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PubMed1989

Retinal light damage in rats exposed to intermittent light. Comparison with continuous light exposure.

Visible light-induced photoreceptor cell damage resulting from exposure to multiple intermittent light-dark periods was compared with damage resulting from continuous light in albino rats maintained in a weak cyclic-light environment or in darkness before light treatment. The time course of retinal damage was determined by correlative measurements of rhodopsin and visual cell DNA at various times after light exposure, and by histopathological evaluation. The effect of intense light exposures on rhodopsin regeneration and on the level of rod outer segment docosahexaenoic acid was also determined. For rats previously maintained in weak cyclic light, 50% visual cell loss was measured 2 weeks after 12 1 hr light/2 hr dark periods, or following 24 hr of continuous light. A comparable 50% loss of visual cells was found in dark-reared rats after only 5 hr of continuous illumination or 2-3 hr of intermittent light. As judged by histology, cyclic-light-reared rats incurred less retinal pigment epithelial cell damage than dark-reared animals. In both experimental rat models intermittent light exposure resulted in greater visual cell damage than continuous exposure. Visual cell damage from intermittent light was found to depend on the duration of light exposure and on the number of light doses administered. Measurements of rhodopsin and DNA 2 hr and 2 weeks after light exposure of up to 8 hr duration revealed that visual cell loss occurs largely during the 2 week dark period following light treatment. The loss of docosahexaenoic acid from rod outer segments was also greater in rats exposed to intermittent light than in animals treated with continuous light. It is concluded that intermittent light exposure exacerbates Type I light damage in rats (involving the retina and retinal pigment epithelium) and the schedule of intense light exposure is a determinant of visual cell death.

Animals↗
PubMed1997

Bee and wasp venom allergy in Turkey.

BACKGROUND: Beekeeping has progressed recently to where bee sting exposure is an important public health problem in Turkey. OBJECTIVE: To investigate the status of bee and wasp sting allergy in a region of Turkey. METHODS: We conducted a questionnaire-based study of 786 subjects (cellulose paper factory personnel and family members older than 16 years of age) in Cay town of Afyon. Skin prick test with common aeroallergens and measurements of total IgE and specific IgE for bee and wasp venom were performed in 212 randomly selected subjects. RESULTS: Cumulative lifetime sting rate was 94.5% (geometric mean: 6.1 times), and last year bee sting rate was 20.4% (geometric mean: 1.6 times). Subjects who had beehives had higher risk of bee sting (P < .05) in the last year, whereas there was no significant difference among the groups for the cumulative lifetime sting exposure. Severe and mild systemic reactions were noted in 2.2% and 5.3%, respectively. Emergency room visits were reported in 9.3%, and familial Hymenoptera allergy in 10.2%. Fatal potential of bee sting was known by 81%. There was no mortality related with Hymenoptera allergy in records of the last 5 years. In 24 subjects with multiple sting exposures, allergic reactions changed severity in the latter exposures, which became less severe in five and more severe in 19 subjects. Atopy rate detected by prick testing was 20.3%. Specific IgE levels were class 1 in 22, class 2 in 11, and class 3 in 2 subjects for bee; and class 1 in 24 and class 2 in 2 subjects for wasp. Nobody had received immunotherapy for venom allergy. None of the factors including atopy, sex, occupation, smoking and family history of bee sting was significantly related with severity of the systemic reaction (P > .05). CONCLUSIONS: Bee and wasp stings are prevalent in Turkey. Severe systemic reactions complicating the sting are frequent (2.2%). Public awareness of potential fatality and treatment of the allergic reaction is not adequate.

Adult↗
PubMed2000

Down will come baby, cradle and all: diagnostic and therapeutic implications of chronic trauma on child development.

OBJECTIVE: This review examines the clinical outcomes associated with exposure to chronic intrafamilial trauma and explores the treatment of the psychological, biological and cognitive sequelae. METHOD: The existing research literature on the subject was collected, using Index Medicus/MEDLINE, Psychological Abstracts and the PILOTS database. The research findings were supplemented with clinical observations by the authors and other clinical writings on this topic. RESULTS: Children with histories of exposure to multiple traumatic experiences within their families or in medical settings usually meet criteria for numerous clinical diagnoses, none of which capture the complexity of their biological, emotional and cognitive problems. These are expressed in a multitude of psychological, cognitive, somatic and behavioural problems, ranging from learning disabilities to aggression against self and others. CONCLUSIONS: Exposure to intrafamilial violence and other chronic trauma results in pervasive psychological and biological deficits. Treatment needs to address issues of safety, stabilise impulsive aggression against self and others, promote mastery experiences, compensate for specific developmental deficits, and judiciously process both the traumatic memories and trauma-related expectations.

Adolescent↗
PubMed1988

Weak associations in occupational epidemiology: adjustment for exposure estimation error.

Epidemiological studies often estimate the health effects of occupational exposures by multiple regression techniques. The standard theory of regression analysis is based on the assumption that the explanatory variables are known without error, and it has long been realised that departures from this assumption will lead to underestimation of the true regression coefficients. In reality, there may be considerable imprecision in the measurement of individuals' exposures to hazards in the workplace, but this is seldom taken into account in analyses. We therefore studied the effect of allowing for imprecision in the exposure estimate with more sophisticated statistical methods, using lung function data from a sample of 348 British miners exposed to mixed coal dust, over an eight-year period. Change in lung function over an eight-year period was regressed on cumulative dust exposure, weight, age and smoking habits. The error in the exposure estimation was assumed to be up to 30% of the total varience of the distribution of the exposure. Adjustment of the regression coefficients of lung function change on dust exposure for the estimation error using linear structural relationships increased the regression coefficient more than threefold compared with those calculated by standard regression analysis. The adjustment led to a change of the coefficients of age as well. The results indicate that a serious underestimation of the relation between lung function change and occupational exposure may occur, which might lead to false interpretations about the relative importance of the occupational exposure as a determinant of disease.

Adult↗
PubMed1991

Characterization of a method for quantitating food consumption for mutation assays in Drosophila.

Quantitation of food consumption is necessary when determining mutation responses to multiple chemical exposures in the sex-linked recessive lethal assay in Drosophila. One method proposed for quantitating food consumption by Drosophila is to measure the incorporation of 14C-leucine into the flies during the feeding period (Thompson and Reeder: Environmental Mutagenesis 10:357-365, 1987). Three sources of variation in the technique of Thompson and Reeder have been identified and characterized. First, the amount of food consumed by individual flies differed by almost 30% in a 24 hr feeding period. Second, the variability from vial to vial (each containing multiple flies) was around 15%. Finally, the amount of food consumed in identical feeding experiments performed over the course of 1 year varied nearly 2-fold. The use of chemical consumption values in place of exposure levels provided a better means of expressing the combined mutagenic response. In addition, the kinetics of food consumption over a 3 day feeding period for exposures to cyclophosphamide which produce lethality were compared to non-lethal exposures. Extensive characterization of lethality induced by exposures to cyclophosphamide demonstrate that the lethality is most likely due to starvation, not chemical toxicity.

Administration, Oral↗
PubMed2000

Comparison of tomosynthesis methods used with digital mammography.

RATIONALE AND OBJECTIVES: The authors performed this study to investigate the potential applicability of tomosynthesis to digital mammography. Four methods of tomosynthesis-tuned aperture computed tomography (TACT)-backprojection, TACT-iterative restoration, iterative reconstruction with expectation maximization, and Bayesian smoothing-were compared to planar mammography and analyzed in terms of their contrast-detail characteristics. Specific comparisons between the tomosynthesis methods were not attempted in this study. MATERIALS AND METHODS: A full-field, amorphous, silicon-based, flat-panel digital mammographic system was used to obtain planar and tomosynthesis projection images. A composite tomosynthesis phantom with a centrally located contrast-detail insert was used as the object of interest. The total exposure for multiple views with tomosynthesis was always equal to or less than that for the planar technique. Algorithms were used to reconstruct the object from the acquired projections. RESULTS: Threshold contrast characteristics with all tomosynthesis reconstruction methods were significantly better than those with planar mammography, even when planar mammography was performed at more than twice the exposure level. Reduction of out-of-plane structural components was observed in all the tomosynthesis methods analyzed. CONCLUSION: The contrast-detail trends of all the tomosynthesis methods analyzed in this study were better than those of planar mammography. Further optimization of the algorithms could lead to better image reconstruction, which would improve visualization of valuable diagnostic information.

Breast Neoplasms↗
PubMed2002

Population pharmacokinetic meta-analysis with efavirenz.

A population-based pharmacokinetic (PK) model has been developed for efavirenz based on 16 phase I studies. The combined data set consisted of 334 healthy volunteers, 2,907 efavirenz dose administrations and 9,342 measured plasma concentrations across a range of doses from 100-600 mg. The pharmacokinetic structural model was a 2-compartment model with first-order absorption with differentiation between single- and multiple-dose exposure to account for known hepatic cytochrome P450 induction of efavirenz metabolism. Model-building was performed on the index data set (66% of the total database), as a data-splitting technique was used to validate the final model using NONMEM. The final model confirmed the appropriateness of separate clearance terms for single and multiple dose administration (2.65 versus 10.2 l/h, respectively). Clearance increased with dose and frequency of administration. A lower clearance was predicted in Asians and Blacks relative to Caucasians. A slightly lower clearance was observed in females relative to males (9.08 compared to 10.2 l/h in males) and interactions on clearance due to co-administration of fluconazole, ritonavir, rifampin, indinavir and azithromycin were identified. The magnitudes of these effects were small and did not suggest dose adjustment in the various subpopulations. With little exception, these results agree with the findings from the non-compartmental analyses. The residual variability was 21% CV and the intersubject variation in CL/F and V/F was 48 and 85%, respectively. The phase I meta-analysis was able to substantiate the pharmacokinetic characteristics of efavirenz derived from the composite of individual well-defined studies. The model was deemed adequate for subsequent evaluation in HIV-infected patients. Covariates and outlier classes identified in this phase I meta-analysis were similarly identified in subsequent analyses of patient data.

Administration, Oral↗
PubMed1981

Interactive effects in 60-Hz electric-field exposure systems.

The level of exposure of laboratory animals to 60-Hz electric fields is commonly specified in terms of the unperturbed field strength present before the introduction of experimental subjects and their cages. In the research reported in this paper, rats were housed in two parallel rows in 12.4 cm x 25.1 cm x 10.2 cm high plastic cages resting on the lower electrode of a parallel-plate exposure system, and the actual perturbed electric fields experienced by an experimental animal were investigated. The most important results are: 1) Reducing the spacing between the exposure electrodes from 8.7 to 1.7 times the height of a singly exposed rat model, while maintaining a constant unperturbed field strength, resulted in a 15% increase in the electric field at the highest point on the surface of the body and a 10% increase in the short-circuit current of the model. 2) For multiple animal exposures, increases of 10% in both the field at the highest point of the body and the short-circuit current were observed when the electrode spacing was reduced from 8.7 to 2.6 times the height of a rat. 3) Plastic cages caused 1--6% reductions in the electric field at the surface of the body, except very near the cage walls, where enhancements of more than 20% were observed. 4) When 16 rats were simultaneously exposed, the short-circuit current, IS, of an individual subject of weight W (in g), that was surrounded on all sides by other rats of weight W, was reduced from the short-circuit current, IU, measurement with the same subject individually exposed as follows: during a 12 h light (sleeping) cycle, IS/IU = 1.00 -- 0.0173W 1/2; during a 12 h night (awake) cycle, IS/IU = 1.00 -- 0.0136W 1/2.

Animals↗
PubMed1994

Toxic interactions among environmental pollutants: corroborating laboratory observations with human experience.

Combined exposures to multiple chemicals may result in interactions leading to a significant increase or decrease in the overall toxicity of the mixture compared to the summation of the toxicity of the components. A large number of chemical interactions have been described in animal studies by administering high doses of chemicals by routes and scenarios often different from anticipated human exposures. Though limited, there is some evidence for the occurrence of several supra-additive (the combined effects are greater than the simple summation of the individual effects) and infra-additive (the combined effects are smaller than the simple summation of the individual effects) chemical interactions in humans. For example, toxicokinetic interactions between several solvents have been found to occur in the workplace, whereas those involving pesticides have been reported less frequently, especially during accidental exposures. Toxic interactions involving nutritionally important metals and metalloids appear to occur more frequently, since several of them have an important role in a variety of physiological and biochemical processes. On the contrary, there is not much evidence to confirm the occurrence of toxic interactions among the commonly encountered inorganic gaseous pollutants in humans. Overall, the majority of chemical interactions observed in animal studies have neither been investigated in humans nor been extrapolated to humans based on appropriate mechanistic considerations. Future research efforts in the chemical interactions arena should address these issues by focusing on the development of mechanistically and biologically based models that allow predictions of the extent of interactions likely to be observed in humans.

Air Pollutants↗
PubMed1979

Sociopsychological factors affecting the human response to noise exposure.

Community noise is reported to be the most often mentioned undesirable neighborhood condition in a recent U.S. Census survey. Understanding community response to noise involves the measurement of a number of complex acoustic and nonacoustic variables and establishing the chain of relationships between physical exposure, perception, annoyance, and acceptability responses and finally complaint behavior. The perceived loudness of a noise is the most important acoustic parameter influencing annoyance and complaints, and the simple dBA unit can be used to integrate spectral characteristics of complex sounds in community studies. Although energy averaging such as Leq or Ldn can be used to describe multiple noise exposures over time, the variable trade-off relationships between number and level of exposures are somewhat obscured by such summary measures. However, they are still the best available descriptors and, until more accurate ones are developed, can be used to measure community noise environments. Perception of an identical noise exposure can vary according to the physiological noise sensitivity of a person and the activity context in which the noise is heard. Although the acoustic quality of the noise itself usually explains about 10 to 25 per cent of the variability in annoyance responses, sociopsychological variables measured in field studies account for 35 to 50 per cent of the variations in human annoyance responses. Three of the most important nonacoustic factors are the connotative fear effects of the noise signal, the feeling that those responsible for the noise are misfeasant in not reducing the noise, and the feeling that harmful health effects are produced by the noise. When residents report great fear, a high misfeasance, and marked health effects, about 90 per cent report a high annoyance level whether their noise exposure level is above 90 Ldn or 65 to 70 Ldn. In contrast, if the feelings are a low fear level, a low degree of misfeasance, and minimal health effects, only 3 to 10 per cent give high annoyance responses. Complaint behavior, although based on intensity of annoyance, is modified by a number of other sociopsychological factors and often is an unreliable indicator of an environmental problem.

Attitude↗
PubMed1966

Effect of poliovirus on deoxyribonucleic acid synthesis in HeLa cells.

Ackermann, W. W. (University of Michigan, Ann Arbor), D. C. Cox, H. Kurtz, C. D. Powers, and S. J. Davies. Effect of poliovirus on deoxyribonucleic acid synthesis in HeLa cells. J. Bacteriol. 91:1943-1952. 1966.-Both poliovirus and arginine stimulated deoxyribonucleic acid (DNA) synthesis in cultures of HeLa cells which were preconditioned by incubation in a medium deficient in arginine. However, the number of cells producing DNA was unaffected. DNA synthesis in such preconditioned cells was 10 to 20% of the maximal value obtained with a full complement of amino acids. Inhibition of DNA synthesis was produced in these cultures either by increasing the multiplicity of exposure above 40 plaque-forming units of virus per cell or by increasing the concentration of the deficient amino acid at the time of virus addition. Inhibition of DNA synthesis resulted from a reduction in the fraction of cells producing DNA. The concentration of arginine required for viral inhibition of DNA synthesis is greater than that for viral multiplication.

Arginine↗
PubMed1986

Intensification and habituation of experimental motion sickness in squirrel monkeys by repeated horizontal rotation.

The aim of this research was to quantify the development of habituation or intensification of experimental motion sickness induced in Bolivian squirrel monkeys by repeated exposures to horizontal rotation. Incidence, frequency, and latency of vomiting responses were recorded from monkeys rotated daily in a transparent testing chamber at 30 rpm for periods of 1 or 2 hours. Data showed that more than half of the subjects revealed habituation in terms of increased latencies for vomiting. Some showed a tendency to vomit increasingly earlier with multiple daily exposures to rotation. The development of habituation and intensification was evident as early as the second day of rotation. The number of emetic episodes per day decreased as a consequence of repeated rotation, but intensification of vomiting frequency did not occur beyond the fifth day.

Animals↗
PubMed1991

Epidemiologic approaches for assessing health risks from complex mixtures in indoor air.

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.

Air Pollution, Indoor↗
PubMed2001

Seizure activity and hyperthermia potentiate the increases in dopamine and serotonin extracellular levels in the amygdala during exposure to d-amphetamine.

Behavioral stereotypy, hyperthermia, and convulsive activity produced by exposure to multiple doses of d-amphetamine (AMPH) were related to changes in the extracellular levels of dopamine and serotonin (5-HT) in the amygdala, using the technique of microdialysis in awake and freely moving rats. Hyperactivity and stereotypy, as well as increases in microdialysis dopamine levels ranging from 100-300% of pre-AMPH basal microdialysate levels (BL), occurred during exposure to 3 doses of 2.5 mg/kg (3 x 2.5 mg/kg) AMPH. Three doses of 5 mg/kg produced a more intense stereotypic behavior as well as hyperthermia, and resulted in large increases in the peak dopamine levels (700% BL) while 5-HT levels were increased to a lesser extent (300% BL). The highest doses tested of 3 x 15 mg/kg produced convulsive activity, seizures, intense stereotypy and hyperthermia with peak microdialysate dopamine (1300% BL) and 5-HT levels (1800% BL) that were 2-fold and 6-fold greater, respectively, than those at the 3 x 5-mg/kg doses. Microdialysate glutamate levels were not changed by AMPH exposure. Rats that did not become hyperthermic when dosed with 15 mg/kg AMPH in a cold environment (10 degrees C) exhibited some hyperactivity and stereotypic behavior, but not overt convulsive behavior. Dopamine and 5-HT levels in these rats were significantly reduced by about 75% and 60%, respectively, compared to the room-temperature group. Inclusion of 2 microM tetrodotoxin (TTX) in the microdialysis buffer significantly reduced the 15-mg/kg AMPH-induced increases in dopamine by 30% and the increase in 5-HT levels by 70% at room temperature. These results indicate that a smaller portion of the dopamine release evoked by doses of AMPH that induce seizure activity is neuronal impulse-dependent while the majority of 5-HT released is impulse-dependent. Irrespective of impulse activity, the hyperthermia alone markedly potentiated dopamine release but had a lesser effect on 5-HT release. Thus, there are differences in the regulation of dopamine and serotonin release in the amygdala from high doses of AMPH, which are known to produce neurotoxicity. Further studies are necessary to determine the impact of these differences in release on AMPH neurotoxicity.

3,4-Dihydroxyphenylacetic Acid↗
PubMed2002

Environmental factors in relation to breast cancer characterized by p53 protein expression.

Findings from studies of cigarette smoking and low-dose ionizing radiation exposure and breast cancer are unclear. Laboratory studies indicate that both exposures can cause DNA damage, potentially increasing cancer risk if such mutations occur in growth control genes, such as p53. We examined the potential etiologic heterogeneity of breast cancer by evaluating whether associations between cigarette smoking and low-dose ionizing radiation and breast cancer differed by p53 protein expression status. Data were obtained from the Carolina Breast Cancer Study, a population-based, case-control study conducted among African-American and white women ages 20-74 years. Questionnaire data were available from 861 women with incident, primary invasive breast cancer and 790 community-based controls. p53 immunostaining was performed on tissue from 683 women with breast cancer; 46% were classified as p53+. Two separate unconditional logistic regression models were used to calculate odds ratios (ORs) for p53+ and p53- breast cancer, as compared with controls, in relation to smoking and low-dose ionizing radiation exposure. Smoking was not differentially associated with p53+ or p53- breast cancer, even when duration, dose, and passive smoking status were considered. Exposure to individual sources of radiation did not differ for p53+ and p53- breast cancers. However, ORs for combined exposure to chest X-rays and occupational radiation were higher for p53+ [OR, 2.2; 95% confidence interval (CI), 1.0-5.3] than p53- breast cancer (OR, 1.2; 95% CI, 0.5-3.4). Combined exposure to radiation from other medical sources as well as occupational exposure was also higher for p53+ (OR, 3.7; 95% CI, 0.8-16.8) than for p53- breast cancer (OR, 1.7; 95% CI, 0.3-10.5). Although preliminary, our results suggest that exposure to multiple sources of low-dose ionizing radiation may contribute to the development of p53+ breast cancer.

Adult↗
PubMed1997

Dysbaric osteonecrosis in divers and caisson workers. An animal model.

Dysbaric osteonecrosis was induced successfully in adult sheep after 12 to 13, 24-hour exposures to compressed air (2.6-2.9 atmospheres absolute) during a 2-month period. All exposed sheep had decompression sickness and extensive bone and marrow necrosis in their long bones. Radiographic analysis of these progressive lesions showed mottled to distinct medullary opacities and endosteal thickening characteristic of dysbaric osteonecrosis. Six months after the last hyperbaric exposure, neovascularization of once ischemic fatty marrow was centripetal from the diaphyseal cortex. Proliferating endosteal new bone, fatty marrow calcification, and appositional new bone formation were widespread. Juxtaarticular osteonecrosis involved marrow fibrosis and loss of osteocytes in subchondral cortical bone. Tidemark reduplication in juxtaarticular bone and cartilage thinning suggested possible early osteoarthritis induction by recurrent episodes of transient ischemia after multiple hyperbaric exposures. Dysbaric osteonecrosis appears to involve a bone compartment syndrome of elevated intramedullary pressure initiated by decompression induced N2 bubble formation in the fatty marrow of the long bones. An animal model that can be used to investigate the pathogenesis, diagnosis, and treatment of dysbaric osteonecrosis is discussed.

Animals↗
PubMed2002

Methylpyridinium (MPP(+))- and nerve growth factor-induced changes in pro- and anti-apoptotic signaling pathways in SH-SY5Y neuroblastoma cells.

The parkinsonian neurotoxin methylpyridinium (MPP(+)) mimics the neuropathology of Parkinson's disease (PD) and likely kills neurons by inhibiting complex I of the electron transport chain and increasing oxidative stress. We examined the time course of activation/inactivation of multiple pro- and anti-apoptotic signaling pathways in MPP(+)-induced apoptotic death of SH-SY5Y neuroblastoma cells. We found an early increase and later decrease of transcriptional activity of the generally anti-apoptotic nuclear factor kappa-beta (NF-kappa B) and early increases in activating phosphorylation of the anti-apoptotic upstream kinase protein kinase B (PKB, also known as AKT). Sequestration-inducing phosphorylation of pro-apoptotic BAD protein increased early then declined. A small biphasic increase in the generally pro-apoptotic p38 kinase activity paralleled the biphasic rise in NF-kappa B-mediated transcription. Inhibition of p38 kinase with 5 micro M SB203540, inhibition of MEK-ERK with 50 micro M U0126, or inhibition of phosphatidylinositol-3-kinase (PI3K) with 10 micro M LY294002 reduced cell viability by 4, 18 or 37%, respectively, after 24 h. All three kinase inhibitors increased cell death in response to 24 h of MPP(+), with the greatest effect shown by LY294002. Nerve growth factor (NGF) caused an early increase in activating phosphorylation of PKB/AKT and MEK-ERK and increased cell survival during MPP(+) exposure. We found that acute MPP(+) exposure activates multiple interacting death- and survival-promoting pathways. Survival-promoting MEK-ERK and PI3K pathways contribute to viability during MPP(+) exposure, both are activated by NGF, and loss of PI3K-mediated signaling and NF-kappa B-mediated transcription may commit cells irreversibly to apoptosis in this model. It remains unknown to what extent these signaling pathways modulate dopamine neuronal death in PD.

1-Methyl-4-phenylpyridinium↗
PubMed1991

Hepatitis C: a sleeping giant?

In the United States, non-A, non-B hepatitis accounts for 20-40% of acute viral hepatitis. Although it has traditionally been considered a transfusion-associated disease, non-A, non-B hepatitis is more likely to occur outside the transfusion setting. Surveillance data from the Centers for Disease Control show that in 1988 6% of patients with non-A, non-B hepatitis reported a history of blood transfusion, 46% parenteral drug use, 10% household or sexual exposure to a contact who had had hepatitis or exposure to multiple sex partners, 2% medical or dental employment involving frequent blood contact, less than 1% hemodialysis, and 40% no known source. Antibody to hepatitis C virus (anti-HCV) is found in the majority of patients with non-A, non-B hepatitis independent of the source of infection; however, antibody may not appear for 6 to 9 months after exposure or onset of illness. Limited serologic studies of the prevalence of anti-HCV in various population groups have found high anti-HCV rates (50-80%) in parenteral drug users and hemophiliacs, intermediate rates among the sexually active (5-15%), and low rates among health care workers (1%). In persons with acute or chronic hepatitis C, the presence of anti-HCV appears to indicate infectivity. Persons with no history of hepatitis who are anti-HCV positive may or may not be infectious. More sensitive and specific markers for the detection of hepatitis C virus will be needed to resolve this question.

Hepacivirus↗