Time course of congener uptake and elimination in rats after short-term inhalation exposure to an airborne polychlorinated biphenyl (PCB) mixture

Abstract

Despite the continued presence of PCBs in indoor and ambient air, few studies have investigated the inhalation route of exposure. While dietary exposure has declined, inhalation of the semivolatile, lower-chlorinated PCBs has risen in importance. We measured the uptake, distribution, and time course of elimination of inhaled PCB congeners to characterize the pulmonary route after short-term exposure. Vapor-phase PCBs were generated from Aroclor 1242 to a nose-only exposure system and characterized for congener levels and profiles. Rats were exposed via inhalation acutely (2.4 mg/m3 for 2 h) or subacutely (8.2 mg/m3, 2 hx10 days), after which pulmonary immune responses and PCB tissue levels were measured. Animals acutely exposed were euthanized at 0, 1, 3, 6, and 12 h post exposure to assess the time course of PCB uptake and elimination. Following rapid absorption and distribution, PCBs accumulated in adipose tissue but decayed in other tissues with half-lives increasing in liver (5.6 h)<lung (8.2 h)<brain (8.5 h)<blood (9.7 h). PCB levels were similar in lung, liver, and adipose tissue, lower in brain, and lowest in blood. Inhalation of the airborne PCB mixture contributed significantly to the body burden of lower-chlorinated congeners. Congeners detected in tissue were mostly ortho-substituted ranging from mono- to pentachlorobiphenyls. Selective uptake and elimination led to accumulation of a distinct congener spectrum in tissue. Minimal evidence of toxicity was observed.

Figure 1

Diagram of the nose-only PCB inhalation exposure system in a secondary containment structure.

Figure 2

Average distribution profile of all congeners during 10 d exposure (A, inset plot showing 0–2.5% on y axis) and day-to-day profile of most prevalent congeners (B) in generated PCB vapor mixture.

Figure 3

Time course of ΣPCB and selected congener concentration in rat liver (A), lung (B), blood (C), adipose tissue (D) and brain (E) following 2 hr inhalation exposure.

Figure 4

Comparison of congener distribution profiles in: generated vapor mixture, and tissue load at different time points post exposure as sorted by mono-, di, tri-, tetra- and pentachlorobiphenyls. ^aAcute exposure (time course experiment), hours post exposure for tissue data. ^bSubacute exposure, hours post exposure for tissue data.

Figure 5

Time course of total TEQ concentration change in rat liver, lung, blood, adipose tissue and brain following 2 hr inhalation exposure.