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Beane Freeman L.E.,U.S. National Institutes of Health | Blair A.,U.S. National Institutes of Health | Lubin J.H.,U.S. National Institutes of Health | Stewart P.A.,Stewart Exposure Assessments LLC | And 2 more authors.
American Journal of Industrial Medicine | Year: 2013

Background: Formaldehyde, a widely used chemical, is considered a human carcinogen. Methods: We extended follow-up of the largest industrial cohort of workers in formaldehyde industries (n=25,619) by 10 years through 2004. Standardized mortality ratios (SMRs) and rate ratios (RRs) were calculated for deaths from solid tumors using quantitative formaldehyde exposure estimates. Results: During 998,239 person-years, 13,951 deaths occurred. With one additional death, previously observed excesses for nasopharyngeal cancer (n=10) persisted for peak, average intensity and cumulative exposure; RRs in the highest exposure categories were 7.66 (95% CI: 0.94, 62.34), P-trend=0.005, 11.54 (95% CI: 1.38, 96.81), P-trend=0.09, and 2.94 (95% CI: 0.65, 13.28), P-trend=0.06, respectively. For all cancer, solid tumors and lung cancer, SMRs among exposed workers were elevated, but internal analyses revealed no positive associations with formaldehyde exposure. Conclusions: Consistent with previous analyses of this cohort, this update continues to suggest a link between formaldehyde exposure and nasopharyngeal cancer. © 2013 Wiley Periodicals, Inc.

Gilboa S.M.,Centers for Disease Control and Prevention | Desrosiers T.A.,University of North Carolina at Chapel Hill | Lawson C.,Centers for Disease Control and Prevention | Lupo P.J.,University of Texas Health Science Center at Houston | And 6 more authors.
Occupational and Environmental Medicine | Year: 2012

Objective: To examine the relation between congenital heart defects (CHDs) in offspring and estimated maternal occupational exposure to chlorinated solvents, aromatic solvents and Stoddard solvent during the period from 1 month before conception through the first trimester. Methods: The study population included mothers of infants with simple isolated CHDs and mothers of control infants who delivered from 1997 through 2002 and participated in the National Birth Defects Prevention Study. Two methods to assess occupational solvent exposure were employed: an expert consensus-based approach and a literature-based approach. Multiple logistic regression was used to calculate adjusted ORs and 95% CIs for the association between solvent classes and CHDs. Results: 2951 control mothers and 2047 CHD case mothers were included. Using the consensus-based approach, associations were observed for exposure to any solvent and any chlorinated solvent with perimembranous ventricular septal defects (OR 1.6, 95% CI 1.0 to 2.6 and OR 1.7, 95% CI 1.0 to 2.8, respectively). Using the literature-based approach, associations were observed for: any solvent exposure with aortic stenosis (OR 2.1, 95% CI 1.1 to 4.1) and Stoddard solvent exposure with d-transposition of the great arteries (OR 2.0, 95% CI 1.0 to 4.2), right ventricular outflow tract obstruction defects (OR 1.9, 95% CI 1.1 to 3.3) and pulmonary valve stenosis (OR 2.1, 95% CI 1.1 to 3.8). Conclusions: The authors found evidence of associations between occupational exposure to solvents and several types of CHDs. These results should be interpreted in light of the potential for misclassification of exposure.

Silverman D.T.,U.S. National Cancer Institute | Samanic C.M.,U.S. National Cancer Institute | Lubin J.H.,U.S. National Cancer Institute | Blair A.E.,U.S. National Cancer Institute | And 12 more authors.
Journal of the National Cancer Institute | Year: 2012

Background Most studies of the association between diesel exhaust exposure and lung cancer suggest a modest, but consistent, increased risk. However, to our knowledge, no study to date has had quantitative data on historical diesel exposure coupled with adequate sample size to evaluate the exposure-response relationship between diesel exhaust and lung cancer. Our purpose was to evaluate the relationship between quantitative estimates of exposure to diesel exhaust and lung cancer mortality after adjustment for smoking and other potential confounders.MethodsWe conducted a nested case-control study in a cohort of 12315 workers in eight non-metal mining facilities, which included 198 lung cancer deaths and 562 incidence density-sampled control subjects. For each case subject, we selected up to four control subjects, individually matched on mining facility, sex, race/ethnicity, and birth year (within 5 years), from all workers who were alive before the day the case subject died. We estimated diesel exhaust exposure, represented by respirable elemental carbon (REC), by job and year, for each subject, based on an extensive retrospective exposure assessment at each mining facility. We conducted both categorical and continuous regression analyses adjusted for cigarette smoking and other potential confounding variables (eg, history of employment in high-risk occupations for lung cancer and a history of respiratory disease) to estimate odds ratios (ORs) and 95% confidence intervals (CIs). Analyses were both unlagged and lagged to exclude recent exposure such as that occurring in the 15 years directly before the date of death (case subjects)/reference date (control subjects). All statistical tests were two-sided.ResultsWe observed statistically significant increasing trends in lung cancer risk with increasing cumulative REC and average REC intensity. Cumulative REC, lagged 15 years, yielded a statistically significant positive gradient in lung cancer risk overall (P trend = .001); among heavily exposed workers (ie, above the median of the top quartile [REC ≥ 1005 μg/m 3-y]), risk was approximately three times greater (OR = 3.20, 95% CI = 1.33 to 7.69) than that among workers in the lowest quartile of exposure. Among never smokers, odd ratios were 1.0, 1.47 (95% CI = 0.29 to 7.50), and 7.30 (95% CI = 1.46 to 36.57) for workers with 15-year lagged cumulative REC tertiles of less than 8, 8 to less than 304, and 304 μg/m 3-y or more, respectively. We also observed an interaction between smoking and 15-year lagged cumulative REC (P interaction = .086) such that the effect of each of these exposures was attenuated in the presence of high levels of the other.ConclusionOur findings provide further evidence that diesel exhaust exposure may cause lung cancer in humans and may represent a potential public health burden. © 2012 The Author.

Attfield M.D.,ERS Inc | Schleiff P.L.,U.S. National Institute for Occupational Safety and Health | Schleiff P.L.,Stewart Exposure Assessments LLC | Lubin J.H.,U.S. National Cancer Institute | And 6 more authors.
Journal of the National Cancer Institute | Year: 2012

Background Current information points to an association between diesel exhaust exposure and lung cancer and other mortality outcomes, but uncertainties remain.MethodsWe undertook a cohort mortality study of 12315 workers exposed to diesel exhaust at eight US non-metal mining facilities. Historical measurements and surrogate exposure data, along with study industrial hygiene measurements, were used to derive retrospective quantitative estimates of respirable elemental carbon (REC) exposure for each worker. Standardized mortality ratios and internally adjusted Cox proportional hazard models were used to evaluate REC exposure-associated risk. Analyses were both unlagged and lagged to exclude recent exposure such as that occurring in the 15 years directly before the date of death.ResultsStandardized mortality ratios for lung cancer (1.26, 95% confidence interval [CI] = 1.09 to 1.44), esophageal cancer (1.83, 95% CI = 1.16 to 2.75), and pneumoconiosis (12.20, 95% CI = 6.82 to 20.12) were elevated in the complete cohort compared with state-based mortality rates, but all-cause, bladder cancer, heart disease, and chronic obstructive pulmonary disease mortality were not. Differences in risk by worker location (ever-underground vs surface only) initially obscured a positive diesel exhaust exposure-response relationship with lung cancer in the complete cohort, although it became apparent after adjustment for worker location. The hazard ratios (HRs) for lung cancer mortality increased with increasing 15-year lagged cumulative REC exposure for ever-underground workers with 5 or more years of tenure to a maximum in the 640 to less than 1280 μg/m 3-y category compared with the reference category (0 to <20 μg/m 3-y; 30 deaths compared with eight deaths of the total of 93; HR = 5.01, 95% CI = 1.97 to 12.76) but declined at higher exposures. Average REC intensity hazard ratios rose to a plateau around 32 μg/m 3. Elevated hazard ratios and evidence of exposure-response were also seen for surface workers. The association between diesel exhaust exposure and lung cancer risk remained after inclusion of other work-related potentially confounding exposures in the models and were robust to alternative approaches to exposure derivation.ConclusionsThe study findings provide further evidence that exposure to diesel exhaust increases risk of mortality from lung cancer and have important public health implications. © 2012 The Author.

Bhatti P.,Fred Hutchinson Cancer Research Center | Stewart P.A.,Stewart Exposure Assessments LLC | Linet M.S.,U.S. National Cancer Institute | Blair A.,U.S. National Cancer Institute | And 2 more authors.
Occupational and Environmental Medicine | Year: 2011

Objectives: There is great interest in evaluating gene-environment interactions with chemical exposures, but exposure assessment poses a unique challenge in case-control studies. Expert assessment of detailed work history data is usually considered the best approach, but it is a laborious and time-consuming process. We set out to determine if a less intensive method of exposure assessment (a job exposure matrix (JEM)) would produce similar results to a previous analysis that found evidence of effect modification of the association between expert-assessed lead exposure and risk of brain tumours by a single nucleotide polymorphism in the ALAD gene (rs1800435). Methods: We used data from a study of 355 patients with glioma, 151 patients with meningioma and 505 controls. Logistic regression models were used to examine associations between brain tumour risk and lead exposure and effect modification by genotype. We evaluated Cohen's κ, sensitivity and specificity for the JEM compared to the expert-assessed exposure metrics. Results: Although effect estimates were imprecise and driven by a small number of cases, we found evidence of effect modification between lead exposure and ALAD genotype when using expert- but not JEM-derived lead exposure estimates. κ Values indicated only modest agreement (<0.5) for the exposure metrics, with the JEM indicating high specificity (∼0.9) but poor sensitivity (∼0.5). Disagreement between the two methods was generally due to having additional information in the detailed work history. Conclusion: These results provide preliminary evidence suggesting that high quality exposure data are likely to improve the ability to detect genetic effect modification.

Hein M.J.,U.S. National Institute for Occupational Safety and Health | Waters M.A.,U.S. National Institute for Occupational Safety and Health | Ruder A.M.,U.S. National Institute for Occupational Safety and Health | Stenzel M.R.,Exposure Assessment Applications LLC | And 2 more authors.
Annals of Occupational Hygiene | Year: 2010

Objectives: Occupational exposure assessment for population-based case-control studies is challenging due to the wide variety of industries and occupations encountered by study participants. We developed and evaluated statistical models to estimate the intensity of exposure to three chlorinated solvents - methylene chloride, 1,1,1-trichloroethane, and trichloroethylene - using a database of air measurement data and associated exposure determinants.Methods: A measurement database was developed after an extensive review of the published industrial hygiene literature. The database of nearly 3000 measurements or summary measurements included sample size, measurement characteristics (year, duration, and type), and several potential exposure determinants associated with the measurements: mechanism of release (e.g. evaporation), process condition, temperature, usage rate, type of ventilation, location, presence of a confined space, and proximity to the source. The natural log-transformed measurement levels in the exposure database were modeled as a function of the measurement characteristics and exposure determinants using maximum likelihood methods. Assuming a single lognormal distribution of the measurements, an arithmetic mean exposure intensity level was estimated for each unique combination of exposure determinants and decade.Results: The proportions of variability in the measurement data explained by the modeled measurement characteristics and exposure determinants were 36, 38, and 54% for methylene chloride, 1,1,1-trichloroethane, and trichloroethylene, respectively. Model parameter estimates for the exposure determinants were in the anticipated direction. Exposure intensity estimates were plausible and exhibited internal consistency, but the ability to evaluate validity was limited.Conclusions: These prediction models can be used to estimate chlorinated solvent exposure intensity for jobs reported by population-based case-control study participants that have sufficiently detailed information regarding the exposure determinants.

Karami S.,U.S. National Cancer Institute | Lan Q.,U.S. National Cancer Institute | Rothman N.,U.S. National Cancer Institute | Stewart P.A.,Stewart Exposure Assessments LLC | And 3 more authors.
Occupational and Environmental Medicine | Year: 2012

Objectives: Inconsistent epidemiological findings, debate over interpretation, and extrapolation of findings from animal studies to humans have produced uncertainty surrounding the carcinogenicity of trichloroethylene (TCE) exposure in occupational settings. We updated meta-analyses of published case-control and cohort studies exploring occupational TCE exposure and kidney cancer risk, incorporating new analytical results from three recently published cohort studies and a case-control study. Methods: PubMed MEDLINE was searched for studies published from 1950 to 2011 assessing occupational exposure to chlorinated solvents, degreasers or TCE. All cohort (N=15) and case-control (N=13) studies included in analyses were stratified by assessment of occupational exposure to TCE specifically and to any chlorinated solvent. Results: Significantly elevated summary estimates were observed for cohort studies (relative risk (RR) 1.26, 95% CI 1.02 to 1.56; p heterogeneity=0.65), case-control studies (OR 1.35, 95% CI 1.17 to 1.57; p heterogeneity=0.41), and cohort and case-control studies combined (RR 1.32, 95% CI 1.17 to 1.50, p heterogeneity=0.63) that specifically assessed TCE exposure after excluding outlier studies that contributed to heterogeneity. Non-significantly elevated summary estimates were generally observed for studies of workers exposed to chlorinated solvents but who were not assessed for TCE specifically. Conclusions: Regardless of study design, significant and stronger estimates were only observed in studies specifically assessing occupational exposure to TCE. Estimates were lower in studies assessing occupational exposure to chlorinated solvents. This updated meta-analysis supports an association between occupational TCE exposure and kidney cancer and provides evidence that exposure misclassification may weaken estimates assessing exposure to the broader class of chlorinated solvents.

Karami S.,U.S. National Institutes of Health | Bassig B.,U.S. National Institutes of Health | Stewart P.A.,U.S. National Institutes of Health | Stewart P.A.,Stewart Exposure Assessments LLC | And 5 more authors.
Occupational and Environmental Medicine | Year: 2013

The carcinogenic potential of trichloroethylene (TCE) continues to generate much controversy, even after the US Environmental Protection Agency raised its classification to 'carcinogenic to humans'. We conducted a meta-analysis of published cohort and case-control studies exploring occupational TCE exposure in relation to five different lymphatic and haematopoietic cancers: non-Hodgkin's lymphoma (NHL, N=24), Hodgkin's lymphoma (HL, N=13), multiple myeloma (MM, N=11), leukaemia (N=12) and chronic/small lymphocytic leukaemia (CLL/SLL, N=7). Studies published between 1950 and 2011 were identified through a PubMed Medline search. All studies included in analyses were classified as those that assessed either occupational TCE exposure specifically ('TCE-exposure' studies) or a broader classification of all chlorinated solvents ('chlorinated solvent-exposure' studies). A significantly raised summary estimate for NHL was seen for all cohort and case-control 'TCE-exposure' studies combined (N=19; relative risk (RR)=1.32, 95% CI 1.14 to 1.54; I2=25.20; p-heterogeneity=0.12) and for cohort 'TCE-exposure' studies (N=10; RR=1.52, 95% CI 1.29 to 1.79; I2=7.09; p-heterogeneity=0.63). A non-significant but raised summary estimate was seen for NHL casecontrol 'TCE-exposure' studies. No significant association with NHL risk was detected overall for any 'chlorinated solvent-exposure' studies. Summary estimates for occupational TCE exposure were not associated with risk of hL, MM, leukaemia or CLL/SLL. Our updated metaanalysis of NHL, which incorporates new analytical results from three cohort and four case-control studies, supports an association between occupational TCE exposure and NHL.

PubMed | University of Houston, Barbara Ann Karmanos Cancer Institute, Stewart Exposure Assessments LLC, University of Alberta and 3 more.
Type: | Journal: Occupational and environmental medicine | Year: 2016

Trichloroethylene, a chlorinated solvent widely used for metal degreasing, is classified by the International Agency for Research on Cancer as a kidney carcinogen. Other chlorinated solvents are suspected carcinogens, most notably the cleaning solvent perchloroethylene, although it is unclear whether they are associated with kidney cancer. We investigated kidney cancer associations with occupational exposure to 6 chlorinated solvents (trichloroethylene, perchloroethylene, 1,1,1-trichloroethane, carbon tetrachloride, chloroform, and methylene chloride) within a case-control study using detailed exposure assessment methods.Cases (n=1217) and controls (n=1235) provided information on their occupational histories and, for selected occupations, on tasks involving potential exposure to chlorinated solvents through job-specific interview modules. Using this information, an industrial hygienist assessed potential exposure to each solvent. We computed ORs and 95% CIs for different exposure metrics, with unexposed participants as the referent group.1,1,1-trichloroethane, carbon tetrachloride, chloroform, and methylene chloride were not associated with kidney cancer. Among jobs with high exposure intensity, high cumulative hours exposed to perchloroethylene was associated with increased risk, both overall (third tertile vs unexposed: OR 3.1, 95% CI 1.3 to 7.4) and after excluding participants with 50% exposure probability for trichloroethylene (OR 3.0, 95% CI 0.99 to 9.0). A non-significant association with high cumulative hours exposed to trichloroethylene was observed (OR 1.7, 95% CI 0.8 to 3.8).In this study, high exposure to perchloroethylene was associated with kidney cancer, independent of trichloroethylene. Additional studies are needed to further investigate this finding.

PubMed | Barbara Ann Karmanos Cancer Institute, University of Illinois at Chicago, Stewart Exposure Assessments LLC and National Cancer Institute
Type: Journal Article | Journal: International journal of cancer | Year: 2016

Epidemiological evidence of a relationship between vitamin D and kidney cancer risk has been inconsistent despite experimental data indicating that vitamin D and its metabolites may inhibit carcinogenesis. Previously we reported an inverse association between renal cell carcinoma (RCC) risk and occupational ultraviolet (UV) exposure among European men. In this study, we examined the association between occupational UV exposure and RCC risk among US residents and investigated whether this association varied by race and sex. Lifetime occupational data for 1,217 RCC cases and 1,235 controls in a population-based case-control study, conducted from 2002 to 2007, were assessed for occupational UV exposure. We evaluated exposure metrics in quartiles based on control exposure levels and calculated associations between RCC risk and occupational UV exposure using unconditional logistic regression adjusted for sex, race, body mass index, smoking, hypertension, center, education, family history of cancer and dietary vitamin D intake. A general pattern of decreasing RCC risk with increasing UV exposure was observed. Cases had significantly lower cumulative occupational UV exposure than controls (fourth quartile vs. first: odds ratio=0.74 [95% confidence interval=0.56-0.99], p-trend=0.03). Similar results were observed for other UV exposure metrics. The association with occupational UV exposure was stronger for women than for men, but did not differ by race. Our findings suggest an inverse association between occupational UV exposure and RCC, particularly among women. Given the sex finding discrepancies in this study versus our previous study, additional research is need to clarify whether the protective effects of occupational UV exposure and RCC risk are real.

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