Biomedical subjects
Publications and source records attributed to J M Samet.
Extensive evidence has now accumulated on the health benefits of smoking cessation. With few exceptions, disease risks are reduced following smoking cessation and continue to drop as abstinence is maintained. The review of the evidence in the 1990 Report of the Surgeon General led to major conclusions that establish smoking cessation as a clear priority for health care providers.
Health care availability and living conditions have improved substantially for American Indians in New Mexico over the past quarter century. To investigate the impact of these changes on health statistics, we examined mortality data collected from 1958 to 1987 for American Indians in the state. We analysed the data for all causes of death combined and for specific causes, and compared these data with figures for nonHispanic whites in the state. Age-adjusted mortality rates were calculated for 5-year periods for each ethnic-gender group, using denominators from US Census reports. Mortality rates for all causes combined did not improve significantly for American Indian males from 1958 to 1987, although the rates for American Indian females showed an 8% decline. Infectious disease-related mortality rates for American Indians decreased dramatically over the 30-year study period; however, mortality rates for cancer and diabetes increased over the 30-year period. Mortality rates for injuries and alcoholism among American Indians increased greatly from 1958 to 1977 and then declined later in the study period, but they were consistently higher than rates for whites. The study indicates that several chronic diseases remain of major public health importance for New Mexico's American Indian population.
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Platelet-activating factor (PAF) is a phospholipid with a wide spectrum of pro-inflammatory properties. In the lung, PAF induces airway hyperresponsiveness, neutrophil sequestration, and increased vascular permeability. The alveolar macrophage and the bronchial epithelium are tissues that are exposed to inhaled ozone (O3). We studied the effect of an in vitro O3 exposure on PAF production in a macrophage-like HL60 human cell line (dHL60), a human bronchial epithelial cell line (BEAS S6), and also in primary human bronchial epithelial cells. PAF was quantified by thin-layer chromatographic separation of lipid extracts from cells radiolabeled with [3H]lysoPAF and by radioimmunoassay. In vitro exposure of dHL60 cells to 0.05 to 1.0 ppm O3 for 15 to 120 min was found to significantly increase PAF levels above air control values at all exposure levels and time points (average increase of 92%). Similarly, BEAS S6 cells grown on collagen-coated filter supports and exposed to 0.05 to 1.0 ppm O3 for 60 min released an average increase in PAF of 626% above control values. Primary human bronchial epithelial cells also demonstrated significant increases in [3H]PAF release (average increase of 289% after exposure to 1.0 ppm O3 for 60 min) compared with paired air controls. These findings suggest that some of the effects of O3 inhalation may be mediated by PAF.
Alveolar macrophages (AM) store arachidonic acid (AA), which is esterified in cellular phospholipids until liberated by phospholipase A2 or C after exposure to inflammatory stimuli. After release, there can be subsequent metabolism of AA into various potent, biologically active mediators including prostaglandins and platelet-activating factor (PAF). To examine the possibility that these mediators may account for some of the pathophysiologic alterations seen in the lung after ozone (O3) exposure, human AM were collected by bronchoalveolar lavage of normal subjects, plated into tissue culture dishes, and the adherent cells were incubated with [3H]AA or [3H]lysoPAF. Human AM exposed to 1.0 ppm O3 for 2 hr released 65 +/- 12% more tritium, derived from [3H]AA, than paired, air-exposed controls into media supernatants. In other studies using a similar O3 exposure protocol, there was also a significant increase in human AM prostaglandin E2 production (2.0 +/- 0.5-fold increase above air-exposure values, p less than 0.01, n = 17). In additional studies, using a similar O3 exposure protocol (1.0 ppm for 1 hr), there was also a significant increase in human AM PAF content (1.7 +/- 0.2-fold increase above air-exposure values, p less than 0.02, n = 5). These potent lipid mediators, originally derived from human AM, may play an important role in the mechanisms of O3 lung toxicity.
An epidemiologist and pulmonologist describes the research that links radon to lung cancer. Although radon poses a risk in many parts of the country, internists can assure their patients that a few, simple precautions can reduce the threat in their homes.
The Contribution of Occupational Exposures to Lung Cancer. The overall importance of occupational agents as a cause of lung cancer has been a controversial subject since the 1970s. A federal report, released in the late 1970s, projected a surprisingly high burden of occupational lung cancer; for asbestos and four other agents, from 61,000 to 98,000 cases annually were attributed to these agents alone. Many estimates followed, some much more conservative. For example, Doll and Peto estimated that 15% of lung cancer in men and 5% in women could be attributed to occupational exposures. A number of population-based case-control studies also provide relevant estimates. In a recent literature review, Vineis and Simonato cited attributable risk estimates for occupation and lung cancer that ranged from 4% to 40%; for asbestos alone, the estimates ranged from 1% to 5%. These estimates would be expected to vary across locations and over time. Nevertheless, these recent estimates indicate that occupation remains an important cause of lung cancer. Approaches to Prevention. Prevention of lung cancer mortality among workers exposed to agents or industrial processes that cause lung cancer may involve several strategies, including eliminating or reducing exposures, smoking cessation, screening, and chemo-prevention. For example, changes in industrial processes that have eliminated or reduced exposures to chloromethyl ethers and nickel compounds have provided evidence of reduced risk of lung cancer following these changes. Although occupational exposures are important causes of lung cancer, cigarette smoking is the most important preventable cause of lung cancer. For adults, the work site offers an important location to target smoking cessation efforts. In fact, the work site may be the only place to reach many smokers. As many as 70% of smokers participating in a work site program reported that they would not seek out other programs for smoking cessation. Furthermore, these programs may be as effective as other smoking cessation programs, with abstinence approaching 30%. By creating a supportive social environment, policies restricting smoking in the workplace may also assist smokers trying to quit. Screening of workers at high risk of lung cancer, with periodic chest radiography and sputum cytology, offers potential methods for early detection that may improve prognosis. However, the failure of those procedures to improve outcome from lung cancer among high-risk smokers makes screening of workers of doubtful value. Both epidemiologic and experimental evidence suggest that dietary factors may modify the risk of lung cancer. To date, attention has been focused on vitamin A and carotenoids.(ABSTRACT TRUNCATED AT 400 WORDS)
High rates of cervical cancer were reported in New Mexico in the early 1970s, with especially high rates for minority women. We examined data collected from 1970 to 1987 for invasive cervical cancer and cervical carcinoma in situ for New Mexico's Hispanic, American Indian, and non-Hispanic white women to determine whether changes had occurred in cervical cancer rates since earlier reports. To further characterize the epidemiology of cervical cancer in New Mexico, we reviewed state vital statistics for cervical cancer deaths occurring between 1958 and 1987. From 1970 to 1987, the incidence for invasive cervical cancer among Hispanic (18.9 per 100,000 person-years) and American Indian women (22.0 per 100,000 person-years) was about double that for non-Hispanic white women (10.3 per 100,000). The incidence in each ethnic group decreased over time for both invasive cancer and carcinoma in situ when the data were examined by 2 time periods (1970 to 1978 and 1979 to 1987). These decreases were most dramatic for invasive cervical cancer. Cervical cancer-related death rates for Hispanics and non-Hispanic whites also decreased from 1958 to 1987. Although our data reflect declines in cervical cancer rates during the study period, further rate decreases, especially for minority women, remain an important public health goal in New Mexico.
Radon is ubiquitous in indoor environments. Epidemiologic studies of underground miners with exposure to radon and experimental evidence have established that radon causes lung cancer. The finding that this naturally occurring carcinogen is present in the air of homes and other buildings has raised concern about the lung cancer risk to the general population from radon. I review current approaches for assessing the risk of indoor radon, emphasizing the extrapolation of the risks for miners to the general population. Although uncertainties are inherent in this risk assessment, the present evidence warrants identifying homes that have unacceptably high concentrations.
The focus of public health concern and research in regard to environmental lung diseases has changed across the century. Illustrative agents include radon, indoor asbestos, environmental tobacco smoke, acidic aerosols, and oxidant gases. Tremendous progress has been made in understanding and preventing environmental lung diseases. However, we remain concerned about adverse consequences of breathing polluted outdoor and indoor air. In the persistent concerns about adverse effects of polluted air on the lung, a new emphasis is pervasive; the focus has shifted from avoiding clinical disease among highly exposed individuals to protecting the population from an unacceptable burden of risk. The technique of quantitative risk assessment has become increasingly important for characterizing the safety of environmental agents. The resulting emphasis on the final risk projection and attendant uncertainties may overly emphasize gaps in our knowledge.
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A cohort of 3469 males with at least 1 y of underground uranium mining experience in New Mexico was assembled and mortality followed up through 31 December 1985. The mean and median cumulative exposures for the cohort were 0.39 J h m-3 and 0.12 J h m-3 (111.4 and 35.0 Working Level Months [WLM]), respectively. Overall, mortality in the cohort was significantly increased (standardized mortality ratio [SMR] = 1.1, 95% confidence interval [CI] = 1.02-1.2) relative to the general population of the state. By cause, significant increases were observed for lung cancer (SMR = 4.0, 95% CI 3.1-5.1) and for external causes of death (SMR = 1.5, 95% CI 1.3-1.7). The risk of lung cancer increased for exposure categories above 100 WLM; the excess relative risk increased by 0.5% per mJ h m-3, 95% CI 0.2-1.5 (1.8% per WLM, 95% CI 0.7-5.4). Data were consistent with a multiplicative interaction between smoking and exposure to Rn progeny in an exponential relative risk model. The risk of lung cancer varied substantially with age at observation; the odds ratios rose more steeply with exposure to Rn progeny for those less than age 55 y at observation.
Familial aggregation of ventilatory function has been described in several populations, but the effects of age and cigarette smoking on the extent of aggregation have not been well characterized. We used data from a survey of a Hispanic population in New Mexico to obtain estimates of heritability for FVC and FEV1 as percentages of predicted value. Product-moment correlations for FVC of spouse pairs were 0.18 (n = 90 pairs) if neither smoked, 0.013 (n = 45 pairs) if only the wife smoked, 0.18 (n = 118 pairs) if only the husband smoked, and -0.04 (n = 83 pairs) if both smoked. Correlations for FEV1 of spouse pairs were similar. Because parent-child correlations did not vary with sex, we calculated product-moment correlations from the pooled data. The parent-child correlations for nonsmoking parents with nonsmoking children 6 to 17 yr of age and living in the same house were 0.16 (n = 335 pairs) and 0.17 for FVC and FEV1, respectively. For parents whose children were 25 yr of age or older, the parent-child correlations for those living in different houses were 0.37 (n = 63 pairs) for FVC and 0.40 for FEV1 if neither smoked, and 0.24 (n = 27 pairs) for FVC and 0.14 for FEV1 if both smoked. Heritability estimates, estimated by path analysis, were 0.43 for FVC and 0.42 for FEV1 if neither family member smoked and 0.65 for FVC and 0.44 for FEV1 if both family members smoked. We conclude that there is a moderate degree of heritability of FVC and FEV1 with no substantial change based on age or smoking status.
Indoor air may be contaminated by diverse gaseous and particulate pollutants that may adversely affect health. As a basis for controlling adverse health effects of indoor air pollution, the presence of a hazard needs to be confirmed, and the quantitative relationship between exposure and response needs to be described. Toxicological, clinical, and epidemiological studies represent complementary approaches for obtaining the requisite evidence. The assessment of the effects of complex mixtures poses a difficult challenge for epidemiologists. Understanding the effects of exposure may require accurate assessment of concentrations and personal exposures to multiple agents and analytical approaches that can identify independent effects of single agents and the synergistic or antagonistic effects that may occur in mixtures. The array of epidemiological study designs for this task includes descriptive studies, cohort studies, and case-control studies, each having potential advantages and disadvantages for studying complex mixtures. This presentation considers issues related to exposure assessment and study design for addressing the effects of complex mixtures in indoor air.
The burden of smoking-related disease can be reduced through smoking prevention and cessation. While physicians should counsel all patients who smoke, disease risks are not uniform among smokers. The smokers of the largest numbers of cigarettes are at greatest risk, as are those who started at younger ages. In addition, other factors determined the likelihood of developing a smoking-related disease. Physicians can use the combination of smoking with these additional risk factors to target smokers for intervention, whether education, cessation, or appropriate screening.
Extensive evidence has now accumulated on the health consequences of smoking cessation. With few exceptions, disease risks are reduced after smoking cessation and continue to drop as abstinence is maintained. The review of the evidence in the 1990 Report of the Surgeon General led to major conclusions that establish smoking cessation as a clear priority for health care providers.