Steven Bayard - Academia.edu (original) (raw)

Papers by Steven Bayard

Environmetrics, Jul 1, 1995

This article is a rejoinder to the article by Gross in this issue, in which he claims that 'any r... more This article is a rejoinder to the article by Gross in this issue, in which he claims that 'any range [of estimates of lung cancer deaths attributable to environmental tobacco smoke (ETS)] must encompass an estimate of zero deaths, and that the uncertainties are so great as to cast serious doubt on the use of any quantitative estimate'. The U.S. Environmental Protection Agency's (EPA) conclusion that ETS is a human lung carcinogen was based on the total weight of evidence, not just the 11 U.S. epidemiology studies of ETS and lung cancer that Gross discusses with respect to the population risk estimates. This conclusion was unanimously endorsed by the Agency's independent Scientific Advisory Board and is in concurrence with the conclusions of other organizations. As for the population risk estimates, the EPA report acknowledges uncertainties in these estimates. However, we maintain that the estimate of 3000 lung cancer deaths per year in U.S. non-smokers is a reasonable point estimate. Furthermore, we have relatively high confidence in this estimate compared to cancer risk estimates for other environmental pollutants, because it is based on human data from actual environmental exposure levels.

Risk Analysis, Jun 1, 1995

Journal of Clinical Epidemiology, Apr 1, 1994

Tobacco Control, Sep 1, 1994

ABSTRACT This document describes the basic principles and assumptions associated with a qualitati... more ABSTRACT This document describes the basic principles and assumptions associated with a qualitative and quantitative carcinogenic risk assessment and illustrates these features using several examples of quantitative risk assessment done by State and local agencies. The report is intended to help readers better understand and interpret a risk assessment rather than to provide instructions that would enable them to conduct a risk assessment. The report is aimed at managers and staff members in State and local agencies who are concerned with the use of qualitative and quantitative carcinogenic risk assessment for evaluating emissions of toxic air pollutants. The report discusses the four steps of risk assessment: hazard identification, dose-response assessment, exposure assessment, and risk characterization, focusing primarily on the dose-response assessment.

Risk Analysis, Feb 1, 1995

After an extensive review and analysis of the scientific evidence on the respiratory health effec... more After an extensive review and analysis of the scientific evidence on the respiratory health effects of passive smoking, the U.S. Environmental Protection Agency concluded that environmental tobacco smoke causes lung cancer in adult nonsmokers and increases the risk of a variety of noncancer respiratory disorders, especially in children. This article is a response to claims in Dr. Gio Gori's article "Policy Against Science: The Case of Environmental Tobacco Smoke," appearing in the same issue of this journal, that such conclusions are unwarranted. This response focuses only on the respiratory health effects of environmental tobacco smoke.

Risk Analysis, Jun 1, 1996

Journal of AOAC INTERNATIONAL, 1976

New methods or modifications of currently used methods in aspiration toxicology must be capable o... more New methods or modifications of currently used methods in aspiration toxicology must be capable of accurately assessing the hazard and toxicity potentials of those products which are capable of being aspirated. The methods evaluated in the rat were intratracheal injections, intravenous injections, and modifications of the Gerarde technique. A product containing petroleum distillates and a standard viscosity petroleum distillate sample were administered to Osborne-Mendel rats, rabbits, and guinea pigs in ml/kg doses. The utility of the methods was determined by comparing lung weight increases, lung-body weight ratios, gross pathological lung changes, and mortality. The modified Gerarde technique showed the best potential for predicting aspiration hazard and toxicity based on the severity of the reactions which, using a radiolabeled oil, was shown to be a function of the amount of product which enters and reacts with the lungs. The influence of preventing the swallowing reflex to assu...

ABSTRACT This document describes the basic principles and assumptions associated with a qualitati... more ABSTRACT This document describes the basic principles and assumptions associated with a qualitative and quantitative carcinogenic risk assessment and illustrates these features using several examples of quantitative risk assessment done by State and local agencies. The report is intended to help readers better understand and interpret a risk assessment rather than to provide instructions that would enable them to conduct a risk assessment. The report is aimed at managers and staff members in State and local agencies who are concerned with the use of qualitative and quantitative carcinogenic risk assessment for evaluating emissions of toxic air pollutants. The report discusses the four steps of risk assessment: hazard identification, dose-response assessment, exposure assessment, and risk characterization, focusing primarily on the dose-response assessment.

Health laboratory science, 1974

Health laboratory science, 1974

New information on cytotoxicity, genotoxicity, and epidemiology has raised some questions about t... more New information on cytotoxicity, genotoxicity, and epidemiology has raised some questions about the federal regulatory agencies' cancer risk assessments for dichloromethane (DCM, methylene chloride). In addition, physiologically based pharmacokinetic models have been developed, showing that tissue-level delivery of metabolically activated DCM may be disproportionately reduced at low exposure levels. These studies suggest to some that the clear carcinogenic response seen

Risk Analysis, 1998

We model nicotine from environmental tobacco smoke (ETS) in office air and salivary cotinine in n... more We model nicotine from environmental tobacco smoke (ETS) in office air and salivary cotinine in nonsmoking U.S. workers. We estimate that: an average salivary cotinine level of 0.4 ng/ml corresponds to an increased lifetime mortality risk of 1/1000 for lung cancer, and 1/100 for heart disease; >95% of ETS-exposed office workers exceed OSHA's significant risk level for heart disease mortality, and 60% exceed significant risk for lung cancer mortality; 4000 heart disease deaths and 400 lung cancer deaths occur annually among office workers from passive smoking in the workplace, at the current 28% prevalence of unrestricted smoking in the office workplace.

Lung Cancer, 1995

After an extensive review and analysis of the scientific evidence on the respiratory health effec... more After an extensive review and analysis of the scientific evidence on the respiratory health effects of passive smoking, the U.S. Environmental Protection Agency concluded that environmental tobacco smoke causes lung cancer in adult nonsmokers and increases the risk of a variety of noncancer respiratory disorders, especially in children. This article is a response to claims in Dr. Gio Gori's article "Policy Against Science: The Case of Environmental Tobacco Smoke," appearing in the same issue of this journal, that such conclusions are unwarranted. This response focuses only on the respiratory health effects of environmental tobacco smoke.

Journal of Clinical Epidemiology, 1994

After an extensive review and assessment of the scientific evidence on the respiratory health eff... more After an extensive review and assessment of the scientific evidence on the respiratory health effects of passive smoking, the U.S. Environmental Protection Agency has determined that the widespread exposure to environmental tobacco smoke in the United States presents a serious and substantial public health impact. The Environmental Protection Agency concluded that environmental tobacco smoke causes lung cancer in adult nonsmokers and increases the risk for a variety of noncancer respiratory disorders, especially in children. This article reviews evidence presented in the Environmental Protection Agency's 1992 report on the respiratory health effects of passive smoking and responds to critical allegations levied by Gio Gori in his article "Science, policy, and ethics: the case of environmental tobacco smoke", appearing in the same issue of this journal. Several recent studies appearing since the cutoff date for inclusion in the EPA report are also discussed. Environmental tobacco smoke Passive smoking Lung cancer Respiratory effects Sudden infant death syndrome Asthma nia. The report estimates that 150,000 to 300,000 cases annually in infants and young children up to 18 months of age are attributable to ETS. CE 4714-B 339 340 JENNIFER JINOT and STEVEN BAYARD ?? ETS exposure is causally associated with cancer, and (3) noncancer respiratory effects. increased prevalence of fluid in the middle This article does not discuss cardiovascular ear, symptoms of upper respiratory tract disease, sick building syndrome, or any other irritation, and a small but significant reissues addressed by Gori that were beyond the duction in lung function. scope of the EPA assessment. ?? ETS exposure is causally associated with additional episodes and increased severity of symptoms in children with asthma. The report estimates that 400,000 to l,OOO,OOO asthmatic childen have their condition worsened by exposure to ETS. ?? ETS exposure is a risk factor for new cases of asthma in childen who have not previously displayed symptoms. The report estimates that ETS may be responsible for 800&26,000 new cases annually. 'A priori probability of significant (p c 0.05) test of effect when true relative risk is 1.5. *RR used for cohort studies [44,46]; OR used for case-control studies. 'One-sided p-value for test of RR = I vs RR > I. +'Relative risks corrected for smoker misclassification. 5RR shown is for all cell types with the two control groups combined. 6Years of exposure as adult (spousal plus workplace). 'Relative risks not corrected for smoker misclassification. *Data not available.

Journal of Clinical Epidemiology, 1994

Human and Ecological Risk Assessment: An International Journal, 2002

The recent advances in biological research, biochemical techniques, molecular epidemiology, biost... more The recent advances in biological research, biochemical techniques, molecular epidemiology, biostatisticalj mathematical methods, and computational power provide opportunities for considerable improvement in the assessment of dose response relationships for risk assessment. This paper describes the discussion and results of a one-day meeting of thineen invited participants (listed as authors) of a dose response workgroup and several additional attending experts in dose response modeling. The workgroup meeting was pan of a three-day workshop exploring research possibilities to improve risk assessments done to suppon occupational and environmental health policies and standards. The charge to the panicipants of the workgroup was to identify five specific research areas that would significantly improve dose response modeling for occupational and environmental risk assessment. Each invited participant was asked to prepare a brief description of research programs that could be the subject of a request for proposals. Table shows titles and authors of each initial written proposal. This paper draws from the proposal writeups, often verbatim, to describe the areas of research the workgroup found most promising. The dose-response workgroup meeting proceeded in three stages. First proposals were soned into broad topic areas, and then each proposal was presented and discussed. Additional topic areas and ideas for proposals were then solicited from the group. Next there was an extended period during which the individual propoã ls were further refined, extended, and consolidated, into ten groups. Finally, each participant was asked to rank the proposal groups giving five points to the top choice in terms of desirability for funding, four for the second choice, three for the third, two for the fourth, one for the fifth and zero for the remaining fIVe proposal groups. In all, thineen people participated in this ranking exercise. The ten areas the group chose to explore, in ranked order are given in Table . Some proposals benefited by the multiplicity of ideas attached within the various groups-and the process of grouping is the principal reason why there is not a oneto-one mapping of the initial proposals listed in Table to the final ranked items in Table . The groupings may well have been a disadvantage to some of the 1422

Environmetrics, Jul 1, 1995

This article is a rejoinder to the article by Gross in this issue, in which he claims that 'any r... more This article is a rejoinder to the article by Gross in this issue, in which he claims that 'any range [of estimates of lung cancer deaths attributable to environmental tobacco smoke (ETS)] must encompass an estimate of zero deaths, and that the uncertainties are so great as to cast serious doubt on the use of any quantitative estimate'. The U.S. Environmental Protection Agency's (EPA) conclusion that ETS is a human lung carcinogen was based on the total weight of evidence, not just the 11 U.S. epidemiology studies of ETS and lung cancer that Gross discusses with respect to the population risk estimates. This conclusion was unanimously endorsed by the Agency's independent Scientific Advisory Board and is in concurrence with the conclusions of other organizations. As for the population risk estimates, the EPA report acknowledges uncertainties in these estimates. However, we maintain that the estimate of 3000 lung cancer deaths per year in U.S. non-smokers is a reasonable point estimate. Furthermore, we have relatively high confidence in this estimate compared to cancer risk estimates for other environmental pollutants, because it is based on human data from actual environmental exposure levels.

Risk Analysis, Jun 1, 1995

Journal of Clinical Epidemiology, Apr 1, 1994

Tobacco Control, Sep 1, 1994

ABSTRACT This document describes the basic principles and assumptions associated with a qualitati... more ABSTRACT This document describes the basic principles and assumptions associated with a qualitative and quantitative carcinogenic risk assessment and illustrates these features using several examples of quantitative risk assessment done by State and local agencies. The report is intended to help readers better understand and interpret a risk assessment rather than to provide instructions that would enable them to conduct a risk assessment. The report is aimed at managers and staff members in State and local agencies who are concerned with the use of qualitative and quantitative carcinogenic risk assessment for evaluating emissions of toxic air pollutants. The report discusses the four steps of risk assessment: hazard identification, dose-response assessment, exposure assessment, and risk characterization, focusing primarily on the dose-response assessment.

Risk Analysis, Feb 1, 1995

After an extensive review and analysis of the scientific evidence on the respiratory health effec... more After an extensive review and analysis of the scientific evidence on the respiratory health effects of passive smoking, the U.S. Environmental Protection Agency concluded that environmental tobacco smoke causes lung cancer in adult nonsmokers and increases the risk of a variety of noncancer respiratory disorders, especially in children. This article is a response to claims in Dr. Gio Gori's article "Policy Against Science: The Case of Environmental Tobacco Smoke," appearing in the same issue of this journal, that such conclusions are unwarranted. This response focuses only on the respiratory health effects of environmental tobacco smoke.

Risk Analysis, Jun 1, 1996

Journal of AOAC INTERNATIONAL, 1976

New methods or modifications of currently used methods in aspiration toxicology must be capable o... more New methods or modifications of currently used methods in aspiration toxicology must be capable of accurately assessing the hazard and toxicity potentials of those products which are capable of being aspirated. The methods evaluated in the rat were intratracheal injections, intravenous injections, and modifications of the Gerarde technique. A product containing petroleum distillates and a standard viscosity petroleum distillate sample were administered to Osborne-Mendel rats, rabbits, and guinea pigs in ml/kg doses. The utility of the methods was determined by comparing lung weight increases, lung-body weight ratios, gross pathological lung changes, and mortality. The modified Gerarde technique showed the best potential for predicting aspiration hazard and toxicity based on the severity of the reactions which, using a radiolabeled oil, was shown to be a function of the amount of product which enters and reacts with the lungs. The influence of preventing the swallowing reflex to assu...

ABSTRACT This document describes the basic principles and assumptions associated with a qualitati... more ABSTRACT This document describes the basic principles and assumptions associated with a qualitative and quantitative carcinogenic risk assessment and illustrates these features using several examples of quantitative risk assessment done by State and local agencies. The report is intended to help readers better understand and interpret a risk assessment rather than to provide instructions that would enable them to conduct a risk assessment. The report is aimed at managers and staff members in State and local agencies who are concerned with the use of qualitative and quantitative carcinogenic risk assessment for evaluating emissions of toxic air pollutants. The report discusses the four steps of risk assessment: hazard identification, dose-response assessment, exposure assessment, and risk characterization, focusing primarily on the dose-response assessment.

Health laboratory science, 1974

Health laboratory science, 1974

New information on cytotoxicity, genotoxicity, and epidemiology has raised some questions about t... more New information on cytotoxicity, genotoxicity, and epidemiology has raised some questions about the federal regulatory agencies' cancer risk assessments for dichloromethane (DCM, methylene chloride). In addition, physiologically based pharmacokinetic models have been developed, showing that tissue-level delivery of metabolically activated DCM may be disproportionately reduced at low exposure levels. These studies suggest to some that the clear carcinogenic response seen

Risk Analysis, 1998

We model nicotine from environmental tobacco smoke (ETS) in office air and salivary cotinine in n... more We model nicotine from environmental tobacco smoke (ETS) in office air and salivary cotinine in nonsmoking U.S. workers. We estimate that: an average salivary cotinine level of 0.4 ng/ml corresponds to an increased lifetime mortality risk of 1/1000 for lung cancer, and 1/100 for heart disease; >95% of ETS-exposed office workers exceed OSHA's significant risk level for heart disease mortality, and 60% exceed significant risk for lung cancer mortality; 4000 heart disease deaths and 400 lung cancer deaths occur annually among office workers from passive smoking in the workplace, at the current 28% prevalence of unrestricted smoking in the office workplace.

Lung Cancer, 1995

After an extensive review and analysis of the scientific evidence on the respiratory health effec... more After an extensive review and analysis of the scientific evidence on the respiratory health effects of passive smoking, the U.S. Environmental Protection Agency concluded that environmental tobacco smoke causes lung cancer in adult nonsmokers and increases the risk of a variety of noncancer respiratory disorders, especially in children. This article is a response to claims in Dr. Gio Gori's article "Policy Against Science: The Case of Environmental Tobacco Smoke," appearing in the same issue of this journal, that such conclusions are unwarranted. This response focuses only on the respiratory health effects of environmental tobacco smoke.

Journal of Clinical Epidemiology, 1994

After an extensive review and assessment of the scientific evidence on the respiratory health eff... more After an extensive review and assessment of the scientific evidence on the respiratory health effects of passive smoking, the U.S. Environmental Protection Agency has determined that the widespread exposure to environmental tobacco smoke in the United States presents a serious and substantial public health impact. The Environmental Protection Agency concluded that environmental tobacco smoke causes lung cancer in adult nonsmokers and increases the risk for a variety of noncancer respiratory disorders, especially in children. This article reviews evidence presented in the Environmental Protection Agency's 1992 report on the respiratory health effects of passive smoking and responds to critical allegations levied by Gio Gori in his article "Science, policy, and ethics: the case of environmental tobacco smoke", appearing in the same issue of this journal. Several recent studies appearing since the cutoff date for inclusion in the EPA report are also discussed. Environmental tobacco smoke Passive smoking Lung cancer Respiratory effects Sudden infant death syndrome Asthma nia. The report estimates that 150,000 to 300,000 cases annually in infants and young children up to 18 months of age are attributable to ETS. CE 4714-B 339 340 JENNIFER JINOT and STEVEN BAYARD ?? ETS exposure is causally associated with cancer, and (3) noncancer respiratory effects. increased prevalence of fluid in the middle This article does not discuss cardiovascular ear, symptoms of upper respiratory tract disease, sick building syndrome, or any other irritation, and a small but significant reissues addressed by Gori that were beyond the duction in lung function. scope of the EPA assessment. ?? ETS exposure is causally associated with additional episodes and increased severity of symptoms in children with asthma. The report estimates that 400,000 to l,OOO,OOO asthmatic childen have their condition worsened by exposure to ETS. ?? ETS exposure is a risk factor for new cases of asthma in childen who have not previously displayed symptoms. The report estimates that ETS may be responsible for 800&26,000 new cases annually. 'A priori probability of significant (p c 0.05) test of effect when true relative risk is 1.5. *RR used for cohort studies [44,46]; OR used for case-control studies. 'One-sided p-value for test of RR = I vs RR > I. +'Relative risks corrected for smoker misclassification. 5RR shown is for all cell types with the two control groups combined. 6Years of exposure as adult (spousal plus workplace). 'Relative risks not corrected for smoker misclassification. *Data not available.

Journal of Clinical Epidemiology, 1994

Human and Ecological Risk Assessment: An International Journal, 2002

The recent advances in biological research, biochemical techniques, molecular epidemiology, biost... more The recent advances in biological research, biochemical techniques, molecular epidemiology, biostatisticalj mathematical methods, and computational power provide opportunities for considerable improvement in the assessment of dose response relationships for risk assessment. This paper describes the discussion and results of a one-day meeting of thineen invited participants (listed as authors) of a dose response workgroup and several additional attending experts in dose response modeling. The workgroup meeting was pan of a three-day workshop exploring research possibilities to improve risk assessments done to suppon occupational and environmental health policies and standards. The charge to the panicipants of the workgroup was to identify five specific research areas that would significantly improve dose response modeling for occupational and environmental risk assessment. Each invited participant was asked to prepare a brief description of research programs that could be the subject of a request for proposals. Table shows titles and authors of each initial written proposal. This paper draws from the proposal writeups, often verbatim, to describe the areas of research the workgroup found most promising. The dose-response workgroup meeting proceeded in three stages. First proposals were soned into broad topic areas, and then each proposal was presented and discussed. Additional topic areas and ideas for proposals were then solicited from the group. Next there was an extended period during which the individual propoã ls were further refined, extended, and consolidated, into ten groups. Finally, each participant was asked to rank the proposal groups giving five points to the top choice in terms of desirability for funding, four for the second choice, three for the third, two for the fourth, one for the fifth and zero for the remaining fIVe proposal groups. In all, thineen people participated in this ranking exercise. The ten areas the group chose to explore, in ranked order are given in Table . Some proposals benefited by the multiplicity of ideas attached within the various groups-and the process of grouping is the principal reason why there is not a oneto-one mapping of the initial proposals listed in Table to the final ranked items in Table . The groupings may well have been a disadvantage to some of the 1422