Juhasz (1977) qualitatively demonstrated that lead-based ammunition was associated with the generation of particles ranging from under 0.3 to 100 μm; most of the particles were smaller than 1 μm. That observation is similar to results regarding the particle size of copper associated with the use of lead-based or lead-free frangible ammunition. For example, the Air Force Institute for Occupational Health (AFIOH 2008) reported that most airborne copper particles associated with an M4 rifle muzzle blast have an aerodynamic diameter under 5 μm. The committee was unable to obtain similar quantitative data on particle size distributions associated with lead-based ammunition used in different small-arms weapons.
The basis of the general industry lead standard of the Occupational Safety and Health Administration (OSHA) and a large scientific literature (IARC 2006; ATSDR 2007; EPA 2012; NTP 2012) document that several personal behaviors can increase lead dose, including tobacco-smoking, eating, and drinking in the workplace and inadequate personal hygiene before leaving the workplace. The OSHA standard therefore mandates no eating, drinking, or smoking in areas that have potential lead exposure and separate facilities for changing clothes and washing before returning home.
The toxicokinetics of lead—that is, its absorption, distribution, metabolism, and excretion—and its relevance to common biomarkers of exposure are schematically represented in Figure 3-1.
Understanding lead’s partitioning in the body provides a useful background for understanding the available biomarkers of lead. After gastrointestinal or pulmonary absorption, lead enters the bloodstream, in which the vast majority of circulating lead (over 95%) is bound to erythrocyte proteins and the remainder is associated with the plasma (Barltrop and Smith 1972; Cake et al. 1996; Bergdahl et al. 1997), before reaching target organs. Lead is distributed widely in the body and can gain access to sites in the central and peripheral nervous, cardiovascular, renal, reproductive, musculoskeletal, hematopoietic, and other organ systems (see reviews by Hu et al. 2007; EPA 2012; NTP 2012). Lead binds to sulfhydryl and carboxyl groups on a wide variety of structural and functional proteins (Rabinowitz et al. 1973), thereby altering their structure or function. Lead can also agonize or antagonize calcium and thereby alter its normal metabolic functions (Rabinowitz 1991). The ability to mimic calcium contributes to lead storage in the bone; at equilibrium, lead-exposed persons have a substantial body burden of lead: over 90% in the bone pool, 2-8% in various soft tissues, and 2-5% in blood (Rabinowitz et al. 1976). In addition, lead’s nonspecific binding to a variety of proteins and its involvement in calcium pathways explain in large part its myriad health effects. Lead is excreted primarily in urine; this pathway can be enhanced by intravenous chelating agents, such as calcium disodium ethylene diamine tetraacetic acid (commonly referred to as