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PubMed1996

Characterization of the major DNA adduct formed by the food mutagen 2-amino-3-methyl-9H-pyrido[2,3-b]indole (MeAalphaC) in primary rat hepatocytes.

Cooking of proteinous food results in the formation of heterocyclic amines. Among these, 2-amino-3-methyl-9H-pyrido[2,3-b]indole (MeAalphaC) has been identified as a mutagenic pyrolysis product of soya protein and has been detected in grilled or pan fried meat. It was subsequently proven to be carcinogenic in mice and, recently, in rats and to form covalent DNA adducts in vitro and in vivo. The corresponding nitro compound, 2-nitro-3-methyl-9H-pyrido[2,3-b]indole (MeNalphaC), was prepared and shown to be a direct acting mutagen in the Ames Salmonella reversion assay. When MeNalphaC was chemically reduced in the presence of DNA a major DNA adduct was detected using the 32P-postlabelling assay. This major adduct was characterized by UV spectroscopy and mass spectrometry as N-(deoxyguanosin-8-yl)-2-amino-3-methyl-9H-pyrido[2,3-b]indole. This structure was corroborated by identification of the modified base as a guanine moiety modified at the C8 position as judged by chromatographic and spectral comparison with a standard synthesized from acetylated guanine-N3-oxide and MeAalphaC was characterized by UV/Vis and 1H NMR spectroscopy and mass spectrometry. Treatment of primary rat hepatocytes with MeAalphaC (100 microM, 24 h) resulted in adduct levels of 9.8 fmol/microg DNA as determined by 32P-postlabelling analysis. Using HPLC analysis, two major 32P-labelled adducts were observed accounting for 80 and 13% of total binding respectively. The major adduct was chromatographically indistinguishable from the synthetic deoxyguanosine-C8 adduct using both ion-exchange thin layer or reversed-phase HPLC. Although MeAalphaC is formed only in low p.p.b. levels in cooked food, the contribution to the human carcinogenic risk that might be imposed by heterocyclic amines is not to be neglected.

Animals↗

PubMed1998

Interindividual variation in the metabolic activation of heterocyclic amines and their N-hydroxy derivatives in primary cultures of human mammary epithelial cells.

The heterocyclic amines, 2-amino-3-methylimidazo[4,5-f]quinoline (IQ), 2-amino-3,4-dimethylimidazo[4,5-f]quinoline (MeIQ) and 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) are pyrolysis products formed when meat is cooked and are rodent mammary carcinogens. They are thought to be metabolically activated by N-hydroxylation, catalysed by cytochrome P450 (CYP), followed by O-acetylation catalysed by N-acetyltransferases. Primary cultures of human mammary epithelial cells (HMECs) prepared from up to 26 individuals for each compound, were treated with IQ, MeIQ, or PhIP (500 microM) or with N-hydroxy-2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (N-OH-PhIP) or N-hydroxy-2-amino-3-methylimidazo[4,5-f]quinoline (N-OH-IQ) (20 microM) and the levels of adduct formation in their DNA analysed by 32P-post-labelling. In order to investigate whether pharmacogenetic polymorphisms influence DNA adduct formation, the NAT2 genotype of each individual was determined by a polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method that distinguishes between the wild-type and four variant alleles. Presence of two variant alleles designates a slow NAT2 acetylator, whereas individuals with one or two wild-type alleles are designated fast NAT2 acetylators. Interindividual variations in total DNA adduct levels ranged for IQ from 0.64-63.1 DNA adducts per 10(8) nucleotides (mean 7.80), for MeIQ from 1.99-17.8 (mean 6.63), for PhIP from 0.13-4.0 (mean 0.96), for N-OH-PhIP from 6.32-497 (mean 176) and for N-OH-IQ from 0.92-30.6 (mean 9.24). The higher adduct levels observed in cells treated with the N-OH metabolites suggests that N-hydroxylation is the rate-limiting step in HMECs and this may be due to low CYP levels. In contrast, the Phase II reaction catalysed by N-acetyltransferases is probably the major step in the metabolic activation of heterocyclic amines that occurs in the breast. Higher mean levels of heterocyclic amine-DNA adduct formation were detected in the cells of NAT2 fast acetylators compared with slow acetylators, with mean adduct levels per 10(8) nucleotides following IQ treatment, of 12.74 and 3.57 respectively, following PhIP treatment, of 1.20 and 0.74, respectively, following MeIQ treatment, of 7.90 and 5.08, respectively and following N-OH-PhIP-treatment, of 243.1 and 130.0, respectively. However, due to the large variations in adduct levels, these differences in mean values were not statistically significant with the limited number of individuals studied. This appears to be the first pilot study to demonstrate interindividual variations in the metabolic activation of heterocyclic amines and their metabolic intermediates in primary cultures of HMECs in vitro.

Arylamine N-Acetyltransferase↗

PubMed1981

Mass spectral characterisation of the major DNA--carcinogen adduct formed from the metabolically activated carcinogen 15,16-dihydro-11-methylcyclopenta[a]phenanthren-17-one.

E. coli DNA, labelled with [14C]adenine and [14C]-guanine, was allowed to react with the [3H]-labelled carcinogen 15,16-dihydro-11-methylcyclopenta[a]phenanthren-17-one in the presence of a microsomal metabolising system. Enzymatic hydrolysis of the DNA followed by Sephadex LH20 chromatography of its constituent nucleosides established that the major DNA - carcinogen adduct involved guanine, and not adenine. This was confirmed by submitting calf thymus DNA, which had been allowed to react with the unlabelled carcinogen, to pyrolysis electron impact mass spectrometry without further derivatisation. Analysis of a selected ion product (m/z 368) by means of mass-analysed kinetic energy spectrometry, a technique which allows study of the further fragmentation of the single, selected ion, revealed that the guanine moiety was attached via the nitrogen atom of its exocyclic amino group to C-1 of a 1,2,3,4-tetrahydro-2,3,4-trihydroxy derivative of the original carcinogen.

Biotransformation↗

PubMed1999

DNA adducts of heterocyclic amine food mutagens: implications for mutagenesis and carcinogenesis.

The heterocyclic amines (HCAs) are a family of mutagenic/carcinogenic compounds produced during the pyrolysis of creatine, amino acids and proteins. The major subclass of HCAs found in the human diet comprise the aminoimidazoazaarenes (AIAs) 2-amino-3-methylimidazo[4,5-f]quinoline (IQ), 2-amino-3,4-dimethylimidazo[4,5-f]quinoline (MeIQ), 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline (MeIQx), 2-amino-3,4,8-trimethylimidazo[4,5-f]quinoxaline (DiMeIQx) and 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP). All, except DiMeIQx, have been shown to be carcinogenic in animals. These compounds are present in cooked muscle meats at the p.p.b. level. Since the discovery of the HCAs in the late 1970s, many studies have examined the DNA adducts of these compounds. This review compiles the literature on AIA-DNA adducts including their identification and characterization, pathways of formation, mutagenesis in vitro and in vivo, and their association with carcinogenesis in animal models. It is now known that metabolic activation leading to the formation of DNA adducts is critical for mutagenicity and carcinogenicity of these compounds. All of the AIAs studied adduct to the guanine base, the major adduct being formed at the C8 position. Two AIAs, IQ and MeIQx, also form minor adducts at the N2 position of guanine. A growing body of literature has reported on the mutation spectra induced by AIA-guanine adducts. Studies of animal tumors induced by AIAs have begun to relate AIA-DNA adduct-induced mutagenic events with the mutations found in critical genes associated with oncogenesis. Several studies have demonstrated the feasibility of chemoprevention of AIA tumorigenesis. Only a few studies have reported on the detection of AIA-DNA adducts in human tissues; difficulties persist in the routine detection of AIA-DNA adducts in humans for the purpose of biomonitoring of exposure to AIAs. The AIAs are nevertheless regarded as possible human carcinogens, and future research on AIA-DNA adducts is likely to help address the role of AIAs in human cancer.

Animals↗

PubMed2002

Comparison of multiple DNA adduct types in tumor adjacent human lung tissue: effect of cigarette smoking.

Cigarette smokers inhale a broad range of carcinogens derived from tobacco and its pyrolysis products, including free radicals, which induce oxidative stress and subsequent lipid peroxidation (LPO). Miscoding carcinogen-DNA adducts are formed by cigarette smoke constituents and are thought to initiate lung carcinogenesis. The presence of various types of DNA damage was therefore analyzed in tumor adjacent uninvolved lung tissues of 13 smoking and 11 non-smoking operated lung cancer patients. O(4)-ethylthymidine (O(4)etT), 1,N(6)-ethenodeoxyadenosine ( epsilon dA) and 3,N(4)-ethenodeoxycytidine ( epsilon dC) were determined by immuno-enriched (32)P-postlabeling. Polycyclic aromatic hydrocarbon (PAH)-DNA adducts were measured as diagonal radioactive zones after nuclease P1 enriched (32)P-postlabeling. Mean O(4)etT and PAH-DNA adduct levels were higher in lung DNA of smokers than of non-smokers (O(4)etT/10(8) thymidine: 3.8 versus 1.6, P < 0.01; PAH-DNA adducts/10(8) nucleotides: 11.2 versus 2.2, P < 0.01). Pulmonary etheno-DNA adduct levels did not differ between smokers and non-smokers, but large inter-individual variations were observed (80- and 250-fold differences for epsilon dA and epsilon dC, respectively). As all smokers (except one) refrained from smoking at least for 1 week before surgery, our results demonstrate the persistence of O(4)etT and PAH-DNA adducts in human lung. A positive correlation obtained between O(4)etT and PAH-DNA adducts (R = 0.65, P < 0.01) suggests that both adducts are formed from cigarette smoke as the main exposure source. We conclude that in addition to the DNA adducts derived from PAH and tobacco-specific nitrosamines, miscoding O(4)etT lesions are formed by cigarette smoke that contribute to the increased genomic instability and increased lung cancer risk in smokers.

Aged↗

PubMed1983

Specificity of rat liver cytochrome P-450 isozymes in the mutagenic activation of benzo[a]pyrene, aromatic amines and aflatoxin B1.

The ability of three purified forms of rat liver cytochrome P-450 to metabolically activate benzo[a]pyrene, trans-benzo-[a]pyrene-7,8-dihydrodiol, 2-aminofluorene, aflatoxin B1, dimethylnitrosamine, and a pyrolysis product of tryptophan(3-amino-1-methyl-5H-pyrido(4,3-b)indole) (Trp-P-2) to mutagenic products was examined using Salmonella typhimurium strains TA98 and G46 in a reconstituted monooxygenase system. The isozymes examined were cytochrome P-450-PB (the major phenobarbital inducible form), and the two major 3-MC inducible forms (cytochromes P-448(52) and P-448(55)). Cytochromes P-448(52) and P-448(55) preferentially metabolize 2-aminofluorene and Trp-P-2 to mutagenic products. However, only cytochrome P-448(55) metabolizes benzo[a]pyrene and its 7,8-dihydrodiol derivative to mutagenic products. Both cytochrome P-448(52) and P-448(55) metabolize aflatoxin B1 to mutagenic products at a much faster rate than cytochrome P-450-PB. Dimethylnitrosamine was not activated by any of the isozymes tested.

Aflatoxin B1↗

PubMed1983

Syntheses of hydroxyamino, nitroso and nitro derivatives of Trp-P-2 and Glu-P-1, amino acid pyrolysate mutagens, and their direct mutagenicities towards Salmonella typhimurium TA98 and TA98NR.

Hydroxyamino, nitroso and nitro derivatives of 3-amino-1-methyl-5H-pyrido[4,3-b]indole (Trp-P-2) and 2-amino-6-methyldipyrido[1,2-a:3',2'-d]imidazole (Glu-P-1), mutagens-carcinogens produced on pyrolysis of amino acids, were synthesized from Trp-P-2 and Glu-P-1. 3-Hydroxyamino-1-methyl-5H-pyrido[4,3-b]indole (N-OH-Trp-P-2) and 2-hydroxyamino-6-methyldipyrido[1,2-a:3',2'-d]imidazole (N-OH-Glu-P-1) were obtained with good yields by controlled catalytic reduction of 3-nitro-1-methyl-5H-pyrido[4,3-b]indole and 2-nitro-6-methyldipyrido[1,2-a:3',2'-d]imidazole. Subsequent oxidation of N-OH-Trp-P-2 and N-OH-Glu-P-1 with gamma-manganese dioxide yielded 3-nitroso-1-methyl-5H-pyrido[4,3-b]indole and 2-nitroso-6-methyldipyrido[1,2-a:3',2'-d]imidazole. All six synthesized compounds were mutagenic to Salmonella typhimurium TA98 without mammalian activation systems. The mutagenic activities of hydroxyamino and nitroso derivatives were identical for both S. typhimurium TA98 and TA98NR, the nitroreductase deficient strain. However, nitro derivatives were essentially mutagenic only towards S. typhimurium TA98.

Carbolines↗

PubMed1983

Induction of SCE by opium pyrolysates in CHO cells and human peripheral blood lymphocytes.

The induction of sister chromatid exchange (SCE) by opium pipe scrapings (sukhteh, Su) and the pyrolysis products of opium (Op) and of its major alkaloids, morphine (Mo), have been compared with that of cigarette smoke condensate (CSC). All pyrolysates induced SCE and the frequency was further increased by the inclusion of S9-mix in the protocol. The pyrolysates of Op induced considerably more SCE than CSC when the same concentrations were compared on a weight basis, and the rank in order of potency in CHO cells was MO greater than Op greater than CSC greater than Su. The Op pyrolysates may therefore contribute a significant risk factor to the observed high incidence of oesophageal cancer in areas of Iran where heavy Op usage occurs.

Animals↗

PubMedDate not supplied

Determination of sodium monofluoroacetate (compound 1080) in tissues and baits as its benzyl ester by reaction-capillary gas chromatography.

A reaction-capillary gas-chromatographic procedure using photo-ionization (PID) or flame-ionization (FID) detection was developed for the determination of sodium monofluoroacetate (compound 1080), a pesticide, in tissues and baits. Fluoroacetic acid from tissue (1 g) and bait (10 g) extracts was first partitioned into ethyl acetate and then into 0.5 M benzyldimethylphenylammonium hydroxide. Benzylation was achieved by pyrolysis of the quaternary ammonium salt in the injection port. Chloroacetic acid was used as the internal standard. A linear relationship (r = 0.999) was observed between the peak area ratio of the substrate/internal standard and the fluoroacetic acid concentration. The detection limit for compound 1080 using the described analytical procedure, was 15 micrograms/kg with PID and 100 micrograms/kg with FID.

Animals↗

PubMed1994

Pharmacokinetics and pharmacodynamics of smoked heroin.

Despite the current popularity of smoking as a route of drug self-administration, there have been few human studies characterizing the pharmacokinetics and pharmacodynamics of smoked drugs of abuse. A variety of technological difficulties are encountered in the design of smoking studies, such as delivering reproducible doses and limiting the amount of pyrolysis of parent drug. As part of a concerted research effort to deliver precise, smoked doses of drug, a computer-assisted smoking device was utilized that delivered single puffs of heroin vapor to human subjects under controlled clinical conditions. Recovery studies indicated that the smoking device delivered approximately 89% of parent heroin to subjects. Although only two qualified heroin smokers could be identified as eligible volunteers, their participation provided the unique opportunity to study the pharmacokinetics and pharmacodynamics of smoked heroin. The two subjects were administered four smoked heroin doses in ascending order. In addition, four intravenous doses of heroin were administered for comparison of effects and estimation of bioavailability. Concurrent physiological, behavioral, and performance measures were collected along with blood samples. Blood was analyzed for heroin, 6-acetylmorphine, and morphine by solid-phase extraction gas chromatography-mass spectrometry. Heroin appeared rapidly in blood after administration and peaked 1-5 minutes after smoking, which is similar to that observed following intravenous administration. Heroin concentrations declined rapidly to the limit of detection (1.0 ng/mL) by 30 minutes. 6-Acetylmorphine blood concentrations also peaked and declined rapidly after smoked heroin with peak concentrations occurring at 1-2 minutes after smoking. Morphine levels rose and decayed more slowly. Mean elimination half-lives for heroin, 6-acetylmorphine, and morphine were 3.3 min, 5.4 min, and 18.8 min, respectively, by the smoked route. The bioavailability of smoked heroin was highly variable. Physiological measures such as pupil diameter demonstrated a counterclockwise hysteresis compared with heroin blood levels. The rapid onset of pharmacological effects together with the early appearance of heroin and metabolites in blood following smoked heroin demonstrated the effectiveness of this route of drug administration. It is evident that the smoking route enables individuals to obtain similar pharmacological effects as are produced by intravenous administration of heroin.

Administration, Inhalation↗

PubMedDate not supplied

Studies on in vitro degradation of anhydroecgonine methyl ester (methylecgonidine) in human plasma.

The presence of the cocaine pyrolysis product anhydroecgonine methyl ester (AEME, methylecgonidine) in plasma indicates the smoking of cocaine. The stability of this analyte in human plasma has not been studied. In the present investigation AEME and its hydrolysis product anhydroecgonine (AE, ecgonidine) were assayed in plasma and buffers using gas chromatography-mass spectrometry. It was found that 50% of AEME in human plasma was hydrolyzed to AE within 5 days at room temperature and within 13 days at 4 degrees C. Addition of esterase inhibitors such as sodium fluoride or echothiophate iodide reduced the hydrolysis significantly. Hydrolysis of AEME also occurred in buffers with pH values above 5, but the hydrolysis rate was significantly lower when compared with plasma and could be markedly increased by the addition of butyrylcholine esterase. The data suggest that AEME is degraded via two mechanisms: chemical hydrolysis at basic pH and enzymatic hydrolysis by butyrylcholine esterase. Therefore, proper storage conditions must be provided for the assay of AEME in plasma.

Buffers↗

PubMedDate not supplied

The extraction and analysis of quaternary ammonium compounds in biological material by GC and GC/MS.

An injection port pyrolysis method for the analysis of quaternary ammonium compounds is reported. Identification and confirmation of the analyte was accomplished by gas chromatography/mass spectrometry. With minor modifications to pH used and solvent composition, a common ion-pair method of extraction of quaternary ammonium compounds from biological matrices with an iodide counter ion is described. Although the combined extraction-identification methodology was limited to neostigmine, succinylcholine, and paraquat, it should easily be applicable to any of the other compounds examined in this study.

Chromatography, Gas↗

PubMed1998

Microsomal metabolism and activation of the environmental carcinogen 2-amino-3-methyl-9H-pyrido[23-b]indole.

2-Amino-3-methyl-9H-pyrido[2,3-b]indole (MeA alpha C) is a mutagenic and carcinogenic heterocyclic amine formed as a pyrolysis product during cooking of food and combustion of tobacco. Hepatic microsomes from PCB-induced rats metabolized MeA alpha C to four products, of which three were non-mutagenic and one was mutagenic without S9 activation. The three non-mutagenic products, which accounted for 83% of the metabolism of MeA alpha C, were characterized by mass spectrometry and NMR spectroscopy as 6-hydroxy-MeA alpha C, 7-hydroxy-MeA alpha C and 3-hydroxy-methyl-A alpha C. The mutagenic metabolite, accounting for 17% of the metabolism of MeA alpha C, was characterized as N2-hydroxy-MeA alpha C by comparison with the HPLC retention time and UV spectrum of N2-hydroxy-MeA alpha C obtained by chemical synthesis. N2-Hydroxy-MeA alpha C was very reactive and a part of it bound covalently to microsomal proteins during incubation and a part was degraded to other products during incubation or chromatography. N2-Hydroxy-MeA alpha C was mutagenic in Salmonella typhimurium TA98 without metabolic activation, resulting in 5070 revertants/microgram, which was > 20 times the specific mutagenic activity of the parent compound.

Animals↗

PubMed1989

Acute health effects among firefighters exposed to a polyvinyl chloride (PVC) fire.

Firefighters are frequently being called on to fight fires that are chemical in nature. In the aftermath of a chemical fire in Plainfield, New Jersey on March 20-21, 1985, the authors conducted a retrospective cohort study which surveyed 80 firefighters exposed to burning polyvinyl chloride (PVC) as well as 15 nonexposed firefighter subjects. By means of an 81-item symptom checklist, exposed firefighters reported more frequent and severe symptoms at 5-6 weeks post incident. This was true for a total symptomatology score as well as 19 individual items. Some of the items with an elevated risk were consistent with exposure to hydrogen chloride, the main pyrolysis product of polyvinyl chloride. Other items with an elevated risk appeared to be related to smoke inhalation while others seemed psychosocial in nature. Analyses conducted within the exposed firefighter group showed that fighting the fire the first day, being a truckman, and residence within 1 mile (1.6 km) of the firehouse were significant risk factors for high total symptom scores. These risk factors may have been associated with level or duration of exposure to the toxic substances produced during the fire.

Acute Disease↗

PubMed1997

Selective enrichment of bifidobacteria in the intestinal tract of broilers by thermally produced kestoses and effect on broiler performance.

A series of kestose oligosaccharides have been produced from pyrolysis of sucrose and the effects of feeding these thermal kestoses on broiler performance and cecal microbial populations were evaluated. Eighty-four broiler chicks (day-old Hubbard x Hubbard) were fed either a nutritionally complete basal starter diet (control), the starter diet dressed with 8% of other sugars found in the thermal kestoses mixture (glucose, sucrose, and fructose), or the starter diet dressed with 10% crude thermal kestoses (2% kestoses, 8% other sugars) for a 4-wk period. Body weight and feed intake were measured weekly. After 4 wk the birds were killed, cecal contents were collected, and selected microbial populations were enumerated. Weight gains were 938, 968, and 989 g for control, other sugars, and thermal kestoses groups, respectively. There were no dietary effects on weight gain, feed conversion, or concentrations of total aerobic bacteria, coliforms, aerobically enumerated lactobacilli, total anaerobes, or clostridia. Cecal bifidobacterial concentrations were increased (P < 0.001) 24-fold in kestose-treated birds compared with controls, with bifidobacterial concentrations being 8.98, 9.09, and 10.36 log10 cfu/g cecal DM in birds fed the control, other sugars, and thermal kestoses diets, respectively. Anaerobically enumerated lactobacilli concentrations in kestose-treated birds were increased (P < 0.007) sevenfold compared with controls, with lactobacilli concentrations being 9.56, 9.53, and 10.36 log10 cfu/g cecal contents, respectively. Thermally produced kestoses altered intestinal bacterial populations in broilers and may have potential to enhance health and performance under the appropriate conditions.

Actinomycetales Infections↗

PubMed2006

Assessment of Populus wood chemistry following the introduction of a Bt toxin gene.

Unintended changes in plant physiology, anatomy and metabolism as a result of genetic engineering are a concern as more transgenic plants are commercially deployed in the ecosystem. We compared the cell wall chemical composition of three Populus lines (Populus trichocarpa Torr. & A. Gray x Populus trichocarpa Bartr. ex Marsh., Populus trichocarpa x Populus nigra L. and Populus deltoides x Populus nigra) genetically modified to express the Cry3A or Cry3B2 protein of Bacillus thuringiensis (Bt) with the cell wall chemistry of non-transformed isogenic control lines. Three genetically modified clones, each represented by 10 independent transgenic lines, were analyzed by pyrolysis molecular beam mass spectrometry, gas chromatography/mass spectrometry and traditional wet chemical analytical methods to assess changes in cell wall composition. Based on the outcome of these techniques, there were no comprehensive differences in chemical composition between the transgenic and control lines for any of the studied clones.

Bacillus thuringiensis↗

PubMed2001

Determination of heavy metal contents in human colostrum samples by electrothermal atomic absorption spectrophotometry.

Determination of lead, cadmium, nickel, chromium, manganese and copper levels in colostrum samples (n = 30), collected from middle-class mothers, was carried out by electrothermal atomic absorption spectrophotometer (ETAAS) with Zeeman effect background correction using a tungsten-palladium-citric acid chemical modifier mixture. A wet-ashing procedure was applied to dissolve the samples and to remove the fat. The graphite furnace temperature programme for analytes determined by ETAAS was studied, and the optimum pyrolysis temperatures of Pb, Cd, Ni, Cr, Mn and Cu were determined in the presence of the modifier mixture. Detection limits of Pb, Cd, Cu, Mn and Cr were determined using a modifier mixture solution. Zinc and iron levels were determined by Zeeman flame atomic absorption spectrometer (F-AAS). Heavy metal levels (mean values) found in colostrum samples were 14.6 microg/l of Pb, 2.8 microg/l of Cd, 27.8 microg/l of Ni, 8.6 microg/l of Cr, 43.2 microg/l of Mn, 278 microg/l of Cu, 12.9 mg/l of Zn, and 3.5 mg/l of Fe. These metal levels were compared with results from other studies in different countries.

Adult↗

PubMed1995

Mechanism of induction of asthmatic attacks initiated by the inhalation of particles generated by airbag system deployment.

OBJECTIVE: We have previously demonstrated that inhalation of the dust produced by dual frontal airbag deployment can result in significant bronchospasm in approximately 40% of mild to moderate asthmatics. This study was performed to determine the cause of the asthmatic response. DESIGN: Controlled laboratory study. MATERIALS AND METHODS: Asthmatics who were previously tested for their response to airbag effluents were exposed for twenty minutes to either 1) airbag effluents from airbag systems in which the airbag was insulated from the hot deployment module; 2) non-sulfur containing airbag effluents; 3) sodium chloride aerosol; or 4) sodium carbonate-bicarbonate aerosol (pH 10). Pre-exposure, post-exposure, and 2 hour post exposure pulmonary spirometry and mechanics were measured. Subject's filled out symptoms questionnaires before exposure, 2, 4, 8, 12, and 19 minutes into the exposure, immediately post-exposure, and 2 hours post-exposure. MEASUREMENTS AND MAIN RESULTS: Prevention of the pyrolysis of the passenger-side bag as it rested on the hot module after deployment did not diminish the asthmatic response. Removal of sulfur-containing oxidants from the airbag pyrotechnic chemistry, which may have led to sulfite production, similarly did not alleviate the asthmatic response to the airbag effluents. Lastly, when asthmatics were exposed to sodium chloride and sodium carbonate-bicarbonate aerosols at approximately the same concentration (approximately 220 mg/m3) as the airbag aerosol concentration that occurred in the in-car tests, they had responses similar to those produced by the airbag exposures. CONCLUSIONS: We conclude that the amount of soluble particulate contained in the aerosol discharged into the passenger compartment by dual frontal airbag deployment is largely the cause of the observed evoked asthmatic attacks. The alkaline pH of the airbag and carbonate aerosols may have added an additional degree of provocation.

Adolescent↗