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Year : 2002  |  Volume : 4  |  Issue : 14  |  Page : 49-61
Chemical asphyxiants and noise

Center for Toxicology, University of Oklahoma Health Sciences Center,Oklahoma City OK 73190, USA

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  Abstract 

The damaging effects of noise on auditory function can be altered significantly by exposure to additional agents that may or may not by themselves be ototoxic. This chapter focuses on the ability of chemical asphyxiants present in both occupational settings and ambient environments to potentiate noise induced hearing loss in a laboratory animal model. Since the chemical agents under study do not produce permanent impairment of hearing by themselves, the finding of auditory impairment in excess of that which is produced by noise exposure alone can be defined as noise potentiation. This chapter focuses both on the exposure conditions that favour such potentiation and also on potential mechanisms for potentiation. The data show that low to moderate exposure levels of carbon monoxide (CO) and hydrogen cyanide can potentiate noise induced hearing loss (NIHL) and the relationship between such levels and those permitted in work environments is provided. Finally, evidence is presented that free oxygen radicals may be responsible for potentiation of NIHL by the chemical asphyxiants. First, the ability of a free radical spin trap agent, PBN, to prevent the adverse effects of CO is demonstrated. Then, in an additional experiment, electron paramagnetic spin resonance is used to demonstrate a high level of free radicals in the cochlea with combined exposure to CO + noise while individual exposures to CO and noise do not produce free radicals at levels detectable by this method.

Keywords: chemical asphyxiants, carbon monoxide, hydrogen cyanide, mixed exposures, potentiation of NIHL.

How to cite this article:
Fechter LD, Chen Gd, Rao D. Chemical asphyxiants and noise. Noise Health 2002;4:49-61

How to cite this URL:
Fechter LD, Chen Gd, Rao D. Chemical asphyxiants and noise. Noise Health [serial online] 2002 [cited 2019 May 21];4:49-61. Available from: http://www.noiseandhealth.org/text.asp?2002/4/14/49/31809

  Introduction Top


Noise induced hearing loss (NIHL) is the most common occupational disease in the United States (US DHHS, 1996). Approximately 30 million U.S. workers are exposed to potentially hazardous noise levels in the workplace (Franks et al., 1996) and, consequently, the Occupational Safety and Health Administration (OSHA) has adopted a permissible exposure level (PEL) designed to prevent NIHL (in the Hearing Conservation Amendment (46 Fed. Reg. 4078, 1983) to the US Occupational Safety and Health Act of 1970 (PL 91-596). Nevertheless, NIHL remains a critical occupational concern in the United States and around the world. It is estimated that noise is a significant contributor to hearing loss in roughly 30% of Americans with hearing loss. The reasons for this failure to protect workers against NIHL are many. They include substantial individual differences in susceptibility, difficulty in controlling noise exposure of particular individuals in the workplace (dosimetry), the uncertainty involved in assigning effective trade-off rules for noise intensity and duration of exposure, and, probably, the under-studied phenomenon of potentiation of NIHL by co-exposure to particular chemical ototoxicants. Auditory system injury can result from exposure to a wide variety of drug and chemical exposures as well as the physical agent, noise (e.g. Rybak 1986; 1992; Fechter & Liu, 1997). While cochlear impairment can be a predictable outcome in cases of noise exposure, its occurrence following chemical exposure is far less easily predicted and, therefore, less appreciated.

A potential risk factor for the occurrence of significant hearing loss even under conditions of relatively low noise exposure is the influence of other environmental agents present along with noise. Organic solvents (e.g. Crofton et al., 1994; Campo et al., 1997; Johnson, 1988; Crofton and Zhao, 1994; Fechter et al. 1998; Morata et al., 1993, 1994, 1997 a, b), metals (e.g. Rice and Gilbert, 1992; Wu et al., 1985; Schwartz and Otto, 1987; Fechter et al., 1992), and chemical asphyxiants (e.g. Young et al., 1987; Fechter et al., 1988; Fechter, 1989; Chen and Fechter, 1999; Chen et al., 1999) are all known to have ototoxic potential. Simultaneous and even successive exposure to certain of these agents in combination with noise can greatly increase susceptibility to NIHL (e.g. Johnson et al., 1988, 1990; Fechter et al., 1988; Johnson, 1993, Lataye and Campo, 1997; Morata et al, 1993; Chen and Fechter, 1999). While in most instances the mechanisms responsible for chemical ototoxicity have not been elucidated, there are sufficient data relating oxygen delivery and cochlear function to begin to focus on the process by which chemical asphyxiants and noise interact to permanently disrupt hearing at least in a laboratory animal model. Another compelling reason to study the interaction of noise and chemical asphyxiants stems from their frequent association in many different workplace environments.

The focus of this chapter is on understanding the mechanisms by which chemical asphyxiants present in many occupational settings can potentiate noise-induced hearing loss (NIHL). To do this, the individual acute effects of cyanide and carbon monoxide will be discussed briefly. Once the targets and timing of ototoxicity are noted, the combined effects of noise and chemical asphyxiant are presented.

Workplace Exposures to Noise and Chemical Asphyxiants:

Chemical asphyxiants are the most common chemicals to which workers are exposed. Some of the most notable examples of such occupational exposures are presented here. Cyanides are used intentionally in the extraction of low-grade ores, in electroplating, and as chemical intermediates (US Dept. HHS, 1995). They may be generated by blast furnaces and coke ovens. A list of occupations in which cyanides are used intentionally includes: steel, electroplating, mining, and chemical industries, metal leaching operations, metal cleaning, and analytical chemistry. Cyanides are used in the manufacture of synthetic fibres, various plastics, dyes, pigments, and nylon. In addition to the inadvertent exposure to cyanide as a combustion product, cyanide is also a significant breakdown product of acrylonitriles that are used as grain fumigants, manmade fibres, and in certain plastics. The OSHA PEL for HCN is 10 ppm as an 8-hr time weighted average.

Carbon monoxide exposure is ubiquitous, as it is a major combustion-related pollutant of air. All workers whose employment involves vehicles using internal combustion engines have potential exposure to carbon monoxide including car, bus and truck drivers, toll takers, mechanics, garage attendants, and police officers (Lipsett et al., 1994, p4524). Hosey (1970) notes that the number of people potentially exposed to carbon monoxide in the workplace exceeded that for any other chemical or physical agent. NIOSH (1972) estimated that nearly 1 million workers are occupationally exposed to high levels of CO.

In addition to being the major air pollutant and a waste gas generated by incomplete combustion, CO exposure may occur among acetylene workers, steel and coke oven workers, pulp and paper workers among others (USEPA, 1991). It may also be produced through the metabolism in vivo of the paint stripper, methylene chloride, and of similar chemicals (Stewart et al., 1972). The OSHA 8 hr. time weighted PEL for CO is 50 ppm with an instantaneous ceiling of 200 ppm. The ACGIH time weighted threshold limit value (TLV) is 25 ppm. The NIOSH recommended exposure level is 35 ppm averaged over 8 hr. with a 200 ppm ceiling.

Among occupations where significant exposure to both noise and chemical asphyxiants can be predicted to occur are firefighters, truck drivers, vehicle repair workers, and toll booth takers. Rates of hearing loss and of exposure to both CO and HCN are widely available particularly for firefighters.

Ototoxicity of chemical asphyxiants alone: acute studies:

The mammalian cochlea is a highly metabolically active structure and as such is particularly vulnerable to hypoxia and chemical asphyxiants. In fact, disruption of blood supply (ischemia) and reduction in available oxygen levels (hypoxia) have been suggested to be fundamental mechanisms responsible for many forms of sudden hearing loss and drug ototoxicity (Hawkins, 1967; Lawrence, 1970; Thorne and Nuttall, 1987). Severe hypoxic hypoxia disrupts cochlear function acutely in laboratory animals (Russell and Cowley, 1983; Brown et al., 1983; Nuttall, 1984). In addition, the disruption of blood supply (ischemia) and reduction in available oxygen levels have been suggested as fundamental mechanisms responsible for many forms of sudden hearing loss and drug ototoxicity (Hawkins, 1967; Lawrence, 1970; Thorne and Nuttall, 1987) perhaps by producing reactive oxygen species and excitotoxicity. Seidman and colleagues (1991) have published evidence that auditory impairment following ischemia stems from free oxygen radicals. Hypoxic hypoxia (Nuttall and Lawrence, 1980; Russell and Cowley, 1983; Brown et al., 1983; Nuttall, 1984), CO exposure (Sato, 1966; Goto et al., 1972; Makishima et al., 1977; Fechter et al., 1997; Liu and Fechter, 1995) and cyanide (van Heijst et al.1994; Konishi and Kelsey, 1968; Evans & Klinke 1982; Tawakoli et al, 2001) all impair aspects of cochlear function acutely under severe exposure conditions [Figure - 1]. Disruption in auditory threshold sensitivity and loss of IHC tuning have been commonly reported.

In this paper, we focus on the acute ototoxicity of carbon monoxide (CO) and cyanide (CN-) not only because these agents are common occupational contaminants with the potential to impair the health of millions of workers world­wide, but also because both of these agents can potentiate permanent threshold shifts induced by noise. Studies of acute cochlear impairment due to CO have focused upon ip injection of pure CO gas in order to produce high carboxyhemoglobin levels with a very rapid onset. Such studies are useful in determining potential mechanisms of toxicity, but also produce less specific impairment than would be seen using more moderate inhalation exposures. Such CO injection studies have shown that the generation of the CAP is particularly vulnerable to CO with smaller shifts observed in the CM amplitude (Fechter et al., 1987). The loss in CAP sensitivity can be fully or partially blocked by the NMDA receptor blocker, MK801 (Liu & Fechter, 1995) whether it is injected systemically or placed directly on the round window membrane. The latter route of drug exposure eliminates the potential confounding factor of hypothermia that may result from MK-801. These data suggest that excitotoxicity contributes to acute CO-induced auditory impairment. Putative inhibitors of free oxygen radicals such as PBN and allopurinol (Fechter et al., 1997) may also reduce the acute ototoxicity of CO. PBN is a free radical spin trapping agent that has also been used to facilitate measurement of free radicals using electron paramagnetic spin resonance. Allopurinol is able to reduce free radical generation by inhibiting xanthine oxidase activity. The ability of these drugs to block or reduce CO-induced cochlear impairment has been interpreted to suggest that CO has its predominant effect at the inner hair cell or the synaptic contact between the inner hair cell and the spiral ganglion cell. Presumably, acute injection of CO gas ip enhances glutamate release from the inner hair cell and promotes free radical formation. However, it is of note that subjects treated with such high bolus doses of CO do show recovery of auditory function (Fechter et al., 1987) though it is possible that some residual impairment may occur that is not apparent using CAP threshold sensitivity as a measure of auditory function [Figure - 2].

Unlike the case for hypoxic hypoxia, CO, and ischemia, the effect of cyanide on the cochlea has not been well defined. That cyanide might impair auditory function is predicted not only from studies using other chemical asphyxiants (reviewed above), but also from limited human data suggesting a permanent hearing loss due to cyanide exposure. Van Heijst et al. (1994) studied 20 patients in Tanzania with sudden onset polyneuropathies that included hearing loss in nine cases. Blood cyanide and plasma thiocyanate levels were significantly elevated. The source of exposure was believed to be increased dietary intake of cassava due to food shortages.

Direct experimental evidence that cyanide can produce hearing loss is also limited. Konishi and Kelsey (1968) showed a significant reduction in the endocochlear potential (EP), an indication of impaired stria vascularis function, when 50 mM NaCN-Ringer solution was perfused through the guinea pig cochlea. The stria vascularis contains very high concentrations of Na-K ATPase and plays a critical role in pumping potassium into the region of the cochlea surrounding the organ of Corti. The loss in EP was accompanied by a loss in the CM which is generated mainly by outer hair cells in response to sound, and which is dependent upon the EP. In addition, the CAP amplitude was also depressed. By contrast, Evans & Klinke (1982) working at a much lower concentration range (0.1-1 mM) perfused potassium cyanide (KCN) directly into the scala tympani and monitored both sharpness of tuning curves from individual neuronal units as well as the CAP and CM responses recorded from the round window in the cat. They reported a rapid, but reversible loss in N 1 sensitivity restricted to the characteristic frequency of the unit with no loss observed either in sensitivity of the broad low frequency tail region of the tuning curve, or in spontaneous firing rate. They rejected the view that cyanide impairs stria vascularis function at the low KCN concentrations employed by them largely because they observed an intact CM response and unit responses.

Recent findings of Tawackoli et al (2001) demonstrate in rats that acute injection of KCN rapidly and profoundly reduces both the EP amplitude and the CAP threshold [Figure - 3]. Both effects are closely correlated with blood cyanide levels and both the EP and CAP sensitivity return to baseline values within the few minutes necessary to clear CN from the blood. The effect of high doses of CO, by contrast, occur more slowly than do those of KCN and are predominantly observed on CAP threshold [Figure - 3]. There is little if any impairment of the EP by CO administration. Thus, the apparent cochlear targets for these two chemical asphyxiants appear to be quite different. Against this background it is of interest to determine whether both CO and cyanide can potentiate noise induced hearing loss.

Permanent hearing loss produced by chemical asphyxiants in combination with noise

The risk of producing NIHL under noise exposure conditions that might appear to be safe is underscored by laboratory studies demonstrating the potentiation of NIHL by CO exposure in rats (Young et al., 1987; Fechter et al., 1988; Fechter, 1989). In those studies, broad band noise exposure that, by itself, did not produce an auditory threshold shift, produced significant auditory impairment when CO was presented simultaneously with noise. As noted above, CO by itself has no permanent effects on auditory sensitivity (Young et al., 1987; Fechter et al., 1988; Fechter, 1989).

The role of CO and CN dose in potentiating NIHL

Dose-response studies in which the efficacy of CO and HCN concentration to potentiate NIHL are essential not only in order to determine a function relating chemical asphyxiant concentration to potentiation of NIHL but also to determine the most appropriate exposure conditions for investigating the mechanisms by which such potentiation occurs.

To establish the relationship between CO dose and potentiation of NIHL, subjects were exposed to octave band noise centred at 13.6 kHz for 8 hours duration. CO concentrations varied between 300 and 1500 ppm for different treatment groups. The data show a linear relationship between CO concentration and extent of potentiation of NIHL [Figure - 4]. Statistically significant elevations in threshold are observed with CO exposures of 500 ppm and higher, yet correctional analysis suggests that the theoretical CO level at which auditory thresholds might be elevated lies about 350 ppm CO in rats. The predicted threshold levels at which CO exposure potentiates NIHL far exceed permissible exposure levels for CO. In the United States, the Environmental Protection Agency permits ambient exposure levels of 9 ppm averaged over 8 hr and 35 ppm averaged over 1 hr. For work environments, the standards proposed by ACGIH and by OSHA are 50 ppm averaged over an 8 hr workday, with a peak level of 200 ppm. However, actual workplace CO levels may exceed these permissible levels at least for short time intervals. Moreover, it is an established practice to utilize safety factors in setting permissible human exposure levels so as to assure adequate protection.

Parallel studies have been undertaken also using hydrogen cyanide inhalation along with simultaneous octave band noise exposure for 2 hours [Figure - 5]. Here we have demonstrated that hydrogen cyanide exposures as low as 10 ppm for two hours can significantly promote auditory impairment by octave band noise. As in the case of CO, increasing HCN concentrations tend to increase the extent of NIHL. While the limited number of HCN concentrations tested preclude an estimate of a reference dose at this time, the finding of adverse effects at concentrations slightly below the permissible exposure level in humans raises serious concerns about potential interactions in the workplace.

Finally, studies were conducted using repeated exposures to combined noise and CO exposure over successive days at levels of CO and noise that did not affect auditory function when presented on a single occasion [Figure - 6]. This was done in order to determine whether or not repeated exposure might yield adverse effects. The study of repeated exposure is important in developing a model for certain occupational exposures to noise and CO and for understanding mechanisms that might be involved in the potentiation phenomenon.

Not only is asphyxiant concentration relevant in determining the extent of potentiation of NIHL, but also noise programming also plays a role. Recently, Chen et al. (1999) compared the extent of CO-induced NIHL potentiation by varying the noise duty cycle (the proportion of time that an intermittent noise is turned on) [Figure - 7]. In subjects exposed only to noise, it can be anticipated from many prior studies (e.g. Campo and Lataye, 1992; Fredelius and Wersall, 1992; Patuzzi, 1998) that with the introduction of rest periods in noise that less NIHL would result. The question being asked was whether or not periods of silence introduced into the noise exposure would provide an opportunity for recovery of auditory function damaged as a result of combined exposure to CO and noise? Such a question has immediate practical importance for occupational exposures and it also provides opportunities to probe the mechanism(s) by which potentiation of NIHL occurs. If combined exposure to CO and interrupted noise did not produce comparable consequences for NIHL as seen in the noise only group, it might reflect either more severe initial cochlear stress from which recovery is not possible or it might reflect the blockage of normal recovery pathways by the continued presence of CO in the environment during periods of silence. Because the uptake and elimination of CO from blood takes several hours to occur, it was not possible to add an additional study group in which both CO and noise were turned off during the rest periods. This study is important because it shows that simultaneous exposure to CO and noise renders rest periods inserted into noise ineffective in reducing NIHL. While for subjects exposed to noise only the extent of permanent auditory impairment increased as the noise exposure became more persistent, this relationship was eliminated for subjects receiving the combined exposure. In this study, rats were exposed to noise alone with increasing duty cycles ranging from 40% to 67% and with simultaneous exposure to 1200 ppm CO + noise at each of these duty cycles. The actual exposures consisted of noise exposure for a total of two hours with silence interspersed into the noise exposure. Thus, actual exposures consisted of 2­60 min, 3-40 min, and 4-30 min noise periods with 1 hr periods of silence inserted between blocks of noise. Here equivalent levels of NIHL were detected for all duty cycles studied. Whether the combined exposure to noise and CO produced significant damage to cells or whether it blocked recovery from the noise exposure (since CO was present during periods of quiet) is not known at this time.

Mechanisms by which chemical asphyxiants may potentiate NIHL:

There are two related lines of investigation that suggest that combined exposure to noise and CO increases free oxygen radical levels in the cochlea. This hypothesis was addressed by investigating the protective effects of the free­radical spin-trap, PBN, against NIHL and its potentiation by CO. The drug was administered both prior to and following combined exposure and also only following exposure in order to address the potential for this agent to serve in a therapeutic strategy. While both administration strategies reduced the extent of NIHL by combined exposure, PBN given before and after exposure provided significantly better protection against potentiation of NIHL by CO when compared to post-exposure administration alone (Rao and Fechter, 2000) [Figure - 8].

Repeated post-exposure administration of PBN within 4 hr of exposure revealed somewhat greater protection than a single administration of PBN. While not providing definitive evidence, such data suggest that free radicals may be generated during the combined exposure leading to cochlear impairment. In this experiment, the disruptive effect of noise by itself on the CAP threshold was quite small and it is not certain whether or not the PBN might serve to reduce NIHL as well as its potentiation by CO.

Direct evidence for the production of free radicals following combined exposure to noise + CO comes from studies in which we measured free radicals directly using electron paramagnetic spin resonance. In these studies, rats were first exposed to CO and air alone for 90 minutes to permit equilibration of blood gases with the external environment. The subjects then received an injection of the spin trap agent, POBN followed by 30 minutes of continued gas exposure with and without octave band noise. At the conclusion of this period, the subjects were euthanized and the cochleae harvested to yield samples for EPR spectroscopy. Combined exposure to 1200ppmCO + 100dB OBN for 2 hr exposure generates free radicals in the cochlea (see [Figure - 9]). Neither CO nor noise alone produced a free radical signal in cochlea or in brain samples.


  Summary Top


The current investigation demonstrates the potential of chemical asphyxiants to potentiate NIHL. CO and HCN, chemical neurotoxic agents, which have only acute effects on hearing, are able to enhance permanent NIHL when both noise and chemical agent are presented together. The investigation does not fully address the possibility that potentiation of NIHL by CO can occur under noise conditions that produce no hearing loss whatsoever. In all cases where CO potentiation of NIHL was observed, the appropriate comparison group that received only noise exposure did show at least some limited NIHL. However, earlier studies which provided longer recovery periods of up to eight weeks following exposure (e.g. Young et al., 1987; Fechter et al. 1988) did show that CO could potentiate NIHL at noise exposure conditions that had no significant effects on auditory function. In any case, when studying occupational noise exposure, there are a considerable number of individuals who do ultimately develop a threshold shift. The current data suggest that these cohorts are at greatest risk for the potentiating effects of simultaneous CO exposure.


  Acknowledgements Top


Supported in part by NIOSH grant OH03481and NIH-NIEHS grant ES08082.[52]

 
  References Top

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Correspondence Address:
Laurence D Fechter
Center for Toxicology, The University of Oklahoma, Health Sciences Center, P.O. Box 26901, Oklahoma City, OK 73190
USA
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Source of Support: None, Conflict of Interest: None


PMID: 12678928

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