Biomedical subjects
D Ozonoff
Publications and source records attributed to D Ozonoff.
Tetrachloroethylene-contaminated drinking water in Massachusetts and the risk of colon-rectum, lung, and other cancers.
We conducted a population-based case-control study to evaluate the relationship between cancer of the colon-rectum (n = 326), lung (n = 252), brain (n = 37), and pancreas (n = 37), and exposure to tetrachloroethylene (PCE) from public drinking water. Subjects were exposed to PCE when it leached from the vinyl lining of drinking-water distribution pipes. Relative delivered dose of PCE was estimated using a model that took into account residential location, years of residence, water flow, and pipe characteristics. Adjusted odds ratios (ORs) for lung cancer were moderately elevated among subjects whose exposure level was above the 90th percentile whether or not a latent period was assumed [ORs and 95% confidence intervals (CIs), 3.7 (1.0-11.7), 3.3 (0.6-13.4), 6.2 (1.1-31.6), and 19.3 (2.5-141.7) for 0, 5, 7, and 9 years of latency, respectively]. The adjusted ORs for colon-rectum cancer were modestly elevated among ever-exposed subjects as more years of latency were assumed [OR and CI, 1.7 (0.8-3.8) and 2.0 (0.6-5.8) for 11 and 13 years of latency, respectively]. These elevated ORs stemmed mainly from associations with rectal cancer. Adjusted ORs for rectal cancer among ever-exposed subjects were more elevated [OR and CI, 2.6 (0. 8-6.7) and 3.1 (0.7-10.9) for 11 and 13 years of latency, respectively] than were corresponding estimates for colon cancer [OR and CI, 1.3 (0.5-3.5) and 1.5 (0.3-5.8) for 11 and 13 years of latency, respectively]. These results provide evidence for an association between PCE-contaminated public drinking water and cancer of the lung and, possibly, cancer of the colon-rectum.
Health status of Persian Gulf War veterans: self-reported symptoms, environmental exposures and the effect of stress.
BACKGROUND: Most US troops returned home from the Persian Gulf War (PGW) by Spring 1991 and many began reporting increased health symptoms and medical problems soon after. This investigation examines the relationships between several Gulf-service environmental exposures and health symptom reporting, and the role of traumatic psychological stress on the exposure-health symptom relationships. METHODS: Stratified, random samples of two cohorts of PGW veterans, from the New England area (n = 220) and from the New Orleans area (n = 71), were selected from larger cohorts being followed longitudinally since arrival home from the Gulf. A group of PGW-era veterans deployed to Germany (n = 50) served as a comparison group. The study protocol included questionnaires, a neuropsychological test battery, an environmental interview, and psychological diagnostic interviews. This report focuses on self-reported health symptoms and exposures of participants who completed a 52-item health symptom checklist and a checklist of environmental exposures. RESULTS: The prevalence of reported symptoms was greater in both Persian Gulf-deployed cohorts compared to the Germany cohort. Analyses of the body-system symptom scores (BSS), weighted to account for sampling design, and adjusted by age, sex, and education, indicated that Persian Gulf-deployed veterans were more likely to report neurological, pulmonary, gastrointestinal, cardiac, dermatological, musculoskeletal, psychological and neuropsychological system symptoms than Germany veterans. Using a priori hypotheses about the toxicant effects of exposure to specific toxicants, the relationships between self-reported exposures and body-system symptom groupings were examined through multiple regression analyses, controlling for war-zone exposure and post-traumatic stress disorder (PTSD). Self-reported exposures to pesticides, debris from Scuds, chemical and biological warfare (CBW) agents, and smoke from tent heaters each were significantly related to increased reporting of specific predicted BSS groupings. CONCLUSIONS: Veterans deployed to the Persian Gulf have higher self-reported prevalence of health symptoms compared to PGW veterans who were deployed only as far as Germany. Several Gulf-service environmental exposures are associated with increased health symptom reporting involving predicted body-systems, after adjusting for war-zone stressor exposures and PTSD.
Tetrachloroethylene-contaminated drinking water and the risk of breast cancer.
We conducted a population-based case-control study to evaluate the relationship between cases of breast cancer and exposure to tetrachloroethylene (PCE) from public drinking water ( n = 258 cases and 686 controls). Women were exposed to PCE when it leached from the vinyl lining of water distribution pipes. The relative delivered dose was estimated using an algorithm that accounted for residential history, water flow, and pipe characteristics. Only small increases in breast cancer risk were seen among ever-exposed women either when latency was ignored or when 5 to 15 years of latency was considered. No or small increases were seen among highly exposed women either when latency was ignored or when 5 years of latency was considered. However, the adjusted odds ratios (ORs) were more increased for highly exposed women when 7 and 9 years of latency, respectively, were considered (OR 1.5 95% CI 0.5-4.7 and OR 2.3, 95% CI 0.6-8.8 for the 75th percentile, and OR 2.7, 95% CI 0.4-15.8 and OR 7.6, 95% CI 0.9-161.3 for the 90th percentile). The number of highly exposed women was too small for meaningful analysis when more years of latency were considered. Because firm conclusions from these data are limited, we recently undertook a new study with a large number of more recently diagnosed cases.
Cancer risk and residential proximity to cranberry cultivation in Massachusetts.
OBJECTIVES: This study evaluated the relationship between cancer risk and residential proximity to cranberry cultivation. METHODS: A population-based case-control study was conducted. Cases, diagnosed during 1983 through 1986 among residents of the Upper Cape Cod area of Massachusetts, involved incident cancers of the lung (n = 252), breast (n = 265), colon-rectum (n = 326), bladder (n = 63), kidney (n = 35), pancreas (n = 37), and brain (n = 37), along with leukemia (n = 35). Control subjects were randomly selected from among telephone subscribers (n = 184), Medicare beneficiaries (n = 464), and deceased individuals (n = 723). RESULTS: No meaningful increases in risk were seen for any of the cancer sites except for the brain. When latency was considered, subjects who had ever lived within 2600 ft (780 m) of a cranberry bog had a twofold increased risk of brain cancer overall (95% confidence interval [CI] = 0.8, 4.9) and a 6.7-fold increased risk of astrocytoma (95% CI = 1.6, 27.8). CONCLUSIONS: Residential proximity to cranberry bog cultivation was not associated with seven of the eight cancers investigated; however, an association was observed with brain cancer, particularly astrocytoma. Larger, more detailed studies are necessary to elucidate this relationship.
Environmental medicine for all: getting there form here.
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Carboxyhemoglobin levels in patients with cocaine-related chest pain.
Carboxyhemoglobin (COHb) levels were measured in patients who came to an emergency department complaining of acute chest pain. For subjects not receiving prior oxygen therapy, those with cocaine-related chest pain (n = 10) had a higher mean COHb level than a comparison group (n = 28) with nonischemic chest pain (4.50 +/- 2.40 vs 2.73 +/- 0.66; p < 0.05). Four of the seven (57 percent) who smoked crack had COHb levels greater than 4.5 percent, while only one of six (17 percent) smokers of only tobacco had such a level. These findings suggest an additional mechanism, the formation of COHb, which could aggravate cocaine-induced cardiotoxicity.
Compliance with EPA guidelines for follow-up testing and mitigation after radon screening measurements.
A survey was taken of 314 individuals, 55 of whom had residences that exceeded the EPA action level of 148 Bq m-3 (4 pCi L-1) of radon as measured by a medical center radon testing service. The survey was designed to assess whether these individuals followed the 1986 EPA guidelines for follow-up testing and mitigation. The survey indicated 41% of respondents performed follow-up tests and 16% of the respondents performed some form of mitigation. Some respondents had performed mitigation after inadequate or no follow-up radon tests. There was a positive relationship between follow-up testing and mitigation and higher initial radon screening values.
Trihalomethanes and maximum contaminant levels: the significance of inhalation and dermal exposures to chloroform in household water.
Our review of the literature on the importance of inhalation and dermal exposures to volatile organic compounds in household water relative to ingestion exposures sought to answer two questions. First, how well do the inhalation and dermal doses predicted by simple models, complex simulations, and measurements agree with one another? And second, what are the implications for the cancer risk from chloroform in household water? The literature yields a coherent and credible range of dose estimates: the ratio of lifetime inhalation dose to lifetime ingestion dose is probably in the range of approximately 0.6 to approximately 1.5, but may be as high as approximately 5.7; and the ratio of lifetime dermal dose to lifetime ingestion dose is probably about approximately 0.3, but may be as high as approximately 1.8. However, because the U.S. Environmental Protection Agency's (EPA's) Cancer Potency Factor (CPF) for inhalation of chloroform is much higher than the CPF for ingestion, the ratios of incremental lifetime cancer risk from inhalation of chloroform to risk from ingestion are much larger than the corresponding ratios for dose. The incremental lifetime cancer risk from chloroform by all three pathways is probably approximately 9 to approximately 21 times the ingestion risk and may be as much as approximately 79 times the ingestion risk. As the EPA reviews the drinking water standard for total trihalomethanes, it is essential that the Agency take account of all exposure pathways in estimating cancer risk.
Epidemiologic approaches to assessing human cancer risk from consuming aquatic food resources from chemically contaminated water.
Epidemiologic approaches to assessing human cancer risk from consuming fish from contaminated waters must confront the problems of long latency and rarity of the end point (cancer). The latency problem makes determination of diet history more difficult, while the low frequency of cancer as an end point reduces the statistical power of the study. These factors are discussed in relation to the study designs most commonly employed in epidemiology. It is suggested that the use of biomarkers for persistent chemicals may be useful to mitigate the difficulty of determining exposure, while the use of more prevalent and timely end points, such as carcinogen-DNA adducts or oncogene proteins, may make the latency and rarity problems more tractable.
Unusual lymphocyte subset distribution in some depressed patients.
Depression has been previously associated with immunologic dysfunction. The lymphocyte subsets of 10 patients with major depression were found to show a mean T4-T8 (helper-suppressor) ratio lower than that of controls, a difference attributable to increased numbers of suppressor cells in the depressed group. One possible cause of increased suppressor cells is prior or current viral infection.
Medical and legal causation.
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A microcomputer-based vital records data base with interactive graphic assessment for states and localities.
Vital records data bases describe large populations over long periods of time, yet their organization and size often preclude or discourage their use. We constructed a microcomputer-based data base of all singleton births in Massachusetts, 1975-84. The original data were stored in 700,000 records, each 174 bytes long, occupying a total of over 120 megabytes (MB). By removing redundant information and unique identifiers, and packing the data, we store 21 fields of this information in a 16-byte record resulting in a data base of 11.1 MB, a saving of over 90 percent of disk space. By using programs written expressly for this data base, we can display a birth weight frequency plot of the entire data set in under 65 seconds on an IBM-compatible PC-AT. Comparable assessments in SAS-PC took over 105 minutes and in main frame SAS on an AS-9000 took over 37 CPU seconds. Implementing similar systems for state registries on births, deaths, cancers, and birth defects potentially offers investigators easy access to vast stores of information and would enable public health officials to produce timely reports, initiate a variety of surveillance activities, and respond rapidly to residents' inquiries about clusters and anomalous disease patterns.
Science and persuasion: environmental disease in U.S. courts.
The U.S. system for determining liability for environmental disease requires plaintiffs to demonstrate that the defendant was the legal cause of their illnesses. The determination of cause takes place in an adversary setting. Both sides in the dispute present evidence about causation to a lay judge or jury, who is responsible for deciding whether the defendant is legally responsible. In injury cases this generally means providing evidence of a specific, concrete event or condition that gave rise to the plaintiff's harm. Environmental disease usually presents a very different picture, one in which there is considerable uncertainty about the relationship between exposure to toxic substances and the plaintiff's disease. Scientific evidence about this uncertain link is often an essential part of the case. The reliance on scientific evidence appears to present almost insurmountable problems of proof of causation to the plaintiff. The law requires the plaintiff to demonstrate that, without the defendant's action, the harm would not have occurred. This strict requirement appears incompatible with the substantial scientific uncertainty about the cause of many environmental diseases. A second attribute of legal causation is that it is based on common experience, and is easily understood by lay citizens who are likely to be the final arbiters of causation. Scientific explanations of environmental disease causation, on the other hand, may not draw on common experience and may not have the intuitive appeal necessary to convince a lay decision-maker. Because scientific evidence of causation is difficult for a lay judge or jury to understand, and because of the adversary use of experts with very different opinions about causation, it might be expected that plaintiffs would have a great deal of difficulty demonstrating causation in environmental liability cases. However, the U.S. legal system appears to have accommodated to the plaintiff's difficulty in meeting the formal burden of persuasion. The courts allow juries considerable leeway in using their own experience and beliefs to determine causation, as long as there is some scientific evidence to support the plaintiff's contention. The U.S. environmental disease liability system has been criticized by some for plaintiffs' difficulty in proving causation and by others because plaintiffs can win cases without evidence that would be convincing to a scientist.(ABSTRACT TRUNCATED AT 400 WORDS)
Health problems reported by residents of a neighborhood contaminated by a hazardous waste facility.
A symptom prevalence survey was conducted of a neighborhood exposed to airborne hazardous wastes. Residents' responses were compared to those of a nearby control population. The results revealed that the exposed group had more self-reported complaints referable to the respiratory system (wheezing, shortness of breath, chest discomfort, persistent colds, coughs), constitutional complaints (always fatigued, bowel dysfunction), and irregular heart beat. When the effect of a documented irritant source in a small portion of the control population was removed, the exposed group also complained more often of irritation of the eyes and nose. There was a biological gradient for several of these effects. Efforts to eliminate the influence of confounding and recall bias are discussed. The results suggest either that the general population reacts to chemicals at levels much lower than the available occupational literature would indicate or that the effects are more long lasting than previously thought.
Leukemias and blood dyscrasias following exposure to chlordane and heptachlor.
We present 25 new cases of blood dyscrasia, including leukemias, production defects, and thrombocytopenic purpura, generally following home termite treatment with the chlorinated hydrocarbon pesticides chlordane and heptachlor (C/H). These newly reported cases are consistent with 34 previously published case reports associating blood dyscrasias with C/H exposure. Additionally, the newly reported leukemias are consistent with epidemiologic evidence of excess risk of leukemia and other cancers in C/H-exposed populations and with the carcinogenic action of C/H in animals. The importance of case reports in warning of the association of blood dyscrasias to C/H exposure is emphasized. Until the voluntary halt in production in July 1987, millions of homes in the United States were treated with chlordane and heptachlor for termites even though their agricultural uses were phased out in 1978, largely on the grounds of "imminent hazard" because of carcinogenicity. In view of the recognized myelotoxicity, carcinogenicity, and other chronic toxic effects of these pesticides, a national program for monitoring all homes treated is urgently needed to detect persistent contamination.