/ml (42.1 SEM f/ml) according to the brake weighting and mixing and clutch mixing process, respectively. The geometrical mean concentrations were 0.63 PCM f/ml (31 SEM f/ml), which is considerably higher than threshold limit value (TLV) of the American Conference of Governmental Industrial Hygienists (ACGIH) which is 0.1f/ml. The SEM data demonstrate that the fibrous particles consisted, approximately, of chrysotile (50%), tremolite (30%), and actinolite (20%). Based on these findings, the 50% of airborne fibers inhaled by the workers were amphiboles asbestos with fibers equal and greater than 5 microm in length and 0.2 microm in diameter, and thus not included in the PCM-based fiber counts. Therefore, it might be expected that workers who worked in the brake and clutch manufacture will suffer from negative health effects of exposing to the amphibole asbestos fibers., ((c) 2009 Elsevier Inc. All rights reserved.)

The purpose of the present study was to investigate the impact of carcinogenic polycyclic aromatic hydrocarbons and volatile organic compounds on sperm quality in a group of city policemen in Prague during a period of increased concentrations of ambient air-pollutants (winter season) compared to a period of low exposure (spring). Polymorphisms in metabolic genes (CYP1A1, EPHX1, GSTM1, GSTP1, GSTT1), folic acid metabolism genes (MTR, MTHFR) and DNA repair genes (XRCC1, XPD6, XPD23, hOGG1) were evaluated in these men as potential modifiers of associations between air pollution exposure and changes in sperm quality. The study population was a group of 47 policemen working in the center of the city. Seasonal differences in exposure were verified by ambient and personal monitoring. Markers of sperm injury included semen volume, sperm concentration, sperm morphology, sperm motility, and sperm DNA damage measured with the sperm chromatin structure assay The sperm chromatin structure assay (SCSA) includes a measure of DNA damage called DNA Fragmentation Index (DFI). The % of cells with detectable DFI (detDFI) by this assay includes sperm with either medium or high DNA damage; the term hDFI is used to define the % of sperm with only high DNA damage. The assay also detects immature sperm defined by high density staining (HDS). No significant differences were found in any of the standard semen parameters between the sampling periods except for vitality of sperms. Both DFI and HDS were significantly higher in winter than in spring samples for all men and for non-smokers. At the bivariate level, significant associations between hDFI or detDFI and polymorphisms of the repair genes XRCC1, XPD6 and XPD23 were observed. In multivariate models, polymorphisms of the genes XPD6, XPD23 and CYP1A1MspI were associated with hDFI and HDS. Moreover, HDS was significantly associated with polymorphisms in GSTM1 gene.

Background: Welding processes emit fine and ultrafine aerosol particles which are potentially harmful to the lungs of welders. In the past, changes in lung function were mostly determined by conventional spirometry. In this study spirometry was combined with new techniques such as Impulse Oscillometry (IOS) and Capnovolumetry (CVS) in order to assess welding associated changes in lung function., Methods: 45 Male welders and 24 non-welders were investigated at two time points: before work shift (baseline) and after work shift., Results: At baseline there were no differences between both study populations in spirometric, IOS, and CVS parameters. However, parameters of the flow-volume curve decreased with increasing long-term welding fume exposure (welding years). Airway resistances measured by IOS increased with welding years. IOS central airway resistance and several parameters of CVS increased during the work shift indicating airway narrowing and more inhomogeneous ventilation., Conclusions: In this study it has been shown that welding associated long-term and short-term effects could be detected in a population of welders, although exposure conditions were quite heterogeneous. The parameters of IOS and Capnovolumetry showed effects even more pronounced than conventional lung function parameters. Thus, these techniques may be considered as an additional tool for occupational medicine research.

Nanomaterials have novel properties and functions because of their small size. The unique nature of nanomaterials may be associated with potentially toxic effects. The aim of this study was to evaluate the in vivo genotoxicity of rats exposed with Aluminum oxide nanomaterials. Hence in the present study, the genotoxicity of Aluminum oxide nanomaterials (30 and 40 nm) and its bulk material was studied in bone marrow of female Wistar rats using chromosomal aberration and micronucleus assays. The rats were administered orally with the doses of 500, 1000 and 2000 mg/kg bw. Statistically significant genotoxicity was observed with Aluminum oxide 30 and 40 nm with micronucleus as well as chromosomal aberration assays. Significantly (p < 0.05 or p < 0.001) increased frequency of MN was observed with 1000 and 2000 mg/kg bw dose levels of Aluminum oxide 30 nm (9.4 +/- 1.87 and 15.2 +/- 2.3, respectively) and Aluminum oxide 40 nm (8.1 +/- 1.8 and 13.9 +/- 2.21, respectively) over control (2.5 +/- 0.7) at 30 h. Likewise, at 48 h sampling time a significant (p < 0.05 or p < 0.001) increase in frequency of MN was evident at 1000 and 2000 mg/kg bw dose levels of Aluminum oxide 30 nm (10.6 +/- 1.68 and 16.6 +/- 2.66, respectively) and Aluminum oxide 40 nm (9.0 +/- 1.38 and 14.7 +/- 1.68, respectively) compared to control (1.8 +/- 0.75). Significantly increased frequencies (p < 0.05 or p < 0.001) of chromosomal aberrations were observed with Aluminum oxide 30 nm (1000 and 2000 mg/kg bw) and Aluminum oxide 40 nm (2000 mg/kg bw) in comparison to control at 18 and 24 h. Further, since there is need for information on the toxicokinetics of nanomaterials, determination of these properties of the nanomaterials was carried out in different tissues, urine and feces using inductively coupled plasma mass spectrometry (ICP-MS). A significant size dependent accumulation of Aluminum oxide nanomaterials occurred in different tissues, urine and feces of rats as shown by ICP-MS data. The results of our study suggest that exposure to Aluminum oxide nanomaterials has the potential to cause genetic damage.

Mean volatile organic compound (VOC) concentrations in 16 newspaper stands and in two printing shops were monitored for the purpose of quantifying the various VOCs in these areas and to relate the results. In each site halogenated, oxygenated, aliphatic, and aromatic compounds were monitored during one workweek. They were sampled with diffusive samplers for thermal desorption and analysed by GC-MS. The results showed that in all newspaper stands the indoor levels of toluene were much higher than the outdoor levels; some sites had toluene indoor concentrations 100 times higher than their correspondent outdoor levels. The investigations in two printing shops confirmed that newspapers, in particular the inks, are the main sources of toluene in the newspaper stands.

Background: The relationship between occupational exposures and COPD has been analyzed in population-based and occupational cohort studies. However, the influence of these exposures on the clinical characteristics of COPD is not well known. The aim of this study was to analyze the impact of occupational exposures on respiratory symptoms, lung function, and employment status in a series of COPD patients., Methods: We conducted a cross-sectional study of 185 male COPD patients. Patients underwent baseline spirometry and answered a questionnaire that included information on respiratory symptoms, hospitalizations for COPD, smoking habits, current employment status, and lifetime occupational history. Exposure to biological dust, mineral dust, and gases and fumes was assessed using an ad hoc job exposure matrix., Results: Having worked in a job with high exposure to mineral dust or to any dusts, gas, or fumes was associated with an FEV(1) of < 30% predicted (mineral dust: relative risk ratio, 11; 95% confidence interval [CI], 1.4 to 95; dusts, gas, or fumes: relative risk ratio, 6.9; 95% CI, 1.1 to 45). High exposure to biological dust was associated with chronic sputum production (odds ratio [OR], 4.3; 95% CI, 1.6 to 12), dyspnea (OR, 2.7; 95% CI, 1.1 to 6.7), and work inactivity (OR, 2.4; 95% CI, 1.4 to 4.2). High exposure to dusts, gas, or fumes was associated with sputum production (OR, 2.8; 95% CI, 1.2 to 6.7) and dyspnea (OR, 1.2; 95% CI, 1.1 to 1.4)., Conclusions: Occupational exposures are independently associated with the severity of airflow limitation, respiratory symptoms, and work inactivity in patients with COPD.

Grunerite asbestos (amosite) has been shown in epidemiological and experimental animal studies to cause lung cancer, mesothelioma and pulmonary fibrosis commonly referred to as asbestosis. An overview of the human and experimental animal studies describing the health hazards of grunerite asbestos (amosite) is presented. Of the many human studies describing the health hazards of asbestos, only three factories using mainly, if not exclusively, grunerite asbestos (amosite) have been studied. The first is a series of reports on a cohort of 820 workers from a plant located in Paterson, NJ. Among this cohort, 18.7% died of lung cancer and 17 mesotheliomas occurred. The Paterson factory closed in 1954 and moved to Tyler, Texas where it operated until 1972. Among the 1130 former workers in the Tyler plant 6 mesotheliomas were reported with 15.8% lung cancer mortality. The third grunerite asbestos (amosite) exposed cohort was an insulation board manufacturing facility in Uxbridge, United Kingdom. Here 17.1% of the workers died of lung cancer and 5 mesotheliomas occurred. The lung content from 48 Uxbridge workers was analyzed by analytical transmission electron microscopy for mineral fibers. The relationship between grunerite asbestos (amosite) concentrations in the lung correlated with grades of fibrosis and asbestos bodies and was lower than the concentration found in the cases with malignant tumors. The lung cancer cases contained more grunerite asbestos (amosite) than mesothelioma cases, and in the cases of non-malignant disease the concentrations were still lower. In both types of malignancies the concentration of grunerite asbestos (amosite) was very high-over a billion fibers per gram of dried lung tissue. Occupational exposure to airborne concentrations of between 14 and 100 fibers of grunerite asbestos (amosite) per milliliter after 20 year latency causes marked increases in lung cancer, mesothelioma and pulmonary fibrosis (asbestosis).

Amphiboles are hydrated mineral silicates five of which occur in asbestiform habits as asbestos grunerite (amosite) asbestos, riebeckite (crocidolite) asbestos, anthophyllite asbestos, tremolite asbestos and actinolite asbestos] and non-asbestiform habits (grunerite, riebeckite, anthophyllite, tremolite and actinolite). The asbestiform varieties are characterized by long, thin fibers while non-asbestiform varieties such as cleavage fragments form short fibers with larger widths. The U.S. regulatory method for counting asbestos fibers (aspect ratio > or = 3:1, length > or = 5 microm) does not distinguish between asbestos and cleavage fragments. The method biases toward increased counts of non-asbestiform cleavage fragments compared to long, thin asbestos fibers. One consequence of this regulatory approach is that workers can be erroneously classified as exposed to concentrations of asbestos (asbestiform amphiboles) above the U.S. 0.1 f/mL exposure standard when in fact they are not exposed to asbestos at all but non-asbestiform amphibole cleavage fragments. Another consequence is that the known carcinogenic effects of asbestos may be falsely attributed to non-asbestiform amphibole cleavage fragments of the same mineral. The purpose of this review is to assess whether amphibole cleavage fragments pose the same risk of lung cancer and mesothelioma characteristic of amphibole asbestos fibers. We identified three groups of workers exposed to non-asbestiform amphiboles: two groups exposed to grunerite (Homestake gold miners and taconite miners) and one group exposed to industrial talc containing non-asbestiform tremolite and anthophyllite in St. Lawrence County, NY. In addition to assessing strength of association and exposure-response trends in the non-asbestiform amphibole cohorts, comparisons were also made with cohorts exposed to the asbestiform counterpart (positive control) and cohorts exposed to the mineral (e.g. talc) that does not contain amphiboles (negative controls). The cohorts exposed to non-asbestiform amphiboles had no excesses of lung cancer or mesothelioma. Similar results were observed in the negative control groups, in stark contrast to the excess risks of asbestos-related disease found in the asbestos cohorts. The only possible exception is the twofold increased risk of lung cancer where exposure was to industrial talc containing cleavage fragments of tremolite and anthophyllite. However, this risk is not considered attributable to the talc or amphibole cleavage fragments for several reasons. A similar increased risk of lung cancer was found in Vermont talc workers, studied in the same time period. Their exposure was to relatively pure talc. There was no relationship between lung cancer mortality and exposure measured as mg/m(3)years and years worked. A case-control study reported that all the lung cancer cases were smokers (or former smokers) and attributed the excess to smoking. There were two mesothelioma cases among the NY State talc workers exposed to cleavage fragments of tremolite and anthophyllite, but talc is not a plausible cause because of too short latency and potential for previous asbestos exposure. The positive controls of tremolite asbestos and anthophyllite asbestos exposed workers showed excess risks of both lung cancer and mesothelioma and positive exposure-response trends. St. Lawrence, NY talc does not produce mesotheliomas in animals while amphibole asbestos does. In sum, the weight of evidence fully supports a conclusion that non-asbestiform amphiboles do not increase the risk of lung cancer or mesothelioma.

The current state of knowledge concerning mesothelioma risk estimates is reviewed. Estimates of the risk of mesothelioma exist for the commercial asbestos fiber types chrysotile, amosite and crocidolite. Data also exist on which to assess risks for winchite (sodic tremolite) and anthophyllite asbestos. Uncertainty in estimates is primarily related to limitations in measurements of exposure. Differences in the dimensions of the various fiber types and of the same fiber types at different stages of processing add a further complication. Never-the-less, in practical terms, crocidolite presents the highest asbestos related mesothelioma risk. The risk associated with sodic tremolite (winchite) appears to be similar. In chrysotile miners and millers, the mesothelioma risk has been linked with exposure to asbestiform tremolite. Exposure to chrysotile in a pure form seems likely to present a very low if any risk of mesothelioma. While the majority of mesothelial tumors result from exposure to the asbestos minerals, there are other well established and suspected etiological agents. While a practical threshold seems to exist for exposure to chrysotile, it is unlikely to exist for the amphibole asbestos minerals, especially for crocidolite. To date there is no indication of an increased risk of mesothelioma resulting from non-commercial fiber exposure in the taconite industry.

Exposure-response relationships between the relative risk of lung cancer and quantitative measures of exposure to asbestos are available from a number of epidemiological studies. Meta-analyses of these relationships have been published by Lash et al. (1997) [Lash, T.L., Crouch, E.A.C., Green, L.C., 1997. A meta-analysis of the relation between cumulative exposure to asbestos and relative risk of lung cancer. Occup. Environ. Med. 54, 254-263] and Hodgson and Darnton (2000) [Hodgson, J.T., Darnton, A., 2000. The quantitative risks of mesothelioma and lung cancer in relation to asbestos exposure. Ann. Occup. Hyg. 44, 565-601]. In this paper, the risks derived in these meta-analyses have been compared. Lash et al., concentrated on process and found that the risk of lung cancer increased as the asbestos is refined by processing. Hodgson and Darnton concentrated on fibre type and found that the risk was highest for exposure to amphibole asbestos (crocidolite and amosite), lowest for chrysotile and intermediate for mixed exposure. Some of the differences between the conclusions from the two meta-analyses are a consequence of the choice of studies included. The range of asbestos types included in the studies in the analysis of Hodgson and Darnton was wider than that in Lash et al., enabling differences between fibre types to be analyzed more readily. There are situations where occupational exposure to chrysotile asbestos has shown no detectable increase in risk of lung cancer. Taconite miners have shown no increased risk of mortality due to lung cancer.

A 70% excess of mesothelioma, an asbestos-related cancer, has been reported among men in northeastern Minnesota, where iron mining has been the major industry. The Minnesota Department of Health has studied iron miners who developed mesothelioma to identify possible sources of asbestos exposure. A database of all Minnesota residents diagnosed with mesothelioma between 1988 and 1996 was linked to a database of approximately 72,000 current and former Minnesota iron-mining employees to identify cases who had ever worked in the mining industry. The job histories of the cases were examined to determine if any of their jobs could have involved exposure to commercial asbestos. Seventeen individuals diagnosed with mesothelioma in Minnesota between 1988 and 1996 were found to have worked in the iron mining industry. Of the 15 for whom adequate work histories were available, 14 had identifiable sources of exposure to commercial asbestos in jobs held both inside and outside of the mining industry. The time between employment in these asbestos-exposed occupations and the diagnosis of mesothelioma is consistent with the 20 or more year latency period that has been observed in other studies of this cancer.