CSTE ANNUAL MEETING POSITION STATEMENT 1999 ENV 2 COMMITTEE: Environmental TITLE: Surveillance Case Definition for Adult Blood Lead Levels to be Reported to the  National Public Health Surveillance System, NPHSS POSITION TO BE ADOPTED An adult blood lead level that should be maintained under surveillance by the NPHSS is defined as an adult (16 or older) with a venous (or comparable) blood lead level equal to or greater than 25 micrograms per deciliter (mcg/dL) of whole blood.  BACKGROUND AND JUSTIFICATION The CSTE adopted a position in 1995 recommending the addition of elevated adult blood lead levels to the NPHSS; this position statement adds the case definition to the previously adopted position. The case definition above is in accordance with the current U.S. Public Health Service objective for adult lead exposures (Objective 10.8 in Healthy People 2000), “Eliminate exposures which result in workers having blood lead concentrations greater than 25 micrograms per deciliter (mcg/dL) of whole blood.” (1) However, current research indicates that some of the adverse effects on the developmental nervous system and on the cardiovascular system which can be measured in exposed populations, occur at blood lead levels (BLLs) as low as 10 mcg/dL. The National Institute for Occupational Safety and Health (NIOSH) recommends that to minimize the risk of adverse health effects in workers and their children, employers should continually strive to reduce workplace lead exposures. Laboratory Criteria The primary source of blood lead level reports is public and private laboratories; physician reporting may supplement laboratory reporting. Laboratory reporting of BLL results to State lead registries must be mandatory under State law and should include basic demographic information, including personal identifiers to differentiate between new and ongoing cases and to account for multiple reports on the same individual. It is strongly recommended that information be included on occupation and/or industry, lead-avocations, and whether the laboratory is approved for occupational lead testing by the Occupational Safety and Health Administration (OSHA). It is also strongly recommended that laboratories report data on all adults tested for lead. The collection of all test results, regardless of BLL, is extremely helpful in following sequential test results on adults who have elevated blood lead levels. The collection of all test results also provides denominator data that allow calculation of screening penetration rates (i.e., compliance with OSHA requirements) and prevalence rates of elevated lead levels among adults tested.  The U.S. Food and Drug Administration has approved a field portable electro-analytic instrument for the on-site testing of childrens blood lead levels which provides test results in about five minutes. This instrument may use capillary blood and has been found to yield results comparable to venous blood lead samples analyzed by approved laboratories. It is possible that field portable instruments will be approved for workplace blood lead testing of adults. If portable, on-site BLL testing for adults is approved, effective State controls must be instituted to make certain that the results of these tests are reported to the State lead registries.  Lead Lead (Inorganic) is a bluish gray metal that has been used since ancient times because of its useful properties, such as low melting point, pliability, and resistance to corrosion. The ancient Romans and Greeks first discovered its toxic effects. Lead is ubiquitous in U.S. urban environments because of the widespread use of lead compounds in industry, gasoline, and paints during the past century.  Lead is not an essential element nor does it serve any useful purpose in the body. It adversely affects multiple organ systems and can cause permanent damage. Research shows that lead has adverse health effects, including reproductive hazards, at levels once believed safe. Despite the fact that sources of lead exposure and effective preventive measures have been known for decades, occupational lead exposure continues to be an important public health problem. Adult Lead Exposure Industries in which workers have been occupationally exposed to lead include: battery manufacturing and recycling, nonferrous foundries, radiator repair shops, lead smelters, construction sites (during activities such as lead-based paint removal), demolition sites, firing ranges, ceramics, aluminum extruded products and the U.S. armed forces. Avocations in which persons are exposed to lead include: making pottery or stained glass, casting ammunition or fishing weights, sport shooting, and renovating or remodeling homes containing lead paint.  Human exposure to inorganic lead occurs when dust and fumes are inhaled and when lead from lead-contaminated hands, food, water, cigarettes, and clothing is ingested. Lead deposited in the respiratory and digestive systems is released to the blood, which distributes the lead throughout the body. More than 90 percent of total body lead content is accumulated in the bones, where it is stored for decades. Lead in bones may be internally released to the body long after the external environmental exposure occurs.  Among adults, lead poisoning is a persistent, mainly occupational, health problem (2). Adult exposure to lead can damage the central and peripheral nervous (3,4), hematological and renal (5,6), reproductive (7,8), and cardiovascular (9,10) systems. Lead that is taken home from the workplace can also harm children and household members (11). Lead has been shown to be an animal carcinogen (12), and authors of recent studies suggest that occupational lead exposure increases the risk of cancer (13,14). Lead poisoning often goes undetected since many of the symptoms such as stomach pain, headaches, anxiety, irritability, and poor appetite, are nonspecific and may not be recognized as symptoms of lead poisoning. Testing for Lead Exposure There are several biological indices of lead exposure. Measurement of protoporphyrin (free or zinc protorporphyrin) concentration in red blood cells can be a good indicator of inhibition of heme synthesis by lead. There are, however, other causes (e.g., iron-deficiency anemia and inflammatory conditions) of elevated protoporphyrin levels. Lead concentrations in urine, bones, teeth, and hair can be used as biological indicators of current or past lead exposure. Recent advances in the measurement of bone lead levels will eventually provide a more accurate method for determining cumulative lead exposure and the total body burden of lead. At present, however, the best available method for monitoring biological exposure to lead is measurement of the BLL in whole blood. The frequency and severity of symptoms associated with lead exposure generally increase as the BLL increases although there is much individual variability. No such relationship between symptoms and the other indices of lead exposure have been established. The federal Occupational Safety and Health Administration’s (OSHA) regulations to protect workers from lead-associated health effects include requirements for monitoring BLLs among employees who meet certain exposure criteria.  The adult BLL of 25 mcg/dL is defined as “elevated” in relation to national data on BLLs among adults in the U.S. Data from the Centers for Disease Control and Prevention (CDC’s) Third National Health and Nutrition Examination (NHANES III) Survey 1988-91 estimated that the geometric mean BLL for U.S. adults ages 20-74 was 3.0 mcg/dL (95% confidence interval, 2.8-3.2) and that 0.4% of the 6,922 in the sample had BLLs of 25 mcg/dL or greater (15). Extrapolated to the entire U.S. population of adults ages 20-74, this suggests that about 700,000 adults had BLLs of 25 mcg/dL or greater.  In the 1978 general industry standard for lead, OSHA advised that the maximum acceptable BLL was 40 mcg/dL and that men or women planning on having children should limit their exposure to maintain a BLL less than 30 mcg/dL. The CDC has recommended an action level of 10 mcg/dL for childrens exposure to lead (16). OSHA said that at that time feasibility constraints prevented it from establishing a lead standard that would prevent all physiologic changes, reproductive effects, and mild signs and symptoms in exposed workers (17). As required by Title X, in 1993 OSHA provided an equivalent level of protection to construction workers in its interim final rule for lead in the construction industry (29 CFR 1926.62). During the 1993 rule making, OSHA performed no additional analysis of health data and did not reexamine the feasibility of protecting workers from all the known health effects of lead. The feasibility and utility of laboratory-based surveillance of BLLs for adults and children have been documented in many states. CDC currently supports adult lead toxicity surveillance activities and collects data from 27 State health departments. Data from the CDC’s Adult Blood Lead Epidemiology and Surveillance Program for 1997 indicated that 12,716 individuals from 27 reporting states had blood lead levels > 25 mcg/dL, including 777 individuals with blood levels > 50 mcg/dL (18). Extrapolated to the entire U.S., this suggests that about 18,000 adults had BLLs > 25 mcg/dL and about 1,100 had BLLs > 50 mcg/dL in 1997. The most recent analysis of the nationwide adult blood lead data suggest that the number of persons with BLLs > 25 mcg/dL has been relatively constant since 1994. ABLES surveillance data underestimate the prevalence of adult lead toxicity because not all workers with significant lead exposure are being tested appropriately for BLL. Reporting of elevated BLLs by clinical laboratories to State occupational lead surveillance systems has led to a wide variety of public health prevention and intervention activities, including industrial hygiene on-site consultations at lead-using work sites, referrals to OSHA for enforcement actions, referral of exposed workers to physicians for clinical follow-up, education of reported individuals and their physicians, and targeted outreach to high-risk industries.  Lead exposure at work can also affect the families and children of lead exposed workers. A meta-analysis of several studies has suggested that about one half of the children of lead-exposed workers have BLLs > 10 mcg/dL. Lead contamination in the homes of workers who have brought lead dust home on their clothing has been documented. Agencies for Response: Agencies for Information: For information on NIOSH policies and data on adult lead exposures,  telephone the NIOSH hotline: 1-800-356-4674. For further information, including contact persons and publications from the 27 states participating in the Adult Blood Lead Epidemiology and Surveillance (ABLES) Program, contact the NIOSH home page: (http://www.cdc.gov/niosh/ables.html). For information on OSHA, EPA and HUD lead policies and publications, contact their home pages at: http://www.osha.gov, http://www.epa.gov, and http://www.hud.gov, respectively. CONTACT: Martha Stanbury New Jersey Department of Health and Family Services 609 984-1863  References 1. DHHS. Healthy people 2000: Midcourse Review and 1995 Revisions. Washington, DC: U.S. Department of Health and Human Services, Public Health Service, 1995.  2. Sussell A, Ashley K, Burr G, Gittleman J, Mickelsen L, Nagy H, Piacitelli G, Roscoe R, Whalen E. Protecting Workers Exposed to Lead-Based Paint Hazards: A NIOSH Report to Congress, Cincinnati, OH: U.S. Department of Health and Human Services, National Institute for Occupational Safety and Health, CDC 1997. 3. Hogstedt C, Hane M, Agrell A, Bodin L. Neuropsychological test results and symptoms among workers with well-defined long-term exposure to lead. Br J Ind Med 1983;40:99-105. 4. Seppäläinen AM, Hernberg S, Vesanto R, Kock B. Early neurotoxic effects of occupational lead exposure: A prospective study. Neurotoxicology 1983;4(2):181-192. 5. Piomelli S. Chemical toxicity of red cells. Environ Health Perspectives 1981;39:65-70. 6. Goyer RA. Mechanisms of lead and cadmium nephrotoxicity. Toxicology Letters 1989;46:153-162. 7. Goyer RA. Transplacental transport of lead. Environ Health Prospectives 1990;89101-105. 8. Mushak P, Davis JM, Crocetti AF, Grant LD. Prenatal and postnatal effects of low-level lead exposure: Integrated summary of a report to the U.S. Congress on childhood lead poisoning. Environ Res 1989;50:11-36. 9. Schwartz J. Lead, blood pressure, and cardiovascular disease in men. Environ Hlth 50, 1995. 10. Hertz-Picciotto I, Croft J. Review of the relation between blood lead and blood pressure. Epidemiologic Reviews 1993;15(2):352-73. 11. US Department of Health and Human Services, Public Health Service, Centers for Disease Control and prevention, National Institute for Occupational Safety and Health. Report to Congress on Workers Home Contamination Study Conducted Under the Workers Family Protection Act (29 U.S.C. 671a). DHHS (NIOSH) Publication No. 95-123, 1995. 12. IARC. IARC Monographs on the evaluation of carcinogenic risks to humans. Overall evaluations of carcinogenicity: updating of IARC monograph volumes 1 to 42. United Kingdom: World Health Organization, International Agency for Research on Cancer. Supp. 7:230-32, 1987.  13. Anttila A, Heikkilä P, Nykyri E, Kauppinen T, Hernberg S, Hemminki K. Excess lung cancer among workers exposed to lead. Scan J Work Environ Health 1995;21:460-469. 14. Cocco P, Dosemeci M, Heineman EF. Brain cancer and occupational exposure to lead. J Occup and Environ Med 1998;40(11):937-42. 15. Brody DJ, Pirkle JL, Kramer RA, Flegal KM, Matte TD, Gunter EW, Paschal DC. Blood Lead Levels in the US Population: Phase 1 of the Third National Health and Nutrition Examination Survey (NHANES III, 1988 to 1991). JAMA 1994;272(4):277-83. 16. Centers for Disease Control and Prevention. Screening Young Children for Lead Poisoning: Guidance for State and Local Public Health Officials. Atlanta: CDC, 1997. 17. OSHA. 43 Fed. Reg. No. 220. Occupational Safety and Health Administration: Final standard for occupational exposure to lead: supplementary information, health effects, pp. 52954-5, 1978. 18. CDC. Adult blood Lead Epidemiology and Surveillance--United States, First Quarter, 1998, and Annual 1994-1997. MMWR 1998;47(42):907-11.