Preventing Lead Poisoning in Children

2 downloads 0 Views 493KB Size Report
these new findings. MICHAEL S. GOTTLIEB, MD. Sherman Oaks, California. REFERENCES. Bacchetti P, Moss AR: Incubation period of AIDS in San Francisco.
THE WESTERN JOURNAL OF MEDICINE

-

MARCH 1990

-

protective effect should eventually be available from longterm follow-up ofthese cohorts. The US Public Health Service has estimated that 600,000 patients should be offered early treatment with zidovudine based on the findings of these two studies. Because of a reluctance to undergo HIV testing, many may be still unaware that they are infected. Most patients with HIV infection in this country became infected in the early 1980s. In view of the median interval of 9.5 years between the infection with HIV and the development of AIDS, the medical profession has a relatively brief window of opportunity to implement any intervention that slows the progression of HIV disease. The two studies prove that zidovudine, while not invariably effective, when administered at an early stage of disease can have a definite impact. The new data make it a particularly opportune time for health professionals to focus on HIV risk assessment and testing with all of their patients and to specifically review histories of sexual activity, substance abuse, and blood product transfusion. If physicians wait for the zidovudine package insert to be changed, they will deprive many patients of the opportunity to benefit from these new findings. MICHAEL S. GOTTLIEB, MD Sherman Oaks, California REFERENCES

Bacchetti P, Moss AR: Incubation period of AIDS in San Francisco. Nature 1989; 338:251-253 Jason J, Lui KJ, Ragni MV, et al: Risk of developing AIDS in HIV-infected cohorts of hemophilic and homosexual men. JAMA 1989; 261:725-727 National Institute of Allergy and Infectious Diseases: Results of controlled clinical trials of zidovudine in early HIV-infection [news release]. AIDS Clin Trials Alert, January 23, 1989

Preventing Lead Poisoning in Children THE CURRENT STANDARD for blood lead concentrations in children is 25 yg per dl. Researchers throughout the world, however, have recently shown that a blood lead level ofas low as 15 /Ag per dl during gestation and infancy is associated with subclinical neuropsychological impairments, particularly in verbal learning, with an average of four IQ points being lost. Recent population-based surveys of children younger than 6 years living in older urban areas in Alameda and Los Angeles counties, California, indicate that many children are exposed to lead-blood concentrations greater than 25 /g per dl in 1 % to 2% and greater than 15 ixg per dl in 10 % to 20 %. Substantial lead contamination was found in indoor and outdoor paint in Alameda and Los Angeles county study areas (Los Angeles results unpublished) and in soil in the Alameda County area. An additional study is planned for Sacramento County, California. Indoor paint contamination occurs because many homes were built before the 1950 voluntary industry standard and the 1977 federal standard for lead in house paints. Soil contamination is from auto emissions, exterior paint, and industrial sources. The California studies only tested paint from homes where paint was chipping or flaking. An additional hazard is present in homes where lead-based paint is in good condition but where renovation can lead to the spread of paint dust and chips into the home environment and exposure to children. In the past few years, several cases of such exposures have come to the attention of the California Department of Health Services; in most cases, the children involved were asymptomatic. Parents and contractors need to be educated about

152

-

289

3

the proper techniques for removing paint that can prevent household contamination. Additional lead hazards to children are posed by dangerous hobbies around the home (common ones are making stained glass and melting down lead shot to make fishing weights or model figures); ethnic folk remedies used for the treatment of diarrhea (used by such diverse ethnic groups as Hispanics, Southeast Asians, and South Indians); lead in drinking water from leaching from leaded solder, particularly from homes built in the past five years; and take-home exposures from parents who work in lead-contaminated workplaces such as radiator repair shops and smelters. Public Health Approaches The two basic approaches that have been proposed involve screening the children and then cleaning up the environment where lead exposure has been found in children or searching for possible environmental sources and regulating exposure.

Lead screening. Childhood lead screening programs are designed to identify elevated blood lead levels in children and investigate and remove lead from contaminated home environments. The US Centers for Disease Control recommend annual screening for children younger than 36 months living in older, dilapidated housing. Screening is not conducted in most ofthe western states. The California Department of Health Services has undertaken educational efforts to provide physicians with the most up-to-date information about lead exposure and to encourage them to increase their efforts to screen for lead poisoning. These efforts need to be increased. Access to information, however, is not the only barrier to physician involvement in lead screening. One barrier is motivation; in most cases no medical intervention is needed, other than identifying potential source(s) of exposure by history, giving nutritional guidance, and educating parents. Possibly some form of incentive could be devised to motivate physicians to screen. The second barrier is technical: when screening for blood lead levels below 40 Ag per dl, the erythrocyte protoporphyrin screening test has a poor predictive value, and capillary blood lead specimens give a high false-positive rate. Providers do not routinely use venipuncture. Technologic breakthroughs in lead screening that would allow a more acceptable process of specimen collection would help overcome this barrier. In the absence of incentives, the development of new, more feasible technologies for screening, or a requirement that screening be done, it is uncertain what role physicians will take in addressing the problem in the future. Environmental regulation. To address the problem of lead-contaminated houses, it is not necessary to first identify lead exposure in children. For example, a program could identify and decontaminate lead houses, using strategies to encourage owner participation. The costs are unknown, however, and the methods for lead removal need further study. For other sources of lead exposure, additional regulatory and educational approaches could be undertaken. Lead is still used by the canning industry, with a voluntary standard for lead in solder. The phaseout of lead in gasoline has been only partially accomplished. Lead-based paint and solder are still

on

the market and are occasionally inappropriately

used

in homes. Laws restricting workplace lead exposures have a

290

EPITOMES-PREVENTIVE MEDICINE AND PUBLIC HEALTH

MEICNEAN --- EPITOMES~~~~~~~~~~~~~~~~~~~~~~~~-PREVENTIVE-

number of exemptions and are only partially enforced. Many household exposures could be prevented by educating parents about lead in paint, pottery, ethnic remedies, and home hobbies. LYNN R. GOLDMAN, MD, MPH ROBERT D. SCHLAG, MSc MARY HAAN, MPH, DrPH Emeryville, California KENNETH W. KIZER, MD, MPH

Sacramento, California REFERENCES

American Academy of Pediatrics: Committee on Environmental Hazards: Statement on childhood lead poisoning. Pediatrics 1987; 79:457-465 California Department of Health Services: Childhood Lead Poisoning in California: Causes and Prevention. Sacramento, California Dept of Health Services, June 1989 Needleman HL: The persistent threat of lead: Medical and sociological issues. Curr Probl Pediatr 1988; 18:697-744 Smith MA, Grant LD, Sors Al: Lead Poisoning and Child Development: An International Assessment. Boston, Kluwer Academic, 1989

The Tuberculosis and HIV Connection EVIDENCE SUGGESTS that clinical tuberculosis eventually develops in a high percentage of persons infected with both the human immunodeficiency virus (HIV) and Mycobacterium tuberculosis. Tuberculosis often precedes other opportunistic diseases in patients with the acquired immunodeficiency syndrome (AIDS), but tuberculosis-infected patients who survive the first episode of AIDS are at a high risk of clinical tuberculosis developing. This has contributed to the increase in the number of tuberculosis cases reported in the United States since 1984, which had been in a general slow decline for many years. In the United States, AIDS has been reported in as many as 12% ofpatients with tuberculosis. The clinical presentation of tuberculosis in HIV-infected persons varies with the immune status, ranging from the more commonly recognized pulmonary apical cavitation in HIV-infected persons with minimal immune impairment to disseminated disease presenting with blood cultures positive for M tuberculosis in persons with advanced AIDS. A 5-mm or more reaction to tuberculin skin testing (purified protein derivative [PPD]) is seen in about a third of those AIDS patients with tuberculosis who are tested. The chest x-ray film often shows an atypical pattern that includes hilar and mediastinal adenopathy. Cavitation is present in less than 25 % of cases, and diffuse reticulonodular infiltrations are frequently seen. M tuberculosis has been found in the sputum of some AIDS patients with normal chest roentgenograms. Extrapulmonary disease occurs frequently, often associated with pulmonary disease. Although Mycobacterium avium-intracellulare is frequently identified in patients with AIDS, acid-fast bacilli identified on staining from any specimen in a high-risk HIV-infected person should be considered and treated as M tuberculosis until proved otherwise by culture. The unusual patterns of tuberculosis in AIDS patients may make diagnosis difficult. Because tuberculosis is both contagious and treatable, every effort should be made to identify M tuberculosis in AIDS patients. The PPD skin test remains the most reliable test for detecting tuberculosis infection and should be done as early as possible in any person infected with HIV or diagnosed with AIDS. Any measurable induration should be considered as potentially significant, but a 5-mm or larger reaction is definitely positive. Any abnormality on a chest x-ray film in an AIDS patient should be considered suspicious for tuberculosis. Because of the

PULI

HELT

high frequency of cases of extrapulmonary tuberculosis in patients with AIDS, any body fluid specimen-sputum, bronchial washings, cerebrospinal fluid, pleural fluid, ascitic fluids, urine-or lung biopsy specimen should be processed for acid-fast staining and culture during an evaluation for infection. Antituberculous medication should be given immediately whenever M tuberculosis is found or suspected in persons with HIV infection or at an increased risk for HIV infection. The recommended regimen is isoniazid, 300 mg daily, plus rifampin, 600 mg daily, and pyrazinamide, 1,500 mg daily. Ethambutol at a dose of 25 mg per kilogram of body weight daily should be added to the regimen when central nervous system or disseminated tuberculosis exists or isoniazid resistance is suspected. Pyrazinamide therapy may be discontinued after two months if the sputum smear results have converted to negative. The treatment of documented tuberculosis should be continued for at least 9 to 12 months or until the patient's cultures are negative for M tuberculosis at least six months. Tuberculosis in patients with HIV infection or AIDS responds well to antituberculous chemotherapy. When tuberculosis patients with AIDS die, it is usually of other complications of AIDS and not the tuberculosis if they are receiving antituberculous medication. Preventive therapy should be given to any HIV-infected person or anyone at high risk for infection, regardless of age, who has a positive reaction to a PPD skin test. Actual disease should be excluded before starting the therapy. Preventive therapy in this circumstance consists of giving isoniazid, 300 mg daily, for at least 12 months. LE QUOC HANH, MD PAUL T. DAVIDSON, MD Los Angeles REFERENCES

Centers for Disease Control: Tuberculosis and acquired immunodeficiency syndrome-New York City. MMWR 1987; 36:785-790, 795 Centers for Disease Control: Tuberculosis and immunodeficiency virus infection: Recommendations of the Advisory Committee for the Elimination of Tuberculosis (ACET). MMWR 1989; 38:236-238, 243-250 Chaisson RE, Schecter GF, Theuer CF, et al: Tuberculosis in patients with the acquired immunodeficiency syndrome-Clinical features, response to therapy, and survival. Am Rev Respir Dis 1987; 136:570-574

Opportunities for Preventing Woman Abuse and Battering WOMAN ABUSE AND BATTERING is a public health problem of epidemic proportions. In a recent national survey, 16% of women reported physical abuse by their spouses; 6% reported severe abuse-that is, punching, kicking, choking, beating, and attacks with a weapon. In 1980 this resulted in 21,000 admissions to hospitals, 99,800 hospital days, 28,700 emergency department visits, 39,900 physician visits, and $44.3 million in medical costs. Woman abuse is only infrequently identified by physicians. The use of simple nursing protocols with direct questioning has shown that 30% of all women presenting with injuries are battered. Only 10% to 25% of these are diagnosed by emergency department physicians, however. In a recent prospective study of women obtaining private and public prenatal services, 8 % reported physical abuse during the current pregnancy and 15 % in the past. Prenatal care providers, however, had never asked about abuse. Early identification and intervention are vital, as violence tends to escalate, and relationship change becomes more

Suggest Documents