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.

Childhood hematologic cancer and residential proximity to oil and gas development.

BACKGROUND: Oil and gas development emits known hematological carcinogens, such as benzene, and increasingly occurs in residential areas. We explored whether residential proximity to oil and gas development was associated with risk for hematologic cancers using a registry-based case-control study design. METHODS: Participants were 0-24 years old, living in rural Colorado, and diagnosed with cancer between 2001-2013. For each child in our study, we calculated inverse distance weighted (IDW) oil and gas well counts within a 16.1-kilometer radius of residence at cancer diagnosis for each year in a 10 year latency period to estimate density of oil and gas development. Logistic regression, adjusted for age, race, gender, income, and elevation was used to estimate associations across IDW well count tertiles for 87 acute lymphocytic leukemia (ALL) cases and 50 non-Hodgkin lymphoma (NHL) cases, compared to 528 controls with non-hematologic cancers. FINDINGS: Overall, ALL cases 0-24 years old were more likely to live in the highest IDW well count tertiles compared to controls, but findings differed substantially by age. For ages 5-24, ALL cases were 4.3 times as likely to live in the highest tertile, compared to controls (95% CI: 1.1 to 16), with a monotonic increase in risk across tertiles (trend p-value = 0.035). Further adjustment for year of diagnosis increased the association. No association was found between ALL for children aged 0-4 years or NHL and IDW well counts. While our study benefited from the ability to select cases and controls from the same population, use of cancer-controls, the limited number of ALL and NHL cases, and aggregation of ages into five year ranges, may have biased our associations toward the null. In addition, absence of information on O&G well activities, meteorology, and topography likely reduced temporal and spatial specificity in IDW well counts. CONCLUSION: Because oil and gas development has potential to expose a large population to known hematologic carcinogens, further study is clearly needed to substantiate both our positive and negative findings. Future studies should incorporate information on oil and gas development activities and production levels, as well as levels of specific pollutants of interest (e.g. benzene) near homes, schools, and day care centers; provide age-specific residential histories; compare cases to controls without cancer; and address other potential confounders, and environmental stressors.

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.

Biomarkers of Exposure to Polycyclic Aromatic Hydrocarbons and Cognitive Function among Elderly in the United States (National Health and Nutrition Examination Survey: 2001-2002).

Recent studies report a link between common environmental exposures, such as particulate matter air pollution and tobacco smoke, and decline in cognitive function. The purpose of this study was to assess the association between exposure to polycyclic aromatic hydrocarbons (PAHs), a selected group of chemicals present in particulate matter and tobacco smoke, and measures of cognitive performance among elderly in the general population. This cross-sectional analysis involved data from 454 individuals aged 60 years and older from the 2001-2002 National Health and Nutrition Examination Survey. The association between PAH exposures (as measured by urinary biomarkers) and cognitive function (digit symbol substitution test (DSST)) was assessed using multiple linear regression analyses. After adjusting for age, socio-economic status and diabetes we observed a negative association between urinary 1-hydroxypyrene, the gold standard of PAH exposure biomarkers, and DSST score. A one percent increase in urinary 1-hydroxypyrene resulted in approximately a 1.8 percent poorer performance on the digit symbol substitution test. Our findings are consistent with previous publications and further suggest that PAHs, at least in part may be responsible for the adverse cognitive effects linked to tobacco smoke and particulate matter air pollution.

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.

Biomarkers of exposure to polycyclic aromatic hydrocarbons (PAHs) and DNA damage: a cross-sectional pilot study among roofers in South Florida.

OBJECTIVE: The main goal of this pilot study was to assess the technical and logistic feasibility of a future study. The research hypothesis is that occupational exposures to polycyclic aromatic hydrocarbons (PAHs) are associated with increased risk of DNA damage among roofers who work with hot asphalt. DESIGN: This is a cross-sectional pilot study. SETTING: The study included roofers from four different construction sites in Miami-Dade County, Florida. PARTICIPANTS: 19 roofers were recruited (six Hispanics and 13 African-Americans, all male), all of whom were eligible (no history of cancer and no history of chronic diseases of kidneys or liver). All participants provided pre-shift samples and 18 provided post-shift samples. Samples of one participant were excluded from the final analyses as they were considered unreliable. RESULTS: Levels of urinary PAH metabolites increased during 6 h of work. Linear regression models of post-shift metabolites included their pre-shift levels, post-shift urinary creatinine levels (for models of 1-OHPyr and 9-OHPhe), and skin burn due to contact with hot asphalt (for models of 1-OHPyr and 1-OHNap). Pre-shift levels of urinary 8-OHdG were not associated with any of the variables considered. For post-shift levels of 8-OHdG, however, post-shift 1-OHPyr (95% CI 0.091 to 0.788) and use of protective gloves (95% CI -1.57 to -0.61) during work explained 86.8% of its variation. Overall, highest levels of urinary PAH metabolites and of 8-OHdG were observed among workers who reported having skin burn and who did not use gloves during work. CONCLUSIONS: Urinary 1-OHPyr is a promising predictor of oxidative DNA damage among roofers. Work-related skin burn and use of protective gloves appear to influence PAH exposure and DNA damage levels in this group, suggesting the importance of dermal absorption.

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.

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.

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.

Earlier age at menopause, work, and tobacco smoke exposure.

OBJECTIVE: Earlier age at menopause onset has been associated with increased all-cause, cardiovascular, and cancer mortality risks. The risk of earlier age at menopause associated with primary and secondary tobacco smoke exposure was assessed. DESIGN: This was a cross-sectional study using a nationally representative sample of US women. A total of 7,596 women (representing an estimated 79 million US women) from the National Health and Nutrition Examination Survey III were asked time since last menstrual period, occupation, and tobacco use (including home and workplace second-hand smoke [SHS] exposure). Blood cotinine and follicle-stimulating hormone levels were assessed. Logistic regressions for the odds of earlier age at menopause, stratified on race/ethnicity in women 25 to 50 years of age and adjusted for survey design, were controlled for age, body mass index, education, tobacco smoke exposure, and occupation. RESULTS: Among 5,029 US women older than 25 years with complete data, earlier age at menopause was found among all smokers and among service and manufacturing industry sector workers. Among women age 25 to 50 years, there was an increased risk of earlier age at menopause with both primary smoking and SHS exposure, particularly among black women. CONCLUSIONS: Primary tobacco use and SHS exposure were associated with increased odds of earlier age at menopause in a representative sample of US women. Earlier age at menopause was found for some women worker groups with greater potential occupational SHS exposure. Thus, control of SHS exposure in the workplace may decrease the risk of mortality and morbidity associated with earlier age at menopause in US women workers.

Declining trends in serum cotinine levels in US worker groups: the power of policy.

OBJECTIVE: To explore trends in cotinine levels in US worker groups. METHODS: Using NHANES III data, serum cotinine levels of US workers not smokers nor exposed to secondhand smoke (SHS) at home were evaluated for trends by occupational/industrial and race/ethnicity-gender sub-groups. RESULTS: Decreases from 1988 to 2002 ranged from 0.08 to 0.30 ng/mL (67% to 85% relative decrease), with largest absolute reductions in: blue-collar and service occupations; construction/manufacturing industrial sectors; non-Hispanic Black male workers. CONCLUSIONS: All worker groups had declining serum cotinine levels. Most dramatic reductions occurred in sub-groups with the highest before cotinine levels, thus disparities in SHS workforce exposure are diminishing with increased adoption of clean indoor laws. However, Black male workers, construction/manufacturing sector workers, and blue-collar and service workers have the highest cotinine levels. Further reductions in SHS exposure will require widespread adoption of workplace clean air laws without exemptions.

Utility of urinary 1-naphthol and 2-naphthol levels to assess environmental carbaryl and naphthalene exposure in an epidemiology study.

We recently reported associations between urinary 1-naphthol (1N) levels and several intermediate measures of male reproductive health, namely sperm motility, serum testosterone levels, and sperm DNA damage. However, because 1N is a major urinary metabolite of both naphthalene and the insecticide carbaryl, exposure misclassification stemming from differences in exposure source was probable and interpretation of the results was limited. As naphthalene, but not carbaryl, is also metabolized to 2-naphthol (2N), the relationship of urinary 1N to 2N within an individual may give information about source of 1N. Utilizing data from two previous studies that measured both 1N and 2N in urine of men exposed to either carbaryl or naphthalene, the present study employed several methods to differentiate urinary 1N arising from exposures to carbaryl and naphthalene among men in the reproductive health study. When re-evaluating the reproductive health data, techniques for identifying 1N source involved exploring interaction terms, stratifying the data set based on 1N/2N ratios, and performing an exposure calibration using a linear 1N to 2N relationship from a study of workers exposed to naphthalene in jet fuel. Despite some inconsistencies between the methods used to distinguish 1N source, we found that 1N from carbaryl exposure is likely responsible for the previously observed association between 1N and sperm motility, whereas 1N from naphthalene exposure is likely accountable for the association between 1N and sperm DNA damage. We demonstrate that studies of health effects associated with carbaryl should utilize a 1N/2N ratio to identify subgroups in which carbaryl is the primary source of 1N. Conversely, studies of naphthalene-related outcomes may utilize 2N levels to estimate exposure.

Dermal exposure to jet fuel JP-8 significantly contributes to the production of urinary naphthols in fuel-cell maintenance workers.

Jet propulsion fuel 8 (JP-8) is the major jet fuel used worldwide and has been recognized as a major source of chemical exposure, both inhalation and dermal, for fuel-cell maintenance workers. We investigated the contributions of dermal and inhalation exposure to JP-8 to the total body dose of U.S. Air Force fuel-cell maintenance workers using naphthalene as a surrogate for JP-8 exposure. Dermal, breathing zone, and exhaled breath measurements of naphthalene were obtained using tape-strip sampling, passive monitoring, and glass bulbs, respectively. Levels of urinary 1- and 2-naphthols were determined in urine samples and used as biomarkers of JP-8 exposure. Multiple linear regression analyses were conducted to investigate the relative contributions of dermal and inhalation exposure to JP-8, and demographic and work-related covariates, to the levels of urinary naphthols. Our results show that both inhalation exposure and smoking significantly contributed to urinary 1-naphthol levels. The contribution of dermal exposure was significantly associated with levels of urinary 2-naphthol but not with urinary 1-naphthol among fuel-cell maintenance workers who wore supplied-air respirators. We conclude that dermal exposure to JP-8 significantly contributes to the systemic dose and affects the levels of urinary naphthalene metabolites. Future work on dermal xenobiotic metabolism and toxicokinetic studies are warranted in order to gain additional knowledge on naphthalene metabolism in the skin and the contribution to systemic exposure.

Determination of dihydroxynaphthalenes in human urine by gas chromatography-mass spectrometry.

A gas chromatography-mass spectrometry (GC-MS) method was developed for measuring 1,2-dihydroxynaphthalene (1,2-DHN) and 1,4-dihydroxynaphthalene (1,4-DHN) in urine. The method involves enzymatic digestion of urinary conjugates to release the DHNs which were then analyzed as trimethylsilyl derivatives by GC-MS. For 1,2-DHN and 1,4-DHN, respectively, the assay limits of detection were 0.21 and 0.15 microg/l, the assay limits of quantitation were 0.69 and 0.44 microg/l, and the coefficients of variation were 14.7 and 10.9%. This method was successfully applied to determine urinary levels of 1,2-DHN and 1,4-DHN in coke workers (14 top workers and 13 side-bottom workers) and 21 matching control workers from the steel industry of northern China. The geometric mean (GM) levels of 1,2-DHN were approximately 100 and 30 times higher than those of 1,4-DHN in exposed and control subjects, respectively. The GM levels 1,2-DHN and 1,4-DHN were significantly higher for coke workers (1,2-DHN: top workers--552 microg/l, side-bottom workers--260 microg/l; 1,4-DHN: top workers--3.42 microg/l, side-bottom workers--3.56 microg/l) than for controls (1,2-DHN: 38.8 microg/l; 1,4-DHN: 1.21 microg/l) (por=0.623; p<0.0001). Also, levels of 1,2-DHN were significantly correlated with those of serum albumin adducts of l,2-naphthoquinone (rs=0.492, p=0.0004). These results indicate that 1,2- and 1,4-DHN are good biomarkers for assessment of naphthalene exposure in coke workers. Since the DHNs are precursors of the naphthoquinones, which have been implicated as toxic products of naphthalene metabolism, measurements of urinary DHNs may have toxicological significance.

Dose-dependent production of urinary naphthols among workers exposed to jet fuel (JP-8).

BACKGROUND: Jet propulsion fuel-8 (JP-8) is one of the largest sources of chemical exposures among Air Force personnel. Urinary naphthols have been suggested as useful biomarkers of exposure to JP-8. METHODS: Multivariate linear regression models were applied to evaluate the effects of environmental and work-related factors upon production of urinary naphthols among 323 Air Force personnel. RESULTS: Naphthalene exposure, smoking status, and their interaction, plus self-reported skin irritation explained about two-thirds of the variation in naphthol levels. The exposure-smoking interaction was consistent with induction by smoking of one or more steps in the metabolism of naphthalene and naphthalene-1,2-oxide (NapO). A supralinear dose-response relationship was observed between urinary naphthols and naphthalene exposure. CONCLUSIONS: Urinary naphthols were associated with specific sources of exposure to JP-8, arising from both inhalation and dermal contact. Smokers and nonsmokers metabolized naphthalene at different rates, consistent with induction of at least two metabolic pathways by smoking.

Naphthalene and its biomarkers as measures of occupational exposure to polycyclic aromatic hydrocarbons.

Polycyclic aromatic hydrocarbons (PAH) include compounds with two or more fused benzene rings, many of which are carcinogens. Industrial sources produce hundreds of PAH, notably in the coke- and aluminium-producing industries. Because PAH are distributed at varying levels between gaseous and particulate phases, exposure assessment has been problematic. Here, we recommend that occupational exposures to naphthalene be considered as a potential surrogate for occupational PAH exposure for three reasons. Naphthalene is usually the most abundant PAH in a given workplace; naphthalene is present almost entirely in the gaseous phase and is, therefore, easily measured; and naphthalene offers several useful biomarkers, including the urinary metabolites 1- and 2-hydroxynaphthalene. These biomarkers can be used to evaluate total-body exposure to PAH, in much the same way that 1-hydroxypyrene has been applied. Using data from published sources, we show that log-transformed airborne levels of naphthalene are highly correlated with those of total PAH (minus naphthalene) in several industries (creosote impregnation: Pearson r= 0.815, coke production: r= 0.917, iron foundry: r= 0.854, aluminium production: r= 0.933). Furthermore, the slopes of the log-log regressions are close to one indicating that naphthalene levels are proportional to those of total PAH in those industries. We also demonstrate that log-transformed urinary levels of the hydroxynaphthalenes are highly correlated with those of 1-hydroxypyrene among coke oven workers and controls (r= 0.857 and 0.876), again with slopes of log-log regressions close to one. These results support the conjecture that naphthalene is a useful metric for occupational PAH exposure. Since naphthalene has also been shown to be a respiratory carcinogen in several animal studies, it is also argued that naphthalene exposures should be monitored per se in industries with high levels of PAH.

Albumin adducts of naphthalene metabolites as biomarkers of exposure to polycyclic aromatic hydrocarbons.

We investigated the utility of adducts formed by the reaction of the naphthalene metabolites naphthalene-1,2-oxide, 1,2-naphthoquinone (1,2-NPQ), and 1,4-naphthoquinone (1,4-NPQ) with serum albumin (Alb) as biomarkers of exposure to polycyclic aromatic hydrocarbons. Cysteinyl serum Alb adducts of 1,2- and 1,4-NPQ (1,2-NPQ-Alb and 1,4-NPQ-Alb, respectively) but not of naphthalene-1,2-oxide were detected in 28 coke oven workers and 22 controls from the steel industry of northern China. The median level of 1,2-NPQ-Alb in coke oven workers (76.6 pmol/g) was significantly higher than that observed in controls (44.9 pmol/g; P = 0.0027). However, the median level of 1,4-NPQ-Alb in exposed subjects was not significantly different from that of controls (48.6 versus 44.2 pmol/g; P = 0.296). Levels of 1,2-NPQ-Alb were significantly correlated with exposure category (controls, side and bottom workers, and top-of-oven workers) as well as with previously measured levels of urinary naphthalene, 1- and 2-naphthol, and 1-pyrenol in these subjects. Multiple linear regression analysis revealed that 35% of the variation in 1,2-NPQ-Alb could be explained by the work category and age. A negative relationship between 1,2-NPQ-Alb and age was observed, suggesting that cytochrome P450 c metabolism diminished with age at approximately 3%/year of life.

Urinary biomarkers of exposure to jet fuel (JP-8).

Benzene, naphthalene, and 1- and 2-naphthol were measured in urine samples obtained from 322 U.S. Air Force personnel categorized a priori as likely to have low, moderate, or high exposure to jet fuel [jet propulsion fuel-8 (JP-8)]. In postexposure samples, levels of these analytes in the high-exposure group were 3- to 29-fold greater than in the low-exposure group and 2- to 12-fold greater than in the moderate-exposure group. Heavy exposure to JP-8 contributed roughly the same amount of benzene and more than three times the amount of naphthalene compared with cigarette smoking. Strong correlations were observed among postexposure levels of naphthalene-based biomarkers in urine and naphthalene in air and breath. We conclude that urinary naphthalene and the naphthols can serve as biomarkers of exposure to jet fuel. Of these, the naphthols are probably more useful because of their greater abundance and slower elimination kinetics.