Laboratory comparison of field portable X-ray fluorescence spectrometer (FP-XRF) and inductively coupled plasma mass spectrometry (ICP-MS) for determination of airborne metals in stainless steel welding fume.

Welding fume is a common exposure in occupational settings. Gravimetric analysis for total particulate matter is common; however, the cost of laboratory analyses limits the availability of quantitative exposure assessment for welding fume metal constituents in occupational settings. We investigated whether a field portable X-ray fluorescence spectrometer (FP-XRF) could provide accurate estimates of personal exposures to metals common in welding fume (chromium, copper, manganese, nickel, vanadium, and zinc). The FP-XRF requires less training and is easier to deploy in many settings than traditional wet laboratory analyses. Filters were analyzed both by FP-XRF and inductively coupled plasma mass spectrometry (ICP-MS). We estimated the FP-XRF limit of detection for each metal and developed a correction factor accounting for the non-uniform deposition pattern on filter samples collected with an Institute of Medicine (IOM) inhalable particulate matter sampler. Strong linear correlation was observed for all metals (0.72

Personal and area exposure assessment at a stainless steel fabrication facility: an evaluation of inhalable, time-resolved PM10, and bioavailable airborne metals.

This study describes a comprehensive exposure assessment in a stainless steel welding facility, measuring personal inhalable PM and metals, time-resolved PM10 area metals, and the bioavailable fraction of area inhalable metals. Eighteen participants wore personal inhalable samplers for two, nonconsecutive shifts. Area inhalable samplers and a time-resolved PM10 X-ray fluorescence spectrometer were used in different work areas each sampling day. Inhalable and bioavailable metals were analyzed using inductively coupled plasma mass spectrometry (ICP-MS). Median exposures to chromium, nickel, and manganese across all measured shifts were 66 (range: 13-300) µg/m3, 29 (5.7-132) µg/m3, and 22 (1.5-119) µg/m3, respectively. Most exposure variation was seen between workers ( 0.79

The State of US Health, 1990-2016: Burden of Diseases, Injuries, and Risk Factors Among US States.

Introduction: Several studies have measured health outcomes in the United States, but none have provided a comprehensive assessment of patterns of health by state. Objective: To use the results of the Global Burden of Disease Study (GBD) to report trends in the burden of diseases, injuries, and risk factors at the state level from 1990 to 2016. Design and Setting: A systematic analysis of published studies and available data sources estimates the burden of disease by age, sex, geography, and year. Main Outcomes and Measures: Prevalence, incidence, mortality, life expectancy, healthy life expectancy (HALE), years of life lost (YLLs) due to premature mortality, years lived with disability (YLDs), and disability-adjusted life-years (DALYs) for 333 causes and 84 risk factors with 95% uncertainty intervals (UIs) were computed. Results: Between 1990 and 2016, overall death rates in the United States declined from 745.2 (95% UI, 740.6 to 749.8) per 100 000 persons to 578.0 (95% UI, 569.4 to 587.1) per 100 000 persons. The probability of death among adults aged 20 to 55 years declined in 31 states and Washington, DC from 1990 to 2016. In 2016, Hawaii had the highest life expectancy at birth (81.3 years) and Mississippi had the lowest (74.7 years), a 6.6-year difference. Minnesota had the highest HALE at birth (70.3 years), and West Virginia had the lowest (63.8 years), a 6.5-year difference. The leading causes of DALYs in the United States for 1990 and 2016 were ischemic heart disease and lung cancer, while the third leading cause in 1990 was low back pain, and the third leading cause in 2016 was chronic obstructive pulmonary disease. Opioid use disorders moved from the 11th leading cause of DALYs in 1990 to the 7th leading cause in 2016, representing a 74.5% (95% UI, 42.8% to 93.9%) change. In 2016, each of the following 6 risks individually accounted for more than 5% of risk-attributable DALYs: tobacco consumption, high body mass index (BMI), poor diet, alcohol and drug use, high fasting plasma glucose, and high blood pressure. Across all US states, the top risk factors in terms of attributable DALYs were due to 1 of the 3 following causes: tobacco consumption (32 states), high BMI (10 states), or alcohol and drug use (8 states). Conclusions and Relevance: There are wide differences in the burden of disease at the state level. Specific diseases and risk factors, such as drug use disorders, high BMI, poor diet, high fasting plasma glucose level, and alcohol use disorders are increasing and warrant increased attention. These data can be used to inform national health priorities for research, clinical care, and policy.

Short-term markers of DNA damage among roofers who work with hot asphalt.

BACKGROUND: Roofers are at increased risk for various malignancies and their occupational exposures to polycyclic aromatic hydrocarbons (PAHs) have been considered as important risk factors. The overall goal of this project was to investigate the usefulness of phosphorylated histone H2AX (γH2AX) as a short-term biomarker of DNA damage among roofers. METHODS: Blood, urine, and dermal wipe samples were collected from 20 roofers who work with hot asphalt before and after 6 h of work on Monday and Thursday of the same week (4 sampling periods). Particle-bound and gas-phase PAHs were collected using personal monitors during work hours. γH2AX was quantified in peripheral lymphocytes using flow cytometry and 8-hydroxy-2-deoxyguanosine (8-OHdG) was assessed in urine using ELISA. General linear mixed models were used to evaluate associations between DNA damage and possible predictors (such as sampling period, exposure levels, work- and life-style factors). Differences in mean biomarker and DNA damage levels were tested via ANOVA contrasts. RESULTS: Exposure measurements did not show an association with any of the urinary biomarkers or the measures of DNA damage. Naphthalene was the most abundant PAH in gas-phase, while benzo(e)pyrene was the most abundant particle-bound PAH. Post-shift levels of γH2AX and 8-OHdG were higher on both study days, when compared to pre-shift levels. Cigarette smoking was a predictor of γH2AX and urinary creatinine was a predictor of urinary 8-OHdG. Between-subject variance to total variance ratio was 35.3 % for γH2ax and 4.8 % for 8-OHdG. CONCLUSION: γH2AX is a promising biomarker of DNA damage in occupational epidemiology studies. It has a lower within-subject variation than urinary 8-OHdG and can easily be detected in large scale groups. Future studies that explore the kinetics of H2AX phosphorylation in relation to chemical exposures may reveal the transient and persistent nature of this sensitive biomarker of early DNA damage.

Potential effects of polychlorinated biphenyls (PCBs) and selected organochlorine pesticides (OCPs) on immune cells and blood biochemistry measures: a cross-sectional assessment of the NHANES 2003-2004 data.

BACKGROUND: Polychlorinated biphenyls (PCBs) and organochlorine pesticides (OCPs) are widely distributed in the environment and may have adverse effects on the immune system. METHODS: Lipid adjusted serum levels of 19 Dioxin Like (DL), 17 Non Dioxin Like (NDL) PCBs, 5 OCPs, and measures of complete blood count and routine biochemistry profile were obtained from the NHANES 2003-2004 cycle. For each of the PCB/OCP variables, individuals were put into four exposure groups and blood markers were compared across these groups. RESULTS: Serum levels of PCBs and OCPs increased with age. Total white blood cell (WBC) count, red blood cells (RBC), hemoglobin, and hematocrit measures were lowest in the group with the highest serum PCBs. Results for the OCPs varied. For Mirex, WBC declined in the highest exposure; no significant differences were observed for p-p'-DDT or p-p'-DDE; and higher levels of WBC were observed at the highest exposure groups of serum trans-nonachlor and oxychlordane. Liver enzymes (AST, ALT, and GGT) were significantly higher in the highest exposure groups of PCBs/OCPs. CONCLUSIONS: We observed significant associations between PCB/OCP levels and blood markers in the general population. All of the levels were within normal ranges but the consistency of results is remarkable and may reflect subclinical effects. Largest differences were observed for NDL PCBs. Thus, routine application of toxic equivalency factors, which assume dioxin like mechanisms and aryl hydrocarbon receptor involvement, may not adequately reflect the effects of NDL PCBs in the mixture.

Exposure to polycyclic aromatic hydrocarbons and serum inflammatory markers of cardiovascular disease.

Polycyclic aromatic hydrocarbons (PAHs) are environmental and occupational carcinogens produced by the incomplete combustion of organic materials, such as coal and petroleum product combustion, tobacco smoking, and food cooking, that may be significant contributors to the burden of cardiovascular disease in human populations. The purpose of this study was to investigate associations between ten monohydroxy urinary metabolites of four PAHs and three serum biomarkers of cardiovascular disease (fibrinogen, homocysteine, and white blood cell count). Using data on 3219 participants aged 20 years and older from the National Health and Nutrition Examination Survey (NHANES) 2001-2004 dataset, the associations between PAH metabolites and serum inflammatory markers were analyzed using the Spearman correlations and multiple linear regression modeling. The PAH metabolites of naphthalene, fluorene, phenanthrene, and pyrene each showed both positive and negative correlations with homocysteine, fibrinogen, and white blood cell count (correlation coefficient range: -0.077-0.143) in nonsmoking participants. Using multiple linear regression models adjusted for age, gender, race/ethnicity, and body mass index, estimates of weighted geometric means of inflammatory marker levels were not significantly different between high and low levels (75th vs. 25th percentiles) for all PAH metabolites in nonsmoking subjects. The results of this study do not provide evidence for a relationship between PAH exposure (as measured by urinary levels of PAH metabolites) and serum biomarkers of cardiovascular disease after controlling for tobacco use.

The utility of naphthyl-keratin adducts as biomarkers for jet-fuel exposure.

We investigated the association between biomarkers of dermal exposure, naphthyl-keratin adducts (NKA), and urine naphthalene biomarker levels in 105 workers routinely exposed to jet-fuel. A moderate correlation was observed between NKA and urine naphthalene levels (p = 0.061). The NKA, post-exposure breath naphthalene, and male gender were associated with an increase, while CYP2E1*6 DD and GSTT1-plus (++/+-) genotypes were associated with a decrease in urine naphthalene level (p < 0.0001). The NKA show great promise as biomarkers for dermal exposure to naphthalene. Further studies are warranted to characterize the relationship between NKA, other exposure biomarkers, and/or biomarkers of biological effects due to naphthalene and/or PAH exposure.

Secondhand smoke exposure and the risk of hearing loss.

Hearing loss has been associated with tobacco smoking, but its relationship with secondhand smoke is not known. We sought to investigate the association between secondhand smoke exposure and hearing loss in a nationally representative sample of adults. The National Health and Nutrition Examination Survey (NHANES), a nationally representative cross-sectional dataset, was utilised to investigate the association between secondhand smoke exposure and hearing loss. Data collected from non-smoking participants aged 20-69 years were included in the analysis if they had completed audiometric testing, had a valid serum continue value, and provided complete smoking, medical co-morbidity and noise exposure histories (N=3307). Hearing loss was assessed from averaged pure-tone thresholds over low- or mid-frequencies (500, 1000 and 2000 Hz) and high-frequencies (3000, 4000, 6000 and 8000 Hz), and was defined as mild or greater severity (pure-tone average in excess of 25 dB HL). Second-Hand Smoke (SHS) exposure was significantly associated with increased risk of hearing loss for low-/mid-frequencies (adjusted OR=1.14; 95% CI 1.02-1.28 for never smokers and 1.30; 1.10-1.54 for former smokers) and high-frequencies (1.40; 1.22-1.81 for former smokers), after controlling for potential confounders. Findings from the present analysis indicate that SHS exposure is associated with hearing loss in non-smoking adults.

Fibronectin stimulates endothelin-1 synthesis in rat hepatic myofibroblasts via a Src/ERK-regulated signaling pathway.

BACKGROUND & AIMS: Liver injury serves as an excellent model of wound healing, characterized by increased synthesis of various cytokines and peptides, including the vasoactive peptide endothelin-1. In the liver, wound healing is mediated by effector cells such as hepatic stellate cells, which cause tissue contraction. Endothelin-1 has autocrine effects on stellate cells and induces their contractile activities. We explored the role of various extracellular matrix components, particularly of fibronectin, in regulating endothelin-1 production during liver injury. METHODS: Hepatic stellate cells were isolated from normal and injured rats. Real-time polymerase chain reaction immunoblot and enzyme-linked immunosorbent assay analyses were used to measure specific variables, including endothelin-1 production. Preproendothelin-1 promoter activity was determined by a luciferase assay. Stellate cell contraction was measured by a gel contraction assay. RESULTS: Fibronectin stimulated transcription of preproendothelin-1 messenger RNA and expression of endothelin through an integrin-dependent pathway in activated hepatic stellate cells. In these cells, fibronectin induced phosphorylation/activation of extracellular signal-regulated kinase (ERK) through a Shc- and Src-dependent mechanism; ERK activation was required for fibronectin-induced endothelin-1 expression. Fibronectin stimulation by stellate cells induced expression of smooth muscle alpha-actin and endothelin-1-mediated autocrine stellate cell contraction. Stellate cells isolated from injured livers of rats exhibited increased basal phosphorylation levels of Src, Shc, and ERK, as well as increased endothelin-1 synthesis. CONCLUSIONS: Fibronectin stimulates activated stellate cells to produce endothelin-1 and contract, via an ERK-dependent signaling pathway. The resulting autocrine functional effects of endothelin-1 are likely to be important in the wound-healing process in injured liver.

Secondhand smoke exposure and depressive symptoms.

OBJECTIVE: To evaluate the association between secondhand smoke (SHS) exposure and depression. Tobacco smoking and depression are strongly associated, but the possible effects of SHS have not been evaluated. METHODS: The 2005 to 2006 National Health and Nutrition Examination Survey (NHANES) is a cross-sectional sample of the noninstitutionalized civilian U.S. population. SHS exposure was measured in adults aged > or =20 years by serum cotinine and depressive symptoms by the Patient Health Questionnaire. Zero-inflated Poisson regression analyses were completed with adjustment for survey design and potential confounders. RESULTS: Serum cotinine-documented SHS exposure was positively associated with depressive symptoms in never-smokers, even after adjustment for age, race/ethnicity, gender, education, alcohol consumption, and medical comorbidities. The association between SHS exposure and depressive symptoms did not vary by gender, nor was there any association between SHS smoke exposure and depressive symptoms in former smokers. CONCLUSIONS: Findings from the present study suggest that SHS exposure is positively associated with depressive symptoms in never-smokers and highlight the need for further research to establish the mechanisms of association.