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Circulatory defects of the optic disk and retina in ocular hypertension and high pressure open-angle glaucoma.

Studies using fluorescein angiography have shown that two types of circulatory defects occur in the optic disk and retina of open-angle glaucomatous eyes. The first is a defect of the microcirculation of the optic disk characterized as a fluorescein defect. Such defects begin as small areas of relatively little filling of the small vessels of the disk with fluorescein. The areas of defect show leakage for both fluorescein and indocyanine green. These defects increase in size and number with the progression of the disease. Fluorescein defects are significantly correlated with visual field loss and retinal nerve fiber layer loss. The second circulatory defect is a decrease of flow of fluorescein in the retinal vessels, especially the retinal veins, so that the greater the age, diastolic blood pressure, ocular pressure and visual field loss, the less the flow. Both the optic disk and retinal circulation defects occur in untreated ocular hypertensive eyes. These observations indicate that circulatory defects in the optic disk and retina occur in ocular hypertension and open-angle glaucoma and increase with the progression of the disease.

Blood Flow Velocity↗

Positron emission tomography detects evidence of viability in rest technetium-99m sestamibi defects.

OBJECTIVES: The purpose of this study was to determine the relative value of single-photon emission computed tomographic (SPECT) imaging at rest using technetium-99m methoxyisobutyl isonitrile (technetium-99m sestamibi) with positron emission tomography for detection of viable myocardium. BACKGROUND: Recent studies comparing positron emission tomography and thallium-201 reinjection with rest technetium-99m sestamibi imaging have suggested that the latter technique underestimates myocardial viability. METHODS: Twenty patients with a previous myocardial infarction underwent rest technetium-99m sestamibi imaging and positron emission tomography using fluorine (F)-18 deoxyglucose and nitrogen (N)-13 ammonia. In each patient, circumferential profile analysis was used to determine technetium-99m sestamibi, F-18 deoxyglucose and N-13 ammonia activity (expressed as percent of peak activity) in nine cardiac segments and in the perfusion defect defined by the area having technetium-99m sestamibi activity < 60%. Technetium-99m sestamibi defects were graded as moderate (50% to 59% of peak activity) and severe (< 50% of peak activity). Estimates of perfusion defect size were compared between technetium-99m sestamibi and N-13 ammonia. RESULTS: Sixteen (53%) of 30 segments with moderate defects and 16 (47%) of 34 segments with severe defects had > or = 60% F-18 deoxyglucose activity considered indicative of viability. Fluorine-18 deoxyglucose evidence of viability was still present in 50% of segments with technetium-99m sestamibi activity < 40%. There was no significant difference in the mean (+/- SD) technetium-99m sestamibi activity in segments with viable (40 +/- 7%) and nonviable segments (49 +/- 7%, p = 0.84). Of the 18 patients who had adequate F-18 deoxyglucose studies, the area of the technetium-99m sestamibi defect was viable in 5 (28%). In 16 patients (80%), perfusion defect size determined by technetium-99m sestamibi exceeded that measured by N-13 ammonia. The difference in defect size between technetium-99m sestamibi and N-13 ammonia was significantly greater in patients with viable (21 +/- 9%) versus nonviable segments (7 +/- 9%, p = 0.007). CONCLUSIONS: Moderate and severe rest technetium-99m sestamibi defects frequently have metabolic evidence of viability. Technetium-99m sestamibi SPECT yields larger perfusion defects than does N-13 ammonia positron emission tomography when the same threshold values are used.

Adult↗

MRI evaluation of patellar tendon defect after harvesting its central third.

PURPOSE: the purpose of this study was to evaluate defect width of patellar tendon after harvest for anterior cruciate ligament reconstruction. MATERIALS AND METHODS: we performed MRI at various time interval after graft harvest (2-96 months) on 28 patients who had had reconstruction of the anterior cruciate ligament using mid-third patellar tendon. T1 and T2 weighted axial images were obtained to assess donor site defect of the patellar tendon. Measurement of the defect width was performed at the level of menisci on the axial images. The patients were divided into two groups according to the time interval between operation and imaging. The defect width of patients with short time interval (2-12 months) was compared to the defect width of patients with long time interval (12-96 months). RESULTS: the average defect width of patients with short time interval was 6.4 mm and it was 2.2 mm for the patients with long time interval. Decreased defect width was obtained from MRI images in the patients with long time interval. Closed donor site defect was detected in 1 out of 14 patients with short time interval and 6 out of 14 patients with long time interval. DISCUSSION AND CONCLUSION: these results show that there is no complete closure of donor site defect up to 1 year. However, it seems to be nearly complete closure of patellar tendon defect in the long time period.

Adult↗

Knee cartilage defects: association with early radiographic osteoarthritis, decreased cartilage volume, increased joint surface area and type II collagen breakdown.

OBJECTIVE: To generate hypotheses regarding the associations between knee cartilage defects and knee radiographic osteoarthritis (ROA), cartilage volume, bone size and type II collagen breakdown in adults. METHODS: A cross-sectional convenience sample of 372 male and female subjects (mean age 45 years, range 26-61) was studied. Knee cartilage defect score (0-4) and prevalence (a defect score of > or =2), cartilage volume, and bone surface area were determined using T1-weighted fat saturation MRI. Urinary levels of C-terminal crosslinking telopeptide of type II collagen (U-CTX-II) were measured by enzyme-linked immunosorbent assay. Height, weight and ROA were measured by standard protocols. RESULTS: In multivariate analysis, the severity and prevalence of knee cartilage defects were significantly and independently associated with tibiofemoral osteophytes (regression coefficient (beta): +0.86 to +1.31/unit, odds ratio (OR): 2.97-3.68/unit, all P<0.05 with the exception of OR in lateral tibiofemoral compartment) and tibial bone area (beta: +0.11 to +0.25/cm2; OR: 1.33-1.58/cm2, all P<0.01). Knee cartilage defects were inconsistently associated with joint space narrowing after adjustment for osteophytes but consistently with knee cartilage volume (beta: -0.27 to -0.70/ml; OR: 0.16-0.56/ml, all P<0.01 except for OR at lateral tibial cartilage site P=0.06). Lastly, knee cartilage defect severity was significantly associated with U-CTX-II (Partial r=+0.18, P<0.001 for total cartilage defect score). CONCLUSION: Osteophytes and increasing knee bone size may be causally related to knee cartilage defects. Furthermore, knee cartilage defects may result in increased cartilage breakdown leading to decreased cartilage volume and joint space narrowing suggesting an important role for knee cartilage defects in early knee OA.

Adult↗

Ultrasound to stimulate mandibular bone defect healing: a placebo-controlled single-blind study in rats.

PURPOSE: Because of the limitations of the body to heal large maxillofacial bone defects, an attempt was made to stimulate mandibular defect healing with low intensity pulsed ultrasound in rats. This ultrasound consists of a 1.5-MHz pressure wave administered in pulses of 200 microsec, with an average intensity over space and time of 30 mW. cm(-2). MATERIALS AND METHODS: In 72 rats, a 5.0-mm-diameter circular mandibular defect was created. Three groups were studied: an ultrasound treatment group, a placebo treatment group, and a control group. Ultrasound and placebo treatment involved a daily treatment for 20 minutes at the site of the defect under general anesthesia. At 2 and 4 weeks, the region of bone growth within the defect was measured using microradiographs and the amount of defect healing was expressed as the percentage of defect closure. RESULTS: At 2 and 4 weeks, there was no statistical significant difference in the percentage of defect closure between the groups. CONCLUSION: Low-intensity pulsed ultrasound does not stimulate bone defect healing in the case of a large mandibular defect in the rat.

Animals↗

Critical size defect in the canine mandible.

OBJECTIVE: The purpose of this study was to determine the minimum size defect in a canine mandible that would not spontaneously heal during the dog's natural life (the critical size defect). STUDY DESIGN: Sixteen adult female mongrel dogs underwent continuity resection on both sides of the mandible to create bilateral defects. In 8 dogs, mandibular defects ranging from 5 to 20 mm were created with periosteal resection. In the other 8 dogs, mandibular defects ranging from 30 to 60 mm were created preserving the periosteum. The dogs were then killed at 6 months and the defects examined using radiographs and histologic analysis. RESULTS: When the periosteum was removed, mandibular defects greater than 15 mm failed to heal across the entire defect. However, when the periosteum was preserved, mandibular defects needed to be greater than 50 mm in order to fail to heal. CONCLUSION: The critical size defect in a canine mandible model is 15 mm when the periosteum is removed and 50 mm when the periosteum is preserved.

Animals↗

Enhancement of bone defect healing in old rats by TGF-beta and IGF-1.

Bone defects are often created in order to repair bone pathologies. In the aging population, the healing of such defects is very limited. Bone healing in aging depends on the availability of various hormone and growth factors. The ability of growth factors to enhance bone formation in femoral defects in old rats was tested. Bone defects were induced in femurs of old rats. A single dose of transforming growth factor-beta (TGF-beta), IGF-1, TGF-beta+IGF-1 or saline was inserted in the defect and bones were tested after 2 and 4 weeks. Radiology revealed that mineralization appeared in the 2 weeks group in defects treated with TGF-beta and in defects treated with TGF-beta, TGF-beta+IGF-1 in the 4 weeks groups. Computerized tomography (CT) coronal and axial images revealed that 4 weeks after treatment with TGF-beta+IGF-1, a complete bone bridge was observed. Morphology revealed that these defects were filled with trabecular bone. A less pronounced bone healing was observed after TGF-beta or IGF-1, while control specimens revealed partial healing of the bone defect. Biomechanical tests indicated that treatment with TGF-beta, IGF-1 or TGF-beta+IGF-1 resulted in a significant increase of bone bending rigidity compared to control in the 4 weeks group and that TGF-beta+IGF-1 was the most inductive in this respect. The ability to induce bone healing in aging by TGF-beta+IGF-1 is of a great clinical importance for restoration of bone strength and biomechanical properties of bone defects in aging.

Aging↗

Positron emission tomography detects tissue metabolic activity in myocardial segments with persistent thallium perfusion defects.

Positron emission tomography with 13N-ammonia and 18F-2-deoxyglucose was used to assess myocardial perfusion and glucose utilization in 51 myocardial segments with a stress thallium defect in 12 patients. Myocardial infarction was defined by a concordant reduction in segmental perfusion and glucose utilization, and myocardial ischemia was identified by preservation of glucose utilization in segments with rest hypoperfusion. Of the 51 segments studied, 36 had a fixed thallium defect, 11 had a partially reversible defect and 4 had a completely reversible defect. Only 15 (42%) of the 36 segments with a fixed defect and 4 (36%) of the 11 segments with a partially reversible defect exhibited myocardial infarction on study with positron tomography. In contrast, residual myocardial glucose utilization was identified in the majority of segments with a fixed (58%) or a partially reversible (64%) thallium defect. All of the segments with a completely reversible defect appeared normal on positron tomography. Apparent improvement in the thallium defect on delayed images did not distinguish segments with ischemia from infarction. Thus, positron emission tomography reveals evidence of persistent tissue metabolism in the majority of segments with a fixed or partially resolving stress thallium defect, implying that markers of perfusion alone may underestimate the extent of viable tissue in hypoperfused myocardial segments.

Aged↗

Healing of segmental bone defects with granular porous hydroxyapatite augmented with recombinant human osteogenic protein-1 or autologous bone marrow.

Hydroxyapatite is a synthetic bone graft, which is used for the treatment of bone defects and nonunions. However, it is a rather inert material with no or little intrinsic osteoinductive activity. Recombinant human osteogenic protein-1 (rhOP-1) is a very potent biological agent, that enhances osteogenesis during bone repair. Bone marrow contains mesenchymal stem cells, which are capable of new bone formation. Biosynthetic bone grafts were created by the addition of rhOP-1 or bone marrow to granular porous hydroxyapatite. The performance of these grafts was tested in a sheep model and compared to the results of autograft, which is clinically the standard treatment of bone defects and nonunions. A 3 cm segmental bone defect was made in the tibia and fixed with an interlocking intramedullary nail. There were five treatment groups: no implant (n=6), autograft (n=8), hydroxyapatite alone (n=8), hydroxyapatite loaded with rhOP-1 (n=8), and hydroxyapatite loaded with autologous bone marrow (n=8). At 12 weeks, healing of the defect was evaluated with radiographs, a torsional test to failure, and histological examination of longitudinal sections through the defect. Torsional strength and stiffness of the healing tibiae were about two to three times higher for autograft and hydroxyapatite plus rhOP-1 or bone marrow compared to hydroxyapatite alone and empty defects. The mean values of both combination groups were comparable to those of autograft. There were more unions in defects with hydroxyapatite plus rhOP-1 than in defects with hydroxyapatite alone. Although the differences were not significant, histological examination revealed that there was more often bony bridging of the defect in both combination groups and the autograft group than in the group with hydroxyapatite alone. Healing of bone defects, treated with porous hydroxyapatite, can be enhanced by the addition of rhOP-1 or autologous bone marrow. The results of these composite biosynthetic grafts are equivalent to those of autograft.

Animals↗

Rotator cuff defect healing: a biomechanical and histologic analysis in an animal model.

Rotator cuff tears are one of the most common causes of pain and disability in the upper extremity. With the use of an animal model, we studied the healing response of a controlled defect in the normal supraspinatus tendon and in a tendon with a reduced intrinsic healing capacity. In 36 Sprague-Dawley rats, defects (2 mm x 2 mm) were created in the supraspinatus tendons bilaterally. To model a tendon with an intrinsically reduced capacity to heal, the tissue adjacent to the defect area in the left shoulder was treated with in situ freezing. The contralateral tendon was not frozen. After 3 (n = 12), 6 (n = 12), and 12 (n = 12) weeks, animals were killed and underwent histologic (n = 4 from each group) and biomechanical (n = 8 from each group) evaluation. An additional group of untreated animals served as a normal control group. On histologic evaluation 78% of tendons had persistent defects (defined as incomplete closure of the defect site). Over time, the tissue from both groups demonstrated an improved histologic grade but did not reach normal levels, even at 12 weeks. No histologic differences were found between defect healing in normal tendons and in those treated with in situ freezing. On biomechanical evaluation there were also no significant differences between treatment groups. Over time, an improvement occurred in tissue properties, indicating that some healing of the defects had occurred. However, these tissue properties remained an order of magnitude lower than those of normal control tendons. These findings indicate that there is an active but inadequate repair response to the defect in the rat supraspinatus tendon, which is not significantly worsened by in situ freezing of the tissue around the defect. This model has applications toward the study of techniques to improve or accelerate cuff defect healing.

Animals↗

Systemic application of growth hormone enhances the early healing phase of osteochondral defects--a preliminary study in micropigs.

Healing of osteochondral defects following trauma remains a significant clinical problem, often leading to osteoarthritis. Growth hormone (GH) has been shown to accelerate formation of bone and cartilage tissue in the growth plates and in cell cultures. To investigate the influence of systemically administered recombinant porcine growth hormone (r-pGH) on the healing of osteochondral defects we performed a histomorphometrical analysis of full-thickness cartilage defects in the femoral condyle of micropigs. Forty-eight mature female Yucatan micropigs were divided into two groups, one receiving a daily injection of r-pGH (100 microg/kg), the other receiving sodium chloride as placebo. A circular 6-mm-diameter full-thickness defect of the cartilage was created, extending 1.5 mm into the subchondral bone. The animals were sacrificed after 4 (n = 24) and 6 (n = 24) weeks. The von-Kossa stain was used to visualise the calcified structures; cartilage and the fibrous tissue were marked with a combined Safranin-O/light-green stain. The defect filling and the percentage of bone, cartilage, and fibrous tissue into the defect were evaluated using an image analysis system. Furthermore, histological grading was performed using the modified Wakitani score. After 4 weeks no differences were observed between both groups. The defect filling after 6 weeks with newly formed bone was significantly higher in the r-pGH-treated group. The formation of cartilage and fibrous tissue showed a trend towards better healing in the GH-treated group; however, there was no significant difference. In the r-pGH-treated group, the percentage of total defect filling was significantly higher. The evaluation of the vascularity showed a significantly lower number of vessels in the GH-treated group after 6 weeks. Histomorphological grading revealed a significantly lower total Wakitani score in the GH-treated group, which represents a better healing result compared to the controls. The results of the present study suggest that circulating r-pGH or one of its mediators may accelerate osteochondral defect healing by stimulating the formation of osseous and chondral tissue. The analysis of the vascularity leads to the assumption of an advanced maturation of the osteochondral defects under the influence of GH.

Actins↗

Periodontal tissue alterations following Emdogain treatment of periodontal sites with angular bone defects. A series of case reports.

UNLABELLED: The aim of the present study was to assess the predictability of probing attachment gain and probing pocket depth reduction following Emdogain treatment at sites with deep angular bone defects. MATERIAL AND METHODS: 108 consecutively-treated periodontal patients (mean age 55.8 years) were included. Each subject exhibited at least 1 deep interproximal intrabony defect that could be identified as an experimental site based on the inclusion criteria: (i) probing pocket depth > or = 5 mm, (ii) probing attachment loss > or = 6 mm, (iii) radiographic evidence of an interproximal bone defect with a > or = 3 mm intrabony component. A total of 145 defects met the criteria for inclusion. All subjects received non-surgical periodontal therapy. This included subgingival instrumentation in all parts of the dentition. At least 6 months after the completion of this treatment, a baseline examination was performed to characterise the experimental site. Reconstructive therapy was subsequently performed. Full-thickness periodontal flaps were elevated, and the root surface scaled and planed. No bone recontouring was performed. A gel containing 24% EDTA was applied on the exposed root and was kept in place for 2 min. A preparation of enamel matrix proteins was applied to the root surface and adjacent defect space. The flaps were replaced and closed with sutures. The experimental sites were re-examined 12 months after reconstructive surgery. RESULTS: The re-examination demonstrated that a treatment including the application of enamel matrix proteins at periodontal sites with angular defects resulted in a mean probing attachment level gain of 4.6 mm and a probing pocket depth reduction of 5.2 mm. 87% of all sites treated exhibited a probing attachment gain of > 2 mm. One site suffered probing attachment loss. The radiographic assessments revealed that the bone defect had been reduced in depth by 2.9 mm on average. The reduction in defect size corresponded to an average bone fill of 69% of the original defect. In 43% of the defects, the bone fill amounted to > or = 80%. CONCLUSION: The overall probing pocket depth reduction, probing attachment level gain, and soft tissue recession, that results following Emdogain therapy, is similar to the corresponding outcome variables following GTR.

Combined Modality Therapy↗

Radiographic detection and assessment of the periodontal endosseous defects.

AIMS: The aim of the present study was to investigate the potential of conventional radiography in detecting and accurately imaging periodontal endosseous (or osseous) defects when compared to surgical measurements. A further objective of the study was the selection of the most successful radiographic method for the assessment of endosseous defects. METHOD: Surgical measurements, during periodontal flap surgery, and radiographic measurements, from periapical and panoramic radiographs, were obtained from 5,072 proximal surfaces of 100 patients presenting with periodontitis. RESULTS: Statistical evaluation of the surgical and radiographic measurements revealed the following. (1) The ability of the radiographs to detect periodontal osseous defects was relatively low. (2) For periapical radiography, it depended, in descending order, on the depth and buccolingual width of the defect, the number of osseous walls and the jaw location. For panoramic radiography, it depended only on buccolingual width. (3) Osseous defects of small depth and/or small buccolingual width were the most difficult to detect radiographically. (4) Periapical radiography was more successful than panoramic in detecting osseous defects, and more accurate in assessing the defect dimensions (depth, mesiodistal width). (5) The difference in the defect detection ability between the 2 radiographic methods, the accuracy of the radiographic defect dimensions assessment as well as the degree of agreement between periapical and panoramic assessment depended on defect location and dimensions. CONCLUSIONS: Periapical radiography is superior to panoramic in detecting and accurately imaging periodontal osseous destruction.

Adolescent↗

Invasive line placement in critically ill patients: do hemostatic defects matter?

BACKGROUND: Blood components are often given prophylactically before the placement of invasive lines in patients with coagulation defects. Little, however, is known about the epidemiology of defects in these patients. The purpose of this study is to ascertain what proportion of intensive care patients who receive invasive lines have hemostatic defects, what actions are taken by physicians to correct these abnormalities before invasive line insertion, and what the incidence is of bleeding complications after invasive line placement. STUDY DESIGN AND METHODS: Charts were retrospectively reviewed for 490 intensive care patients in whom 938 arterial, pulmonary artery, and central venous lines were placed. RESULTS: At least one defect in hemostasis was documented for 388 patients (41%) before line placement, with 253 (27%) of these patients evidencing severe abnormalities. Seventeen percent of patients had no preprocedure laboratory evaluation. Trauma patients showed the highest numbers of abnormalities in hemostatic testing, but medical patients had more-severe defects. The occurrence of isolated abnormal laboratory values did not predict bleeding, but a score derived from a consideration of multiple defects did. Correction of the abnormalities was attempted in 37 percent of patients with hemostatic defects. Sixteen patients had bleeding complications, but only two had complications that were life-threatening. None of the complications were fatal. CONCLUSION: Invasive lines are used frequently in patients with hemostatic defects, often without any attempt to correct the abnormalities. Nevertheless, rates of hemorrhage are low and appear to be closely related to the level of experience of the physician rather than to defects in hemostasis. These findings suggest that the use of blood components for preprocedure correction of hemostatic defects is not necessary, except in those patients who have the most severe hemostatic abnormalities.

Adolescent↗

Reconstruction of segmental defects during revision procedures of the acetabulum with the Burch-Schneider anti-protrusio cage.

Sixty-three Burch-Schneider rings in 62 patients with segmental or combined defects were followed up after a mean of 5.45 years. The mean Harris hip score was 74.9 points. Aseptic loosening occurred in 3 cases, and septic loosening occurred in 2 cases. All cases of aseptic loosening had Paprosky stage IIIb defects and defects of the posterior column. Radiologic migration analysis showed increased migration with increase in the Paprosky defect stage, defects of the posterior column, and cranial defects. The cage has the lowest migration and loosening rate in cases with medial defects or anterior column defects. Surgical treatment of defects of the posterior column is associated with an increased rate of aseptic loosening, whereas implantation with cranial defects shows a higher migration rate with no significant increase in loosening.

Acetabulum↗

Absence of an environmental effect on the recurrence of facial-cleft defects.

BACKGROUND: The rate of recurrence of a broad range of birth defects may decrease among women who change residence after the birth of their first infant. The aim of the present study was to determine the effect of changing residence on the recurrence of congenital facial-cleft defects. METHODS: We identified 4189 women who had infants with facial-cleft defects by linking a data base comprising the records of children with facial clefts born between 1952 and 1987 with the Central Person Registry in Denmark. Among the 4189 mothers, 1902 each had additional children after the first child with a facial-cleft defect. A total of 2692 younger siblings were identified. We compared the proportion of infants with facial-cleft defects among the younger siblings between mothers who had changed municipalities or sexual partners and those who had not. RESULTS: Changing the municipality of residence did not decrease the frequency with which facial-cleft defects recurred in younger siblings. Among the 907 infants of mothers who changed municipalities but not partners, 29 (3.2 percent) had facial-cleft defects, as compared with 48 (3.4 percent) of 1425 infants of mothers who changed neither municipality nor partner (relative risk, 0.9; 95 percent confidence interval, 0.6 to 1.5). However, a change of partner reduced the recurrence risk significantly. Among 236 infants of mothers who changed partners, 1 (0.4 percent) had a facial-cleft defect, as compared with 77 (3.3 percent) of 2350 infants of mothers who did not change partners (relative risk, 0.1; 95 percent confidence interval, 0.02 to 0.9). CONCLUSIONS: Recurrence of facial-cleft defects is not linked to the residence of the mother, but having a different partner reduced a woman's risk of having a second child with this defect.

Cleft Lip↗

Risk for birth defects among premature infants: a population-based study.

OBJECTIVE: To investigate the relationship between prematurity and birth defects. STUDY DESIGN: In a population-based cohort study, infants with birth defects were ascertained through the Metropolitan Atlanta Congenital Defects Program, a surveillance system with active methods of ascertainment. Gestational age data were obtained from birth certificates of liveborn, singleton infants with and without birth defects born in the 5-county metropolitan Atlanta area. RESULTS: Among 264,392 infants with known gestational ages born between 1989 and 1995, 7738 were identified as having birth defects (2.93%). Premature infants (<37 weeks' gestation) were more than two times as likely to have birth defects than term infants (37-41 weeks) (risk ratio = 2.43; 95% CI 2.30-2.56). This relationship was evident for several categories of birth defects. The rate of birth defects varied by gestational age categories, with the highest risk in the 29- to 32-week gestational age category (risk ratio = 3.37). CONCLUSIONS: The risk for birth defects is increased in premature infants. Awareness of this relationship is important for clinicians caring for premature infants. The morbidity and mortality associated with a particular defect may be significantly altered by the presence of prematurity. Further study of this association may provide insight into the etiology of these relatively common problems.

Cohort Studies↗

Elevated birth defects in racial or ethnic minority children of women living near hazardous waste sites.

This case-control study evaluated the relationship between birth defects in racial or ethnic minority children born during 1983-1988 and the potential exposure of their mothers to contaminants at hazardous waste sites in California. Four categories of race or ethnicity were used: black/African American, Hispanic/Latino, American Indian/Alaska Native, and Asian/Pacific Islander. Case subjects were 13,938 minority infants with major structural birth defects (identified by the California Birth Defects Monitoring Program) whose mothers resided in selected counties at the time of delivery. The control group was composed of 14,463 minority infants without birth defects who were randomly selected from the same birth cohort as the case subjects. The potential for exposure was determined by whether the mother resided at the time of delivery in the same census tract as a hazardous waste site that was on the U.S. Environmental Protection Agency's National Priorities List (NPL). Racial/ethnic minority infants whose mothers had been potentially exposed to hazardous waste were at slightly increased risk for birth defects (odds ratio [OR] = 1.12, 95% confidence interval [CI] = 0.98-1.27) than were racial/ethnic minority infants whose mothers had not been potentially exposed. The greatest association was between potential exposure and neural tube defects (OR = 1.54, 95% CI = 0.93-2.55), particularly anencephaly (OR = 1.85, 95% CI = 0.91-3.75). The strongest association between birth defects and potential exposure was among American Indians/Alaska Natives (OR = 1.19, 95% CI = 0.62-2.27). Despite the limitations of this study, the consistency of these findings with previous studies suggests an association between environmental risk factors and birth defects. This is particularly relevant to minority populations. We recommend further investigation of birth defects among minority communities, particularly among American Indians/Alaska Natives. Special attention should also be paid to those defects and contaminants that consistently are associated with exposure to hazardous waste.

Adolescent↗