Biomedical subjects

Robert J McCunney

Publications and source records attributed to Robert J McCunney.

7 recordsLinked to original sources

PubMed2006

Lung cancer mortality and carbon black exposure: Cox regression analysis of a cohort from a German carbon black production plant.

OBJECTIVE: We undertook a lung cancer mortality analysis of 1528 German carbon black workers, followed between the years of 1976-1998, who produced furnace black, lamp black, and gas black. METHODS: We used Cox modeling across age with time-dependent covariates, ie, cumulative and mean carbon black exposure, duration of work in departments, adjusting for calendar time, a smoking indicator, and age at hire. Exposures were lagged up to 20 years. Analyses were performed with the full cohort and after restriction to an inception cohort. RESULTS: A total of 50 lung cancer deaths occurred. No positive association was found with carbon black exposure indices. Some models indicated an increasing risk across duration of work in the lamp black producing department. CONCLUSIONS: Our results do not suggest that carbon black exposure is a human lung carcinogen. The lamp black results, if no artifact, may point at historical exposures to gaseous polycyclic aromatic hydrocarbons.

Age Factors↗

PubMed2006

Lung cancer mortality and carbon black exposure: uncertainties of SMR analyses in a cohort study at a German carbon black production plant.

OBJECTIVE: We undertook a sensitivity analysis of the lung cancer standardized mortality ratios (SMRs) in a study of 1522 German carbon black workers from 1976 to 1998. METHODS: We applied results from a case-control study to adjust the SMR for smoking habits and exposures experienced before the carbon black job. In addition, sensitivity to reference rates was explored. RESULTS: On the basis of 47 lung cancer deaths, the SMRs were 1.62, 1.72, and 2.08 (local, state, and national rates, respectively). Adjustment for previous exposures and smoking yielded additional correction factors of 0.64 or 0.74, varying with the chosen reference. CONCLUSIONS: Lung cancer SMRs (95% confidence intervals) for the full cohort ranged from 1.20 (0.88-1.59) to 2.08 (1.53-2.77) in this sensitivity analysis. Thus, overall SMRs are only weak measures of causal associations and should be complemented by internal modeling of exposure effects whenever possible.

Case-Control Studies↗

PubMed2006

Lung cancer mortality and carbon black exposure: a nested case-control study at a German carbon black production plant.

OBJECTIVE: The objective of this study was to conduct a case-control study of lung cancer nested within a cohort of 1528 German carbon black workers, 1976-1998. METHODS: The authors conducted risk-set sampling of two controls matched on year of birth and conditional logistic regression modeling of cumulative carbon black exposure, duration of work in different departments, feedstock contact, asbestos exposure, smoking, age at hire, exposures before the carbon black job, and serving as a soldier in World War II or being a prisoner of war. Analyses were performed with both the full cohort and members of an inception cohort subset. Exposures were lagged by 10 years. RESULTS: Analysis of 50 lung cancer deaths showed no association to carbon black exposure. CONCLUSIONS: Carbon black exposure was not linked to lung cancer risk. Suggestions of positive associations with asbestos exposure, feedstock contact, and work in specific departments are inconclusive due to small numbers.

Asbestos↗

PubMed2006

Should we screen for occupational lung cancer with low-dose computed tomography?

OBJECTIVE: The objective of this study was to assess the potential value of screening for occupational lung cancer through the use of low-dose computed tomography (LDCT). METHODS: A literature review of Medline was conducted to assess: 1) screening studies of occupational lung cancer that used LDCT; 2) screening studies of nonoccupational lung cancer that used LDCT; and 3) position papers of medical professional societies and nongovernmental health organizations that have addressed the value of screening for lung cancer with LDCT. RESULTS: No screening studies of occupational lung cancer with LDCT were uncovered; however, numerous observational and population-based studies have addressed the value of screening for lung cancer among cigarette smokers. Results of these studies are difficult to interpret in light of numerous biases associated with these types of studies. No randomized, controlled studies on screening for lung cancer have been published at this time. No professional, governmental, or nonprofit health organization recommends screening asymptomatic people at risk of lung cancer with LDCT at this time. CONCLUSION: In the absence of randomized, controlled studies that can address biases commonly encountered in observational and population-based studies, it is unclear whether LDCT reduces mortality from lung cancer. The National Cancer Institute is sponsoring a randomized, controlled study of over 50,000 current and former smokers with the results expected in 2009.

Humans↗

PubMed2006

Particles and cancer.

Explore the source record for details and available documents.

Air Pollutants, Occupational↗

PubMed2005

Asthma, genes, and air pollution.

OBJECTIVE: The objective of this article is to evaluate genetic risks associated with the pulmonary response to air pollutants, including particulates and ozone. METHODS: A comprehensive review of articles related to the genetics of asthma with particular attention to air pollution was conducted through a search of the National Library of Medicine's PubMed database. RESULTS: Asthma, which affects over 15 million people in the United States, is characterized by inflammation leading to reversible airflow obstruction. Triggered by exposure to numerous occupational and environmental agents, asthma has long been considered to occur more frequently in families, with upwards of a 50% higher rate in the offspring of parents with asthma. Asthma genetic studies have used two major methods: mapping techniques that pinpoint gene loci and studies that identify genes and polymorphisms associated with various asthma mechanisms such as inflammatory mediators. The most consistently replicated chromosomal regions associated with asthma have been chromosomes 2q, 5q, 6p, 12 q, and 13q. Because the formation of reactive oxygen species is a major aspect of the inflammatory process of asthma, genetic aberrations associated with antioxidants such as glutathione S-transferase (GST) may shed light on reasons why some people with asthma seem more at risk of exacerbations as a result of air pollution. People with a polymorphism at the GSTP 1 locus, which codes for GST, one of a family of pulmonary antioxidants, have higher rates of asthma. Children in Mexico City with the GSTM1 null genotype demonstrated significant ozone-related decrements in lung function. Animal studies support the key role of antioxidants in reducing the inflammatory response associated with exposure to diesel exhaust particles. CONCLUSIONS: Oxidative stress is a key mechanism underlying the toxic effects of exposure to some types of air pollution. Asthmatics with the null genotype for the antioxidant, GST, seem more at risk of the pulmonary effects of air pollution.

Air Pollution↗

PubMedDate not supplied

Genetic testing: ethical implications in the workplace.

The human genome project has led to impressive scientific advances in understanding the genetic basis of disease. To date, genetic risks associated with occupational illnesses are not well understood. Recent research, however, has uncovered an allele that appears directly related to the risk of contracting chronic beryllium disease; other chromosomal abnormalities have been identified in association with cancer. Progress from the human genome project has potential implications for predicting, screening, and diagnosing occupational diseases. Ethical issues associated with the use of genetic testing in the workplace will present employers, insurers, and physicians with challenging decisions related to promoting health in the workplace while avoiding potential misuse of sensitive genetic information.

Confidentiality↗