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Results of Blood Lead Determinations among Workers Potentially Exposed to Lead -- United States

Determinations of blood lead levels among adult workers in the United States were recently analyzed by the National Institute for Occupational Safety and Health (NIOSH) and the National Center for Health Statistics (NCHS); data were collected during the Second National Health and Nutrition Evaluation Survey (NHANES-II). Blood lead levels were significantly higher among adults working in occupations with potential exposure to lead than in occupations without such potential exposures. Cigarette smokers had consistently higher blood lead determinations than nonsmokers, and men had higher levels than women.

NHANES II, conducted by NCHS from 1976 to 1980, was a cross-sectional survey of a probability sample of 27,801 persons, aged 6 months to 74 years, who were selected as representative of the total non-institutionalized civilian population of the United States. The survey used medical histories, physicians' examinations, and laboratory tests to collect a broad range of information on health status, including measurements of lead concentrations in whole blood (1).

The NHANES-II blood lead determinations were compared with data previously collected during the National Occupational Hazard Survey (NOHS) (2), conducted by NIOSH from 1972 to 1974. NOHS collected information on potential exposures of workers to chemical and physical agents in a probability sample survey of approximately 5,000 workplaces across the United States. These data identified occupations with potential occupational exposure* to lead in the workplace.

The results of blood lead determinations among workers, aged 18-74 years, surveyed by NHANES II were divided into two groups: those for persons working in settings previously identified by NOHS as affording potential exposures to lead and those for persons working in settings without such potential exposures. Preliminary results of this comparison indicate that the mean of blood lead determinations for men in the United States with potential occupational exposures to lead (17.9 ug/dL) was significantly greater than that for men without potential occupational exposure to lead (15.5 ug/dL) (p 0.001) (Table 2). Of the male workers with potential occupational exposure to lead, 5.8% had blood lead levels greater than 30 ug/dL. Of male workers without potential occupational exposure to lead, 1.2% had blood lead levels over 30 ug/dL. Hence, 92% of adult men in the United States found in 1976-1980 with blood lead levels over 30 ug/dL worked in occupations that were judged in 1972 to be associated with potential occupational exposure to lead.

Because NHANES-II also recorded information on the smoking status of examinees, it was possible to demonstrate that smokers have significantly higher blood lead levels than nonsmokers (Figure 2). This was true for adults of both sexes and for workers with and without potential occupational exposures to lead. Smoking appeared to have an additive effect to the potential occupational exposure to lead in producing elevated blood lead levels. Reported by Surveillance Br, Div of Surveillance, Hazard Evaluations, and Field Studies, National Institute for Occupational Safety and Health, CDC.

Editorial Note

Editorial Note: Lead poisoning has been recognized since antiquity as a hazard of working with lead (3). Present-day occupations associated with exposure to lead and the risk of lead poisoning include smelting, recovery of scrap, cutting of steel, and the manufacturing of batteries, lead pigment, and stained glass. The major route of lead absorption in the occupational setting is inhaling lead dust and fumes (4). Ingesting lead dust from fingers, food, and cigarettes (5) has also been shown to contribute to occupational exposure.

Chronic occupational exposure to lead has been shown to cause anemia and peripheral neuropathy, the extent and severity of these effects correlating with observed blood lead levels (6). Occupational lead exposure has also been associated with central nervous system dysfunction that may lead to premature senility (7) and with renal impairment resulting in elevated death rates from end-stage renal disease (8). Finally, lead is toxic to reproductive functions and may cause depressed sperm counts in workers (9).

It is not possible to establish a blood lead level below which symptoms are never found or to indicate a blood lead level at which symptoms will necessarily occur (10). Although various standards have been proposed for maximum blood lead levels and permissible exposure limits (11,12), the present analysis focuses on blood lead levels of 30 ug/dL as an indicator of the need for concern. Coincidentally, this level appears to be about two standard deviations above the average blood lead level observed in adults in NHANES II.

The data indicate that exposure in the workplace had and may continue to have a significant impact on blood lead levels of adults in the United States. Although blood lead levels among workers in the lead industries have declined in recent years, they are still significantly higher than among lead workers in the United Kingdom, Sweden, or Finland (13).

Methods of preventing occupational absorption of lead include: 1) replacing lead with less toxic materials; 2) enclosing work processes that produce exposure to lead; 3) adequately ventilating work areas; 4) altering work practices; 5) using personal protective equipment, such as coveralls and respirators; and 6) modifying personal hygiene practices. The first three measures, which tend to reduce airborne lead at its source, are the most effective.

References

  1. National Center for Health Statistics. Plan and operation of the Second National Health and Nutrition Examination Survey, 1976-1980. (DHHS 81-1317) Washington, D.C.: U.S. Public Health Service 1981.

  2. National Institute for Occupational Safety and Health. National Occupational Hazard Survey, 1972-1974. Volumes 1-3. DHHS 74-127, 77-213, 78-114.

  3. Hunter D. The diseases of occupations. 4th ed. Boston: Little, Brown, 1969.

  4. Legge T. Industrial maladies. London: Oxford University Press, 1934.

  5. World Health Organization. Environmental health criteria 3 - lead. Geneva: WHO, 1977.

  6. Baker EL, Jr, Landrigan PJ, Barbour AG, et al. Occupational lead poisoning in the United States: clinical and biochemical findings related to blood lead levels. Br J Ind Med 1979;36(4):314-22.

  7. Arnvig E, Grandjean P, Beckmann J. Neurotoxic effects of heavy lead exposure determinated with psychological tests. Toxicol Lett 1980;5(6):399-404.

  8. Cooper WC, Gaffey WR. Mortality of lead workers. J Occup Med 1975;17(2):100-7.

  9. Lancranjan I, Popescu HI, Gavanescu O, Klepsch I, Serbanescu M. Reproductive ability of workmen occupationally exposed to lead. Arch Environ Health 1975;30(8):396-401.

  10. Fischbein A. Environmental and occupational lead exposure. In: Rom WN, ed. Environmental and occupational medicine. Boston: Little, Brown 1983:443-47.

  11. Testimony for Occupational Safety and Health Administration rulemaking. E Baier, March 15, 1977.

  12. Occupational Safety and Health Administration. Permissible exposure limit for lead. (29 CFR 1910.1025). Washington, D.C.: U.S. Department of Labor. Revised 1978.

  13. Hernberg S, Tola S. The battle against occupational lead poisoning in Finland. Examinations during the 15-year period 1964-1978. Scand J Work Environ Health 1979; 5(4):336-44.

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