Publications by authors named "James Huff"

63 Publications

Livelihood intervention and mental well-being among women living with HIV in Delhi.

AIDS Care 2021 08 26;33(8):1037-1043. Epub 2020 Oct 26.

Emmanuel Hospital Association, New Delhi, India.

Poverty-alleviation programmes aimed to improved mental well-being among persons living with HIV (PLWH) in low and middle income countries have underscored the importance of understanding how and why such programmes work. We present findings from a six-month ethnographic process evaluation of , an economic livelihood programme locally designed to improve mental well-being among women affected by HIV in Delhi, India. In addition to benefits of improved economic standing, we found that supportive relationships cultivated among participants ( = 9) and with providers ( = 3) provided respite from worry about their illness and reframed what was relationally and practically possible in the context of living with HIV. In acquiring marketable craft skills with peers, participants challenged internalized scripts of being socially devalued and regained agency about their abilities to contribute to their community and support their children's immediate and future needs. We found that the benefits of weighed less on the direct alleviation of mental distress and more on the instillation of hope for their children. Our findings exemplify the importance of re-visiting a priori theories that inform interventions for PLWH and highlight the methodological merits of ethnographic approaches that underscore how theory and intervention praxis are bidirectionally informed.
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http://dx.doi.org/10.1080/09540121.2020.1837336DOI Listing
August 2021

Examining Health Literacy Levels in Homeless Persons and Vulnerably Housed Persons with Mental Health Disorders.

Community Ment Health J 2020 05 19;56(4):645-651. Epub 2019 Dec 19.

Royal Ottawa Health Care Group, 1145 Carling Avenue, Ottawa, ON, K1Z 7K4, Canada.

Health care use is high in persons who are homeless and vulnerably housed, but their health literacy (ability to read and understand health information) is often not known. The purpose of this study was to determine health literacy rates in a Canadian population of homeless and vulnerably housed individuals with mental health disorders. Higher levels of health literacy were associated with being housed, higher levels of education, non-psychotic mental health diagnoses and lower levels of drug use. This suggests that health literacy may be a potential barrier for accessing and utilizing health services and information for vulnerable populations.
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http://dx.doi.org/10.1007/s10597-019-00525-2DOI Listing
May 2020

Commentary: IARC Monographs Program and public health under siege by corporate interests.

Am J Ind Med 2018 Apr 3;61(4):277-281. Epub 2018 Feb 3.

Dean, Faculty of Public Health, Kuwait University, Kuwait, Hawalli.

The International Agency for Research on Cancer (IARC) evaluates causes of cancer with help from independent international experts in an open and transparent manner. Countries, research and regulatory agencies, and other organizations adopt IARC evaluations for communication of human cancer hazards, and for strategies to prevent cancer. Scientists worldwide endorse IARC cancer evaluations and process. Those with economic interests, however, challenge IARC's cancer evaluations, most recently for glyphosate and red and processed meats, and are conducting a campaign including intervention from US Congressional Representatives to discredit IARC's review process and to undermine financial support-a campaign intimidating to IARC and Working Group members. Challenges to scientific interpretations serve to advance science and should be resolved by scientific experts who do not have conflicts of interest. Such interference does not bode well for the free flow of scientific information that informs and protects the public from risks of cancer.
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http://dx.doi.org/10.1002/ajim.22811DOI Listing
April 2018

An Integrated Experimental Design for the Assessment of Multiple Toxicological End Points in Rat Bioassays.

Environ Health Perspect 2017 03 22;125(3):289-295. Epub 2016 Jul 22.

Cesare Maltoni Cancer Research Center, Ramazzini Institute, Bentivoglio, Bologna, Italy.

Background: For nearly five decades long-term studies in rodents have been the accepted benchmark for assessing chronic long-term toxic effects, particularly carcinogenicity, of chemicals. The European Food Safety Authority (EFSA) and the World Health Organization (WHO) have pointed out that the current set of internationally utilized test methods capture only some of the potential adverse effects associated with exposures to these agents over the lifetime.

Objectives: In this paper, we propose the adaption of the carcinogenicity bioassay to integrate additional protocols for comprehensive long-term toxicity assessment that includes developmental exposures and long-term outcomes, capable of generating information on a broad spectrum of different end points.

Discussion: An integrated study design based on a stepwise process is described that includes the priority end points of the Economic Co-operation and Development and the National Toxicology Program guidelines on carcinogenicity and chronic toxicity and developmental and reproductive toxicity. Integrating a comprehensive set of relevant toxicological end points in a single protocol represents an opportunity to optimize animal use in accordance with the 3Rs (replacement, reduction and refinement). This strategy has the potential to provide sufficient data on multiple windows of susceptibility of specific interest for risk assessments and public health decision-making by including prenatal, lactational, neonatal exposures and evaluating outcomes over the lifespan.

Conclusion: This integrated study design is efficient in that the same generational cohort of rats used for evaluating long-term outcomes can be monitored in satellite parallel experiments to measure biomarkers and other parameters related to system-specific responses including metabolic alterations and endocrine disturbances. Citation: Manservisi F, Babot Marquillas C, Buscaroli A, Huff J, Lauriola M, Mandrioli D, Manservigi M, Panzacchi S, Silbergeld EK, Belpoggi F. 2017. An integrated experimental design for the assessment of multiple toxicological end points in rat bioassays. Environ Health Perspect 125:289-295; http://dx.doi.org/10.1289/EHP419.
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http://dx.doi.org/10.1289/EHP419DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5332192PMC
March 2017

IARC monographs: 40 years of evaluating carcinogenic hazards to humans.

Environ Health Perspect 2015 Jun 24;123(6):507-14. Epub 2015 Feb 24.

Department of Medical Statistics, London School of Hygiene and Tropical Medicine, London, United Kingdom.

Background: Recently, the International Agency for Research on Cancer (IARC) Programme for the Evaluation of Carcinogenic Risks to Humans has been criticized for several of its evaluations, and also for the approach used to perform these evaluations. Some critics have claimed that failures of IARC Working Groups to recognize study weaknesses and biases of Working Group members have led to inappropriate classification of a number of agents as carcinogenic to humans.

Objectives: The authors of this Commentary are scientists from various disciplines relevant to the identification and hazard evaluation of human carcinogens. We examined criticisms of the IARC classification process to determine the validity of these concerns. Here, we present the results of that examination, review the history of IARC evaluations, and describe how the IARC evaluations are performed.

Discussion: We concluded that these recent criticisms are unconvincing. The procedures employed by IARC to assemble Working Groups of scientists from the various disciplines and the techniques followed to review the literature and perform hazard assessment of various agents provide a balanced evaluation and an appropriate indication of the weight of the evidence. Some disagreement by individual scientists to some evaluations is not evidence of process failure. The review process has been modified over time and will undoubtedly be altered in the future to improve the process. Any process can in theory be improved, and we would support continued review and improvement of the IARC processes. This does not mean, however, that the current procedures are flawed.

Conclusions: The IARC Monographs have made, and continue to make, major contributions to the scientific underpinning for societal actions to improve the public's health.
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http://dx.doi.org/10.1289/ehp.1409149DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4455595PMC
June 2015

War on Carcinogens: industry disputes human relevance of chemicals causing cancer in laboratory animals based on unproven hypotheses, using kidney tumors as an example.

Int J Occup Environ Health 2013 Oct-Dec;19(4):255-60

Evidence from studies in animals is essential for identifying chemicals likely to cause or contribute to many diseases in humans, including cancers. Yet, to avoid or delay the implementation of protective public health standards, the chemical industry typically denies cancer causation by agents they produce. The spurious arguments put forward to discount human relevance are often based on inadequately tested hypotheses or modes of action that fail to meet Bradford Hill criteria for causation. We term the industry attacks on the relevance of animal cancer findings as the "War on Carcinogens." Unfortunately, this tactic has been effective in preventing timely and appropriate health protective actions on many economically important yet carcinogenic chemicals, including: arsenic, asbestos, benzene, 1,3-butadiene, formaldehyde, methylene chloride, phthalates, tobacco usage, trichloroethylene [TCE], and others. Recent examples of the "War on Carcinogens" are chemicals causing kidney cancer in animals. Industry consultants argue that kidney tumor findings in rats with exacerbated chronic progressive nephropathy (CPN) are not relevant to humans exposed to these chemicals. We dispute and dismiss this unsubstantiated claim with data and facts, and divulge unprofessional actions from a leading toxicology journal.
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http://dx.doi.org/10.1179/1077352513Z.00000000090DOI Listing
April 2014

Long-term toxicology and carcinogenicity of 2,4,6-trichlorophenol.

Authors:
James Huff

Chemosphere 2012 Oct 27;89(5):521-5. Epub 2012 Jun 27.

National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA.

Carcinogenesis bioassays were conducted by giving 2,4,6-trichlorophenol [2,4,6-TCP] in feed to groups of 50 male and female Fischer rats and male B6C3F1 mice for two years. Dietary concentrations were 0 [20/group], 5000 [0.5%], or 10,000 [1%] ppm. Female mice began with 10,000 and 20,000 ppm but after 38 weeks were lowered due to reduced body weights to 2500 and 5000 ppm for 67 weeks; exposures averaged 5200 and 10,400 ppm. Adverse effects at two years were leukocytosis and monocytosis of peripheral blood and hyperplasia of bone marrow in both sexes of rats. In mice, liver toxicity, including individual liver cell abnormalities, focal areas of cellular alteration, and focal and nodular areas of hyperplasia were commonly present. Regarding carcinogenic activity, TCP caused leukemias/lymphomas in male rats, and possibly in female rats and female mice as well, and induced liver tumors in male and female mice. Using NTP categories of evidence indicates 'clear evidence of carcinogenicity' for male rats [hematopoietic system tumors]; 'equivocal evidence of carcinogenicity' for female rats [hematopoietic system tumors]; 'clear evidence of carcinogenicity' for male and female mice [liver tumors].
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http://dx.doi.org/10.1016/j.chemosphere.2012.05.015DOI Listing
October 2012

Hexane fraction of American ginseng suppresses colitis and colon cancer.

Cancer Prev Res (Phila) 2012 Jul 25;5(7):982; author reply 983. Epub 2012 May 25.

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http://dx.doi.org/10.1158/1940-6207.CAPR-12-0079DOI Listing
July 2012

Chemically exacerbated chronic progressive nephropathy not associated with renal tubular tumor induction in rats: an evaluation based on 60 carcinogenicity studies by the national toxicology program.

Toxicol Sci 2012 Aug 26;128(2):346-56. Epub 2012 Apr 26.

Ron Melnick Consulting, LLC, Chapel Hill , North Carolina 27514, USA.

Chronic progressive nephropathy (CPN) is a common age-related degenerative-regenerative disease of the kidney that occurs in both sexes of most strains of rats. Recently, claims have been made that enhanced CPN is a mode of action for chemically induced kidney tumors in male rats and that renal tubular tumors (RTTs) induced by chemicals that concomitantly exacerbate CPN are not relevant for human cancer risk assessments. Although CPN is an observable histopathological lesion that may be modified by diet, the etiology of this disease and the mechanisms for its exacerbation by chemicals are unknown, and it fails to meet fundamental principles for defining carcinogenic modes of action and human relevance. Our comprehensive evaluation of possible relationships between exacerbated CPN and induction of RTTs in 58 carcinogenicity studies, conducted by the National Toxicology Program, in male and 11 studies in female F344 rats using 60 chemicals revealed widespread inconsistency in the claimed association. Because the proposed hypothesis lacks evidence of biological plausibility, and due to inconsistent relationships between exacerbated CPN and kidney tumor incidence in carcinogenicity studies in rats, dismissing the human relevance of kidney tumors induced by chemicals that also exacerbate CPN in rats would be wrong.
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http://dx.doi.org/10.1093/toxsci/kfs156DOI Listing
August 2012

Environmental justice and primary prevention of cancer: the odyssey and legacy of lorenzo tomatis.

New Solut 2012 ;22(1):7-17

NIEHS, P.O. Box 12233, Research Triangle Park, NC 27709, USA.

Lorenzo Tomatis [1929-2007] devoted his private and professional life to the betterment of mankind. As a physician, scientist, and humanitarian he championed against the plight of social injustice and promoted the obvious benefits of primary prevention of diseases compared to treatments that prevent or delay disease progression, especially occupational cancers. An avowed student and scholar of literature, the arts, the history of medicine and science, and chemical carcinogenesis, he believed in and wrote about these issues throughout his storied life. Some of his achievements, with excerpts from his writings, especially on primary prevention and on social injustice, are highlighted herein.
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http://dx.doi.org/10.2190/NS.22.1.bDOI Listing
July 2012

Styrene exposure and risk of cancer.

Mutagenesis 2011 Sep 1;26(5):583-4. Epub 2011 Jul 1.

National Institute of Environmental Health Sciences, Research Triangle Park, 111 T.W.Alexander Drive, NC 27709, USA.

Styrene is widely used in the manufacture of synthetic rubber, resins, polyesters and plastics. Styrene and the primary metabolite styrene-7,8-oxide are genotoxic and carcinogenic. Long-term chemical carcinogenesis bioassays showed that styrene caused lung cancers in several strains of mice and mammary cancers in rats and styrene-7,8-oxide caused tumours of the forestomach in rats and mice and of the liver in mice. Subsequent epidemiologic studies found styrene workers had increased mortality or incidences of lymphohematopoietic cancers (leukaemia or lymphoma or all), with suggestive evidence for pancreatic and esophageal tumours. No adequate human studies are available for styrene-7,8-oxide although this is the primary and active epoxide metabolite of styrene. Both are genotoxic and form DNA adducts in humans.
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http://dx.doi.org/10.1093/mutage/ger033DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3165940PMC
September 2011

Primary prevention of cancer.

Authors:
James Huff

Science 2011 May;332(6032):916-7

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http://dx.doi.org/10.1126/science.332.6032.916-bDOI Listing
May 2011

Lorenzo Tomatis and primary prevention of environmental cancer.

Environ Health 2011 Apr 5;10 Suppl 1:S14. Epub 2011 Apr 5.

Ron Melnick Consulting, LLC, 111 Roundtree Rd, Chapel Hill, NC 25514, USA.

The leading 20th century proponent for primary prevention of environmental cancer was Dr. Lorenzo Tomatis, the former Director of the International Agency for Research on Cancer and founder of the IARC Monographs program. This paper is dedicated to the memory of Dr. Tomatis--eminent scientist, scholar, teacher, humanitarian, and public health champion--and includes many perspectives that he promoted throughout his career, with original quotations from some of his scientific writings on primary prevention of environmental cancer. Any attempt by us to simply summarize his views would only detract from the power and logic of his language."Cancer still remains a mainly lethal disease. Primary prevention remains the most relevant approach to reduce mortality through a reduction in incidence".
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http://dx.doi.org/10.1186/1476-069X-10-S1-S14DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3073192PMC
April 2011

Predicting chemicals causing cancer in animals as human carcinogens.

Authors:
James Huff

Occup Environ Med 2010 Oct;67(10):720

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http://dx.doi.org/10.1136/oem.2009.054569DOI Listing
October 2010

Clarifying carcinogenicity of ethylbenzene.

Regul Toxicol Pharmacol 2010 Nov 17;58(2):167-9; discussion 170-2. Epub 2010 Aug 17.

National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA.

Ethylbenzene has been evaluated for carcinogenic activity in Fischer rats and B6C3F1 mice exposed by inhalation (Chan et al., 1998; Chan, 1999) and in Sprague-Dawley rats after oral exposure (Maltoni et al., 1985,1997). Bioassay findings are summarized below to expand on those not stated clearly or completely in Saghir et al. (2010). Overall in these three studies animals exposed to ethylbenzene had increased tumors in rats for kidneys, testes, head (including rare neuroesthesioepitheliomas), and total malignant tumors, whilst in mice tumor incidences were increased in the lung and liver (Huff, 2002). Thus ethylbenzene was carcinogenic by two exposure routes to both sexes of two species of rodents, two strains of rats, and one strain of mice, causing collectively tumors in five different target organs and a composite of "total malignant" tumors.
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http://dx.doi.org/10.1016/j.yrtph.2010.08.011DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2989615PMC
November 2010

The case for a global ban on asbestos.

Environ Health Perspect 2010 Jul 8;118(7):897-901. Epub 2010 Jun 8.

University of California-San Francisco, USA.

Background: All forms of asbestos are now banned in 52 countries. Safer products have replaced many materials that once were made with it. Nonetheless, many countries still use, import, and export asbestos and asbestos-containing products, and in those that have banned other forms of asbestos, the so-called "controlled use" of chrysotile asbestos is often exempted from the ban. In fact, chrysotile has accounted for > 95% of all the asbestos used globally.

Objective: We examined and evaluated the literature used to support the exemption of chrysotile asbestos from the ban and how its exemption reflects the political and economic influence of the asbestos mining and manufacturing industry.

Discussion: All forms of asbestos, including chrysotile, are proven human carcinogens. All forms cause malignant mesothelioma and lung and laryngeal cancers, and may cause ovarian, gastrointestinal, and other cancers. No exposure to asbestos is without risk. Illnesses and deaths from asbestos exposure are entirely preventable.

Conclusions: All countries of the world have an obligation to their citizens to join in the international endeavor to ban the mining, manufacture, and use of all forms of asbestos. An international ban is urgently needed. There is no medical or scientific basis to exempt chrysotile from the worldwide ban of asbestos.
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http://dx.doi.org/10.1289/ehp.1002285DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2920906PMC
July 2010

Occupational cancer and social inequities.

Authors:
James Huff

Eur J Public Health 2011 Feb 6;21(1):129. Epub 2010 Apr 6.

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http://dx.doi.org/10.1093/eurpub/ckq026DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3031345PMC
February 2011

The limits of two-year bioassay exposure regimens for identifying chemical carcinogens.

Environ Health Perspect 2008 Nov 30;116(11):1439-42. Epub 2008 Jun 30.

National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, North Carolina, USA.

Background: Chemical carcinogenesis bioassays in animals have long been recognized and accepted as valid predictors of potential cancer hazards to humans. Most rodent bioassays begin several weeks after birth and expose animals to chemicals or other substances, including workplace and environmental pollutants, for 2 years. New findings indicate the need to extend the timing and duration of exposures used in the rodent bioassay.

Objectives: In this Commentary, we propose that the sensitivity of chemical carcinogenesis bio-assays would be enhanced by exposing rodents beginning in utero and continuing for 30 months (130 weeks) or until their natural deaths at up to about 3 years.

Discussion: Studies of three chemicals of different structures and uses-aspartame, cadmium, and toluene-suggest that exposing experimental animals in utero and continuing exposure for 30 months or until their natural deaths increase the sensitivity of bioassays, avoid false-negative results, and strengthen the value and validity of results for regulatory agencies.

Conclusions: Government agencies, drug companies, and the chemical industry should conduct and compare the results of 2-year bioassays of known carcinogens or chemicals for which there is equivocal evidence of carcinogenicity with longer-term studies, with and without in utero exposure. If studies longer than 2 years and/or with in utero exposure are found to better identify potential human carcinogens, then regulatory agencies should promptly revise their testing guidelines, which were established in the 1960s and early 1970s. Changing the timing and dosing of the animal bioassay would enhance protection of workers and consumers who are exposed to potentially dangerous workplace or home contaminants, pollutants, drugs, food additives, and other chemicals throughout their lives.
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http://dx.doi.org/10.1289/ehp.10716DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2592260PMC
November 2008

Long-term cancer bioassays of ascorbic acid.

Authors:
James Huff

Toxicol Sci 2008 Dec 28;106(2):570-1. Epub 2008 Aug 28.

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http://dx.doi.org/10.1093/toxsci/kfn185DOI Listing
December 2008

More toxin tests needed.

Authors:
James Huff

Science 2008 Feb;319(5864):725-6

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http://dx.doi.org/10.1126/science.319.5864.725DOI Listing
February 2008

Aspartame bioassay findings portend human cancer hazards.

Int J Occup Environ Health 2007 Oct-Dec;13(4):446-8

National Institute of Environmental Health Sciences, Research Triangle Park, NC 27514, USA.

The U.S. Food and Drug Administration (FDA) should reevaluate its position on aspartame as being safe under all conditions. Animal bioassay results predict human cancer risks, and a recent animal study confirms that there is a potential aspartame risk to humans. Aspartame is produced and packaged in China for domestic use and global distribution. Japan, France, and the United States are also major producers. No study of long-term adverse occupational health effects on aspartame workers have been conducted. The FDA should consider sponsoring a prospective epidemiologic study of aspartame workers.
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http://dx.doi.org/10.1179/oeh.2007.13.4.446DOI Listing
January 2008

American College of Occupational and Environmental Medicine (ACOEM): a professional association in service to industry.

Int J Occup Environ Health 2007 Oct-Dec;13(4):404-26

Division of Occupational and Environmental Medicine, University of California School of Medicine, San Francisco, CA 94143-0924, USA.

The American College of Occupational and Environmental Medicine (ACOEM) is a professional association that represents the interests of its company-employed physician members. Fifty years ago the ACOEM began to assert itself in the legislative arena as an advocate of limited regulation and enforcement of occupational health and safety standards and laws, and environmental protection. Today the ACOEM provides a legitimizing professional association for company doctors, and continues to provide a vehicle to advance the agendas of their corporate sponsors. Company doctors in ACOEM recently blocked attempts to have the organization take a stand on global warming. Company doctors employed by the petrochemical industry even blocked the ACOEM from taking a position on particulate air pollution. Industry money and influence pervade every aspect of occupational and environmental medicine. The controlling influence of industry over the ACOEM physicians should cease. The conflict of interests inherent in the practice of occupational and environmental medicine is not resolved by the ineffectual efforts of the ACOEM to establish a pretentious code of conduct. The conflicted interests within the ACOEM have become too deeply embedded to be resolved by merely a self-governing code of conduct. The specialty practice of occupational and environmental medicine has the opportunity and obligation to join the public health movement. If it does, the ACOEM will have no further purpose as it exists, and specialists in occupational and environmental medicine will meet with and be represented by public health associations. This paper chronicles the history of occupational medicine and industry physicians as influenced and even controlled by corporate leaders.
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http://dx.doi.org/10.1179/oeh.2007.13.4.404DOI Listing
January 2008
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