Economic impact of a community-wide waterborne outbreak of gastrointestinal illness.
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Biomedical subjects
Publications and source records attributed to E L Baker.
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In a survey of occupationally acquired disease in workers at a pesticide plant, we found that 11 (11%) of 102 workers had been hospitalized for illness related to chemical exposures; highest hospitalization rates occurred in packaging (27%), production (22%), and maintenance (9%) workers. Commonest causes of hospitalization were intoxication by the carbamate pesticide methomyl [1-(methylthio)ethylideneamino methyl carbamate], a reversible cholinesterase inhibitor, and methemoglobinemia following exposure to 3,4-dichloroaniline. On clinical evaluation, five (46%) of 11 packaging workers, the group with the highest exposure to methomyl, had experienced blurred vision or pupillary constriction. Seventeen (61%) of 28 production workers with exposure to dichloroaniline and propanil (3'4'-dichloropropionanilide) had chloracne, an acne-form dermatosis caused by the contaminant tetrachlorazobenzene in propanil and dichloroaniline. The chloracnegenic potentials of propanil and dichloroaniline were verified by rabbit ear tests. These findings reemphasize the hazards inherent in the the manufacture and formulation of pesticides and herbicides.
In 1976, epidemic organophosphate insecticide poisoning due to malathion occurred among 7500 field workers in the Pakistan malaria control programme. In July, the peak month of the epidemic, it is estimated that there were about 2800 cases. In field studies low red-cell cholinesterase activities were associated with the signs and symptoms of organophosphate insecticide intoxication. Toxicity was seen with 3 different formulations of the insecticide and was greatest with the products containing increased amounts of isomalathion, a toxic malathion degradation product. Poor work practices, which had developed when D.D.T. was the primary insecticide for malaria control, resulted in excessive skin contact with and percutaneous absorption of the pesticide. Airborne malathion concentrations were very low. Implementation of good work practices and proscription of use of the 2 pesticide formulations most contaminated with isomalathion halted the epidemic in September. An extensive training programme and surveillance system for pesticide toxicity preceded 1977 spraying operations.
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In a community of potters in Barbados where lead glazes traditionally have been used, a survey of 12 potters, 19 of their family members, and 24 controls revealed elevated blood lead levels in the potters, their family members, and the neighbours who used pottery for culinary purposes. Dust from the potters' homes and work areas contained lead in concentrations up to 320,000 ppm. Pottery was found to have lead release levels up to 3,125 microgram/ml. Six people had upper extremity tremor associated with elevated blood lead levels. This survey demonstrates the risk of using lead glazes in pottery production to family members of potters as well as the potters themselves and emphasizes the need for surveillance of occupational hazards in developing countries.
Arsenic, lead, and cadmium absorption levels were determined in 1774 children 1-5 years old living in 19 USA towns with primary nonferrous metal smelters. Results were compared with data on 258 children of the same age in three communities without smelters. Increased systemic absorption of arsenic, as reflected by urine arsenic content, was noted in children near 10 of 11 copper smelters. Blood lead levels were also modestly elevated near two copper smelters. Near lead and zinc smelters, elevated levels of lead and cadmium in hair provided evidence of external exposure to these elements. Levels of lead in blood were not, however, elevated near any of three lead smelters and were elevated near only two of five zinc smelters. Blood cadmium levels were high near one lead and two zinc smelters. The apparent sources of exposure (except in one community with elevated levels of arsenic in drinking water) were air, soil, and dust contaminated by smelting operations. While the full biologic significance of these findings is not known exposure of children to toxic heavy metals emitted by smelters should be reduced to a minimum.
Cholinesterase deficiency was detected in a young girl following an episode of postanesthesia apnea. Subsequently, plasma and serum cholinesterase levels and dibucaine numbers were determined on blood samples from 56 members of her extended family. Including the proband, three individuals were identified with severe cholinesterase deficiency and 12 were found to have mild abnormalities. The occurrence of two genetic variants regulating cholinesterase production, the "silent" gene and the atypical enzyme, is postulated to account for the unusual pattern of inheritance in this family. Screening family members of confirmed cases is essential to prevent the potentially fatal consequences of this hereditary disorder.
Studies to evaluate the prevalence, sources, and health consequences of lead absorption were conducted among children living near a primary lead smelter. Lead levels in air, soil, and dust were highest at the smelter and decreased with distance. Ninety-nine percent of one- to nine-year-old children living within 1.6 kilometers had blood lead levels greater than or equal 40 mug/dl, indicating increased absorption, and 22% had levels greater than or equal 80 mug/dl. The prevalence of lead levels greater than or equal 40 mug/dl decreased with distance; at 72 kilometers from the smelter it was 1%. Erythrocyte protoporphyrin levels increased with blood lead levels: 17% of children with lead levels of greater than or equal 80 mug/dl were anemic. There was no overt neurologic toxicity. Significant negative correlation was found in 202 five- to nine-year-old children between blood lead levels and motor nerve conduction velocity (r = 0.38, p less than 0.02).
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PURPOSE: To establish a safe and effective method for occluding a transjugular intrahepatic portosystemic shunt (TIPS) in patients who develop uncontrollable, disabling encephalopathy. PATIENTS AND METHODS: The study population consisted of five patients who developed refractory encephalopathy following TIPS. The indication for TIPS was bleeding in four patients and ascites in one. Wallstents that were 10 mm in diameter and 68 mm long were used to bridge the hepatic parenchyma in all patients. The onset of encephalopathy from the time of the TIPS procedure ranged from 24 hours to 210 days. Because encephalopathy was not responsive to conventional medical management, shunt thrombosis was induced by means of temporary inflation of an 11.5-mm-diameter latex occlusion balloon within the midportion of the stent. RESULTS: All shunts were successfully thrombosed when the balloon was inflated for 12 hours or more. Encephalopathy resolved in four patients and improved in the remaining patient. One patient experienced recurrent bleeding within 24 hours of the TIPS occlusion that was controlled medically. CONCLUSION: Temporary occlusion of a TIPS with latex balloons successfully induces shunt thrombosis and improves encephalopathy. However, the patient is again exposed to risks related to complications of portal hypertension.
Accidental spillage of 37,900 1 of 100% phenol (carbolic acid) in July 1974 caused chemical contamination of wells in a rural area of southern Wisconsin. Human illness characterized by diarrhea, mouth sores, dark urine, and burning of the mouth was subsequently reported by seventeen individuals who consumed the contaminated water; their estimated intake of phenol was 10 to 240 mg/person/day. Clustering of the illnesses in time and place, as well as the similarity of these cases to previously documented cases of phenol poisoning, suggest that phenol in water caused the illness. Physical and laboratory examinations 6 months after the exposure revealed no residual abnormality in exposed persons. Water testing and geologic evaluations indicate that contamination of the underground water system may persist for many years.
An outbreak of cadmium intoxication in a jewelry factory provided an opportunity for evaluating the usefulness of diagnostic procedures used to evaluate human cadmium toxicity. Blood cadmium levels in workers exposed to cadmium were higher (.93 micrograms/100ml vs .38 micrograms/100 ml) than in unexposed workers. A dose-response relationship was noted between blood cadmium level and symptom prevalence in four symptoms (dyspnea, chest pain, dysuria, and dizziness). Segmental hair analysis revealed highest cadmium levels (up to 19 micrograms/gm) in segments formed prior to cadmium exposure, suggesting that extrinsic contamination was the primary source of cadmium in the hair. beta2-microglobulin levels were within normal limits. No significant renal or pulmonary dysfunction was noted. Symptoms ceased after a cadmium-containing brazing alloy used in jewelry production was replaced, yet urine cadmium levels remained persistently elevated in four workers. Blood cadmium determinations were found to be useful in evaluating symptoms potentially related to cadmium intoxication.
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Planning for the 2000 Sydney Olympic Games may benefit from the experience of the 1996 Atlanta Olympics. Excellent health promotion and prevention activities before and during the Games resulted in fewer medical and public health problems than anticipated. Despite this, there was room for improvement in the level of communication and cooperation between the many service providers to ensure the most appropriate and efficient responses.
Although the American public health system has made major contributions to life expectancy for residents of this country over the past century, the system now faces more complex health problems that require comprehensive approaches and increased capacity, particularly in local and State public health agencies. To strengthen the public health system, concerted action is needed to meet these five critical needs: First, the knowledge base of public health workers needs to be supplemented through on-the-job training and continuing education programs. To this end, self-study courses will be expanded, and a network of regional training centers will be established throughout the country. Second, communities need dynamic leadership from public health officials and their agencies. To enhance leadership skills and expand the leadership role of public health agencies, focused personal leadership development activities, including a Public Health Leadership Institute, and national conferences will provide a vision of the future role of public health agencies. Third, local and State public health agencies need access to data on the current health status of the people in their communities and guidance from the nation's public health experts. To improve access to information resources, state-of-the-art technologies will be deployed to create integrated information and communication systems linking all components of the public health system. Fourth, local and State agencies need disease prevention and health promotion plans that target problems and develop strategies and the capacity to address them. To provide communities with structured approaches to this process, planning tools have been developed and distributed, and technical assistance will be provided to local and State health agencies to involve each community in planning,priority setting, and constituency building.Finally, public health agencies need adequate resources to fund prevention programs. To improve the use of existing Federal support and enhance the availability of new community resources, grant programs will be modified, and innovative approaches to local resource enhancement will be developed and shared.Activities in these five key areas are designed to improve the infrastructure of the public health system and its capacity to carry out effectively the core functions of public health assessment, policy development, and assurance of the availability of the benefits of public health. If the nation is to achieve the health objectives for the year 2000, the public health system-the individuals and institutions that, when working effectively together, promote and protect the health of the people-must be strengthened.
This chapter deals with general principles of conducting medical examinations to detect adverse health effects of workplace exposures and thereby prevent occupational disease or slow its progression. Much of the discussion is most relevant to screening for effects of chemical hazards, but many of the principles presented apply to physical and biological hazards as well. Procedural and administrative aspects of workplace medical examinations that are not "exposure specific" and are applicable to all medical programs are reviewed.