Advertisement

Deterioration of Air Quality in Firing Ranges: A Review of Airborne Lead Exposures

  • Ram K. Tripathi
  • Gerald C. Llewellyn
Part of the Biodeterioration Research book series (BIOR, volume 3)

Abstract

Exposure to airborne lead in indoor (Fischbein et al., 1979; Novotny et al., 1987; Landrigan et al., 1975; Smith, 1976; NIOSH, 1975; Anderson et al., 1977; Olmez et al., 1984;) and outdoor firing ranges (Tripathi et al., 1989a, b) is a documented occupational health hazard. Deterioration of air quality in firing ranges poses a serious health threat to personnel who work in shooting ranges, both commercial and private. Airborne lead, dust, and fumes generated by the firing guns, cause an accumulation of lead in the blood of firearm instructors, maintenance workers, and shooters. A study conducted by the National Institute for Occupational Safety and Health (Anania and Seta, 1975) reported an average airborne lead concentration from nine indoor firing ranges of 2,700 μg/m3, almost 54 times the current Occupational Safety and Health Administration (OSHA) standard of 50 μg/m3 (OSHA, 1978). Another recent study conducted by Tripathi et al., (1989a) from an outdoor firing range reported an average airborne lead concentration of 129 μg/m3.

Keywords

Lead Exposure Blood Lead Level Personal Protective Equipment Blood Lead Concentration Firing Range 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. Anania, T.L., and Seta, J.A. (1975). Lead exposure and design considerations for indoor firing ranges. NIOSH 76-130. Department of Health, Education, and Welfare, Washington, D.C.Google Scholar
  2. Anderson, K.E., Fischbein, A., Kestenbaum, D., Sassa, S., Alveres, A.P., and Kappas, A. (1977). Plumbism from airborne lead in firing range: an usual exposure to a toxic heavy metal. Amer. J. Med., 63, 306–312.CrossRefGoogle Scholar
  3. Annest, J., Dirkle, J., Makuc, C, Nesse, J., Bayse, D., and Kovar, M. (1983). Chronological trends in blood lead levels between 1976 and 1980. N. Engl. J. Med., 308, 1373–1377.CrossRefGoogle Scholar
  4. Barry, P.S.I. (1975). A comparison of concentrations of lead in human tissues. Br. J. Ind. Med., 32, 119–139.Google Scholar
  5. Bellinger, D., Leviton, A., Waternauk, C, Needleman, H., and Robinowitz, M. (1987). Longitudinal analysis of prenatal and postnatal lead exposure and early cognitive development. N. Engl. J. Med., 316, 1037–1043.CrossRefGoogle Scholar
  6. Brown, D.R. (1975). Neonatal lead exposure in the rat: Decreased learning as a function of age and blood lead concentration. Toxicol. Appl. Pharmacol., 32, 628–637.CrossRefGoogle Scholar
  7. Butchthal, F., and Behse, F. (1979). Electrophysiology and nerve biopsy in men exposed to lead. Br. J. Ind. Med., 36, 135–147.Google Scholar
  8. Cramer, K., and Dahlberg, L. (1966). Incidence of hypertension among lead workers: a follow-up study based on regular control over 20 years. Br. J. Ind. Med., 23, 101–104.Google Scholar
  9. EPA (1986). Environmental Protection Agency. Air quality Criteria for lead. EPA 600/8-83/02dF. Vol. 4, 12-221-12-244.Google Scholar
  10. Fahim, M.S., Fahim, Z., and Hall, D.G. (1976). Effects of subtoxic lead levels on pregnant women in the State of Missouri. Res. Commun. Chem. Pathol. Pharmacol., 13, 309–331.Google Scholar
  11. Fischbein, A., Rice, C, Sarkozi, L., Kon, S.H., Petrocci, M., and Selikoff, I.J. (1979). Exposure to lead in firing ranges. J. Amer. Med. Assoc., 241, 1141–1144.CrossRefGoogle Scholar
  12. Fischbein, A., Nicholson, W.J., and Weisman, I. (1980). Comparative lead emissions from conventional and jacketed ammunition. Am. Ind. Hyg. Assoc. J., 41, 525–527.CrossRefGoogle Scholar
  13. Gross, S.B. (1981). Human oral and inhalation exposure to lead: summary of Kehoe balance experiments. J. Toxicol. Environ. Health, 8, 333–377.CrossRefGoogle Scholar
  14. Harlan, W.R., Landis, R., Schmonder, R.L., Goldstein, M.G., and Harlan, L.C. (1985). Blood lead and blood pressure. Relationship in the adolescent and adult population. J. Am. Med. Assoc., 253, 530–534.CrossRefGoogle Scholar
  15. Heard, M.J. and Chamberlin, A.C. (1982). Effects of minerals and food uptake of lead from the gastrointestinal tract in humans. Hum.Toxicol., 1, 411–415.CrossRefGoogle Scholar
  16. Kehoe, R.A. (1961a). The metabolism of lead in man in health and disease: the normal metabolism of lead. J. R. Inst. Public Health Hyg., 24, 81–97.Google Scholar
  17. Kehoe, R.A. (1961b). The metabolism of lead in man in health and disease: the metabolism of lead under abnormal conditions. J. R. Inst. Public Health Hyg., 24, 129–143.Google Scholar
  18. Kehoe, R.A. (1961c). The metabolism of lead in man in health and disease: present hygienic problems relating to the absorption of lead. J. R. Inst. Public Health Hyg., 24, 177–203.Google Scholar
  19. Lampert, P.W., and Schochet, S.S. (1968). Demyelination and remyelination in lead neuropathy: electron microscopic studies. J. Neuropathol. Exp. Neurol., 27, 527–545.Google Scholar
  20. Lancranjan, I., Popescu, H.I., Gavanescu, O., Klepsch, I., and Serbanescu, M. (1975). Reproductive ability of workmen occupationally exposed to lead. Arch. Environ. Health, 30, 396–401.CrossRefGoogle Scholar
  21. Landrigan, P.J., McKinney, A.S., Hopkins, L.C., Rhodes, Jr., W.W., Price, W.A., and Cox, D.H. (1975). Chronic lead absorption: results of poor ventilation in an indoor pistol range. J. Amer. Med. Assoc., 234, 394–397.CrossRefGoogle Scholar
  22. Lauwerys, R.R. (1983). Biological monitoring of exposure to inorganic and organometallic substances, In: Industrial Chemical Exposure: Guidelines for Biological Monitoring, pp.9–50, Biomedicai Publications, Davis, CA.Google Scholar
  23. Muhaffey, K., Annest, J., Roberts, J. and Murphy, R. (1982). National estimates of blood lead levels. United States, 1976-1980, N. Engl. J. Med., 307-573-579.Google Scholar
  24. NBS. (1977). National Bureau of Standards. The reduction of airborne lead in indoor firing ranges by using modified ammunition. Special publication No. 480-130. Washington, D.C.Google Scholar
  25. Needleman, H.L., Rabinowitz, M., and Levington, A. (1983). The risk of minor congenital anomalies in relation to umbelical cord blood lead levels. Pediatri. Res., 17, 1281A.Google Scholar
  26. NIOSH. (1975). National Institute for Occupational Safety and Health. Lead exposure at an indoor firing range. DHEW publication No. (NIOSH) 74-100.Google Scholar
  27. NIOSH. (1983). National Institute for Occupational Safety and Health, Centers for Disease Control. Reducing exposure to airborne lead in indoor firing ranges-United States. MMWR, 32, 483–489.Google Scholar
  28. Novotny, T., Cook, M., Hughes, J., and Lee, S.A. (1987). Lead exposure in a firing range. Amer. J. Public Health, 77, 1225–1226.CrossRefGoogle Scholar
  29. O’Flaherty, E.J., Hammond, P.B., and Lerner, S.I. (1982). Dependance of apparent blood lead half-life on the length of previous lead exposure in humans. Fundam. Appl. Toxicol., 2, 49–54.CrossRefGoogle Scholar
  30. Olmez, I., Kotra, J.P., Lowery, S., and Zoller, W.H. (1984). Airborne lead and trace elements in an indoor shooting range: a study of the DC National Guard Armory Pistol Range. Environ. Toxicol. Chem., 4, 447–452.CrossRefGoogle Scholar
  31. OSHA. (1978). Occupational Safety and Health Administration. Occupational Exposure to Lead. OSHA Final Standard. Fed. Reg. 43. 54353–54616.Google Scholar
  32. Pirkle, J.L., Schwartz, J., Landis, J.R., and Harlan, W.R. (1985). The relationship between blood lead levels and blood pressure and its cardiovascular risk implications. Am. J. Epidem., 121, 246–258.Google Scholar
  33. Rabinowitz, M.D., Wetherill, G.W., and Kopple, J.D. (1974). Studies of human lead metabolism by use of stable isotopetracers. Environ. Health Perspect., 7, 145–153.CrossRefGoogle Scholar
  34. Rabinowitz, M.B., Wetherill, G.W., and Kopple, J.D. (1976). Kinetic analysis of lead metabolism in healthy humans. J. Clin. Invest., 58, 260–270.CrossRefGoogle Scholar
  35. Rabinowitz, M.B., Wetherill, G.W., and Kopple, J.D. (1977). Magnitude of lead intake from respiration by normal man. I. Lab. Clin. Med. 90, 238–248.Google Scholar
  36. Seppalainen, A.M., and Hernberg, S. (1980). Subclinical lead neuropathy. Am. J. Ind. Med., 1, 413–420.CrossRefGoogle Scholar
  37. Seppalainen, A.M., and Herberg, S. (1982). A follow-up study of nerve conduction velocities in lead exposed workers. Neurobehav. Toxicol. Teratol., 4, 721–723.Google Scholar
  38. Smith, D.L. (1976). Lead absorption in police small-arms instructors. J. Soc. Occup. Med., 26, 139–140.CrossRefGoogle Scholar
  39. Tripathi, R.K., Sherertz, P.C., Llewellyn, G.C., Armstrong, C.W., and Ramsey, S. L. (1989a) Overexposures to lead at a covered outdoor firing range. J. Amer. Coll. Toxicol., (in press).Google Scholar
  40. Tripathi, R.K., Sherertz, P.C. Llewellyn, G.C., Armstrong, C.W., and Ramsey, S.L. (1989b). Reducing exposures to airborne lead in a covered outdoor firing range by using totally copper-jacketed bullets. Amer.Indust. Hyg. Assoc. J., (in press).Google Scholar
  41. Victery, W., Vauder, A.J., Schoeps, P., and Germain, C. (1983). Plasma renin is increased in young rats exposed to lead in utero and during nursing. Proc. Soc. Exp. Biol. Med., 172, 1–7.CrossRefGoogle Scholar

Copyright information

© Springer Science+Business Media New York 1990

Authors and Affiliations

  • Ram K. Tripathi
    • 1
  • Gerald C. Llewellyn
    • 1
  1. 1.Bureau of Toxic SubstancesVirginia Department of HealthRichmondUSA

Personalised recommendations