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Pulmonary Immunotoxicology of Select Metals: Aluminum, Arsenic, Cadmium, Chromium, Copper, Manganese, Nickel, Vanadium, and Zinc

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Pulmonary Immunotoxicology of Select Metals: Aluminum, Arsenic, Cadmium, Chromium, Copper, Manganese, Nickel, Vanadium, and Zinc Journal of Immunotoxicology ISSN: 1547-691X (Print) 1547-6901 (Online) Journal homepage: http://www.tandfonline.com/loi/iimt20 Pulmonary Immunotoxicology of Select Metals: Aluminum, Arsenic, Cadmium, Chromium, Copper, Manganese, Nickel, Vanadium, and Zinc Mitchell D. Cohen To cite this article: Mitchell D. Cohen (2004) Pulmonary Immunotoxicology of Select Metals: Aluminum, Arsenic, Cadmium, Chromium, Copper, Manganese, Nickel, Vanadium, and Zinc, Journal of Immunotoxicology, 1:1, 39-69, DOI: 10.1080/15476910490438360 To link to this article: https://doi.org/10.1080/15476910490438360 Published online: 29 Sep 2008. Submit your article to this journal Article views: 163 Citing articles: 24 View citing articles Full Terms & Conditions of access and use can be found at http://www.tandfonline.com/action/journalInformation?journalCode=iimt20 Journal of Immunotoxicology, 1:39–69, 2004 Copyright c Taylor & Francis Inc. ISSN: 1547-691X print / 1547-6901 online DOI: 10.1080/15476910490438360 Pulmonary Immunotoxicology of Select Metals: Aluminum, Arsenic, Cadmium, Chromium, Copper, Manganese, Nickel, Vanadium, and Zinc Mitchell D. Cohen Department of Environmental Medicine, New York University School of Medicine, Tuxedo, New York, 10987, USA INTRODUCTION during host resistance against challenge with a viable bacterial The field of immunotoxicology had its inception in the early or viral pathogen) is provided. For some of the metals, poten- 1970s; the science of pulmonary toxicology has been recognized tial mechanisms of action are presented when the literature had for more than forty years. With increasing research efforts in provided same. both fields, a convergence of the two in the quest to understand While this is a large review, it is impossible to cover all metals, how inhalation of toxic agents can alter the health of a host including some that Readers may think merit more of a place here was inevitable. In general, the majority of the advances in our than those presented. It certainly would be worthwhile to have understanding of pulmonary immunotoxicology have come as had provided information about pulmonary immunotoxicologic the result of studies in humans or animal models that inhaled or effects of lead, beryllium, platinum, mercury, and/or iron. It is were instilled with toxicants. Still, it needs to be emphasized that hoped that in the subsequent issues of this new journal, one or immunomodulation in the lungs can also be caused by agents more authors will take up this challenge to survey the literature that enter the body by non-respiratory routes and that all agents covering these metals, and provide a review of either each alone are not necessarily immunomodulatory. or several in compilation. Pulmonary immunotoxicologic research over the past decade has been increasingly important in elucidating how exactly work- ALUMINUM place/environmental agents can cause those changes in immuno- Aluminum (Al) is one of the most abundant elements in the logic function in the lungs that allow for indirect alterations in environment, and daily exposure is unavoidable. Inhalation of respiratory health and, subsequently, the overall health of ex- Al by the general population is generally considered negligible posed individuals. The purpose of this review is to provide infor- (i.e., 0.14 mg Al dust/d [Jones and Bennett, 1986]). Average air mation about how our understanding of the pulmonary immuno- levels of Al for rural and urban areas are provided in Table 1. toxicology of select inorganic agents, i.e., metals, has evolved In contrast, exposures of workers in several industries often oc- over the past ≈30+ years. Specifically, the review covers the cur at significantly higher levels. Smelters, miners, and others literature to date dealing with aluminum, arsenic, cadmium, involved in various metal industries are often acutely exposed, chromium, copper, manganese, nickel, vanadium, and zinc, in accidentally or intentionally, to these much higher ambient levels each of their various inorganic forms with differing chemistries, (i.e., mgs Al/m3). The most recent National Occupational Expo- sizes, and solubilities. For each metal, information regarding sure Study conducted in the 1980s estimated that the total num- occupational and environmental levels that are readily encoun- bers of workers potentially exposed to Al compounds exceeded tered, as well as permissible levels of exposure (when infor- 3,000,000 (ATSDR, 1999a). To help minimize the risk to work- mation was available), is presented at the outset. Thereafter, ers potentially exposed to Al agents, regulatory standards for specific effects on humoral, cell-mediated, and innate immune permissible levels of ambient Al have been established (Table 1). functions, and potential overall effects within the lungs (i.e., as Al-bearing compounds, the majority of which are the var- ious forms of alumina (Al oxide; Al2O3), are widely used in chemical, abrasive, ceramic, and refractory industries as well Address correspondence to Mitchell D. Cohen, Department of Environmental Medicine, New York University School of Medicine, as in primary Al production. In the latter, the metal is refined 57 Old Forge Road, Tuxedo, New York 10987, USA; e-mail: from bauxite and then recovered by electrolytic reduction of [email protected] an Al2O3/cryolite (3NaF·AlF3)-containing melt; to minimize 39 40 COHEN TABLE 1 lung fibrosis in occupationally exposed subjects (Chen et al., Ambient levels and acceptable workplace levels for Al 1978; Gibbs, 1985; Abramson et al., 1989; Chan-Yeung et al., 1989; Larsson et al., 1989; Schwarz et al., 1994; Sorgdrager a a a Background Rural Urban et al., 1995, 1998; Soyseth et al., 1995; Dufresne et al., 1996; Average air levels 0.005–0.018b 0.27–0.38c 0.4–10.0b Kilburn, 1998; Romundstad et al., 2000; Hull and Abraham, (ng Al/m3) 0.005–0.032d 150–1000e, f 2002; Maier, 2002). Among studies examining effects of Al compounds on devel- a,g Regulations and guidelines opment of pulmonary fibrosis and/or asthma (“potroom Accepted levels OSHA NIOSH ACGIH asthma”), only a few assessed histological changes or inflam- 3 h (mg Al/m ) matory responses after agent deposition. An examination of Total dust 15.0 10.0 10.0 lungs of rats instilled with 1 or 5 mg Al2O3/kg BW noted dose- Respirable 5.0 5.0 N/A dependent increased inflammatory responses (characterized by fraction increased neutrophil [PMN] influx and total numbers of lavage- Al metal dust N/A 10.0 10.0 able cells) and minimal interstitial inflammation/type II cell hy- Al in welding N/A 5.0 5.0 perplasia over a 2-month postexposure period (Lindenschmidt fume et al., 1990). Unlike the increased inflammatory responses as Al soluble salts N/A 2.0 2.0 a function of time postinstillation with fibrogenic dust contain- Al alkyls N/A 2.0 2.0 ing silica, effects from Al2O3 were maximal within the first 7– Aluminum oxide N/A N/A 10.0 14 days postexposure and slowly decreased to normal thereafter. A comparison of the inflammatory effects of virginal Al2O3 a ATSDR (1999a). against those of potroom dust (alumina + AlF3 mixture) indi- b United States. cated that while a single instillate of rats with the Al2O3 induced c Central Canada. lung inflammation and an associated PMN influx, effects from d Rural Hawaii. potroom dust were often greater (albeit not dose-dependent; eselect American and Japanese cities. White et al., 1987). The Authors noted that the dust-induced f Sweet and Vermette, 1993; Tsuchiyama et al., 1997; Yokel and McNamara, 2001. increases in PMN were often accompanied by concurrent de- gMany states set values for each agent (in 8- or 24-hour periods) at creases in lavageable alveolar macrophages (AM). This is impor- from <1–several hundred µg/m3. tant in that in a study of effects of virginal Al2O3 vs fluoride(F)- h Eight (8) hour time-weighted averages (TWA). adhered Al2O3, an instillate of an approximetly 8-fold higher amount (i.e., 40 mg/rat) of virginal Al2O3 failed to induce a change in total cell numbers/PMN at 1 month post-exposure fluoride release, virginal (primary) Al2O3 is used as an adsor- (Tornlinget al., 1993). Conversely, instillation of an equal amount bent. While this clearly suggests that workers might potentially of the secondary F-Al2O3 caused (in same timeframe) a dou- be at risk for exposure to Al2O3 and AlF3, other agents may also bling in recoverable total cells and AM, and a 10-fold increase be present at levels that could pose a health risk (e.g., Al: iso- in PMN. The apparent incongruous results among all of these propylate; sulfate; hydroxide; chloride; nitrate; and phosphide, studies are not surprising given that generation-related varia- and triethyl aluminum and Al metal itself [NIOSH, 1984]). tions in purity/cocontaminant composition of various alumina As reflected by these varying standards, compound solubility samples are sufficient to induce disparate immunotoxicologic is critical to the extent of pulmonary (immuno)toxicity that could effects in the lungs (Ess et al., 1993). evolve after deposition of Al agents in that it ultimately impacts A few studies have examined effects from host inhalation/ on both the extent of agent clearance and Al bioavailability. A exposure to Al agents on bronchoalveolar fluid (BAL) compo- few studies have described the distribution/excretion of Al2O3 sition. Lindenschmidt et al. (1990) reported that a single Al2O3 (Rollin et al., 1991; Priest et al., 1998; Schlesinger et al., 2000), instillate induced short-lived significant increases in the amounts Al flakes (Ljunggren et al., 1991), welding fume-associated Al of lactate dehydrogenase (LDH; index of lung cell membrane (Sjogren et al., 1985, 1988), or aluminum chlorhydrate (Stone damage), total protein (index of potential fibrotic activity et al., 1979) after their inhalation or intratracheal (IT) instillation. and/or vascular damage), β-glucuronidase and N-acetylgluco- Other Investigators have concluded that lung Al burdens tend to saminidase (markers of macrophage/PMN membrane damage) increase with host longevity, irrespective of Al source or agent in rat BAL.
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