Philip Witorsch

Lung Cancer Risk in White and Black Americans

PURPOSE To test whether differences in smoking-related lung cancer risks in blacks and whites can explain why lung cancer incidence is greater in black males than in white males but about equal in black and white females, given that a greater proportion of blacks are smokers, but smoke far fewer cigarettes per day than do whites. METHODS A hospital-based case-control study was conducted between 1984 and 1998 that included interviews with 1,710 white male and 1,321 white female cases of histologically confirmed lung cancer, 254 black male and 163 black female cases, and 8,151 controls. Relative risks were estimated via odds ratios using logistic regression, adjusted for age, education, and body mass index. RESULTS We confirmed prior reports that smoking prevalence is higher but overall dosage is lower among blacks. Overall ORs were similar for blacks and whites, except among the heaviest smoking males (21+ cigarettes per day or 37.5 pack-years), in whom ORs for blacks were considerably greater than for whites. Long-term benefits of cessation were similar for white and black ex-smokers. Smokers of menthol flavored cigarettes were at no greater risk for lung cancer than were smokers of unflavored brands. CONCLUSIONS Lung cancer risks were similar for whites and blacks with similar smoking habits, except possibly for blacks who were very heavy smokers; this sub-group is unusual in the general population of African American smokers. Explanations of racial disparities in lung cancer risk may need to account for modifying factors including type of cigarette (yield, mentholation), diet, occupation, and host factors such as ability to metabolize mainstream smoke carcinogens.

Review : Environmental Tobacco Smoke and Respiratory Health in Children: A Critical Review and Analysis of the Literature from 1969 to 19981

This analysis of parental/household smoking (a surro gate for environmental tobacco smoke, ETS) and respira tory symptoms and disease in children updates an ear lier analysis. Some 94 studies of preschool children and 152 studies of school-age or older children published between 1969 and 1998 were examined. Both analyses have shown an age dependency in the relationship between parental/household smoking and respiratory symptoms and disease in children. A statistically signifi cant, though moderate, relationship between parental/ household smoking and respiratory illness was ob served in most (86%) of the studies in preschool chil dren. While almost two thirds (98 of 152) of the studies of school-age children showed a statistically significant re lationship between parental/household smoking and re spiratory symptoms and disease, there was a general lack of consistency of statistical association for specific respiratory endpoints (e.g., asthma, wheeze, bronchitis,

Review : Effects of Environmental Tobacco Smoke Exposure on Pulmonary Function and Respiratory Health in Adults: Update 1997

Eighteen epidemiology studies have examined the relationship between chronic environmental tobacco smoke (ETS) exposure and pulmonary func tion. A statistically significant relationship between chronic ETS exposure and a specific spirometric endpoint was reported in 5 of 17 studies that measured forced expiratory volume in 1 s (FEV1), 2 of 9 studies that measured forced vital capacity (FVC) and 3 of 5 studies that measured mean forced expiratory flow during the middle half of the FVC. Fourteen of 24 epidemiological stud ies report a statistically significant association between chronic ETS exposure and a clinical endpoint, although there is little consistency from one report to the next when a specific endpoint is considered. A statistically significant asso ciation was reported in 2 of 9 studies for cough, 3 of 9 studies for phlegm and expectoration, 6 of 10 studies for dyspnea and shortness of breath, 3 of 6 stud ies for bronchitis, and 8 of 18 studies dealing with asthma incidence, exacerba tion, or symptoms. The inconsistency of association in the foregoing function al and clinical epidemiology studies could either reflect absence of such an association or methodology problems such as reliability of spirometric mea surement, lack of verification of clinical endpoint, errors in classification of smoking and ETS exposure status and inappropriate control of confounding variables. The effects of acute ETS exposure (at levels equivalent to or exceed ing real-life smoke-polluted environments) have been examined in experimen tal studies in which spirometric measures were obtained prior to, during, and after exposure of subjects to machine-generated tobacco smoke. Six of seven studies suggest that acute ETS exposure, while serving as an irritant to the upper respiratory tract, fails adversely to affect pulmonary function of normal adults. The effect of acute ETS exposure in asthmatic subjects has been exam ined in 15 studies. These studies suggest that acute exposure to ETS does not consistently evoke adverse pulmonary effects in most asthmatics. Several studies from a single research group suggest that a small sub-set of asthmatics may respond to acute ETS exposure with a ≥20% decrement in FEV1 as well as an increased responsiveness to bronchoconstrictors. The mechanism for this responsiveness does not appear to be allergic in nature and is subject to speculation.

Cognitive dysfunction in a patient with long-term occupational exposure to ethylene oxide : role of ethylene oxide as a causal factor

This case illustrates a comprehensive approach to assessing causality in a woman with apparent cognitive dysfunction, as measured by neuropsychological testing, and a 10-year history of occupational exposure to ethylene oxide. The analysis included a multidisciplinary examination of the patient, which took place several years after the termination of her exposure. In addition, all of the patients prior medical and psychiatric records were reviewed, as were the records of her employer to ascertain her exposure history. Our evaluation revealed a pattern of neuropsychological findings not consistent with nervous system damage secondary to an organic effect of ethylene oxide. A more likely causal hypothesis is adopted: the patients apparent cognitive dysfunction had a psychiatric etiology. This case also illustrates the potential impact of a patients involvement in legal proceedings related to claims of neurocognitive dysfunction.

Environmental Tobacco Smoke and Birthweight of Offspring: A Critical Review and Analysis of the Epidemiological Literature:

Forty papers on the association between environmental tobacco smoke (ETS) exposure of the mother and low birthweight of offspring were examined from the point of view of experimental design, criteria for ETS exposure, sample size, methods of statistical analysis, individual confounders considered, spe cific endpoints, and outcome. An approximately equal number of studies employed either the prospective or retrospective design, with very few using the case-control design. The vast majority of studies used a surrogate for ETS exposure (mainly paternal smoking), without verification of such exposure with a biochemical marker. The sample sizes of the studies ranged from under 100 subjects to almost 25,000 subjects. Most studies employed regression analysis. A considerable variation from study to study was noted in the treat ment of potential confounding variables and most studies considered relative ly few of these. Most of the individual confounding variables were considered in a relatively small proportion (one third or less) of the studies. The majority (almost two thirds) of the studies failed to demonstrate a statistically signifi cant association between ETS exposure of the pregnant woman and low birth weight. This general lack of consistency of association could reflect absence of an adverse effect of ETS or methodologic difficulties such as misclassification error, type II error, recall bias, or inadequate adjustment for potential con founders.

Acute Inhalation Lung Disease

A vast number of chemicals may cause acute injury and disease when inhaled. This may be the result of direct injury to the respiratory tract or secondary to the accumulation of toxic levels in the blood after absorption through the respiratory portal of entry. Such chemicals are encountered in a wide variety of occupational, avocational, and accidental settings (Table 1). Any acute injury or disease produced will be determined by the specific chemical properties of the gas or combination of gases inhaled, the presence or absence of particulate materials, the concentration of the toxic substances(s), the conditions of exposure, and the presence of underlying conditions in the exposed individual.