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At least 19 recordsLinked to original sources

Health effects of exposure to automobile exhaust--V. exposure of toll booth operators to automobile exhaust.

The exposures of automobile toll booth collectors in the Boston area to selected air contaminants were monitored during the four seasons from 1972 to 1974. The highest carbon monoxide concentrations were found at the in-city toll booths and the highest lead levels at the surburban booths. Biological monitoring for carbon monoxide and lead exposure were closely related to airborne contaminant levels. The study supports the need for environmental control for toll booths located at busy highway and tunnels.

Air↗

Tumours in mice after subcutaneous injection of automobile exhaust condensates.

Automobile exhaust condensate (AEC), either mixed with benzo[a]pyrene (BaP) or suspended or dissolved in tricaprylin, was injected subcutaneously into NMRI mice in a series of experiments. The addition of AEC decreased the incidence of tumours which developed with 30, 90 and 270 microgram BaP. Reduction of tumour incidence was proportional to the amount of AEC added. With an injection of 10 microgram BaP, the latent period was greatly increased when AEC was added, but the occurrence of tumours was the same. Components of AEC appear to inactivate BaP, at least temporarily. In further experiments AEC and nine fractions thereof were injected subcutaneously into mice. The fraction comprising only polycyclic aromatic hydrocarbons (PAH) induced the highest incidence of tumours. In contrast, when it was administered in combination with other fractions the PAH fraction was less active. Application of the products of further fractionation of PAH showed that polycyclic compounds with seven or more rings can also induce tumours in this model.

Animals↗

[Progresses on adverse health effects of automobile exhaust].

The progresses on the latest studies at home and abroad on adverse health effects of automobile exhaust were reviewed in this paper. Particulates and poisonous gases from automobile exhaust were considered to be harmful to respiratory system, immune system and reproductive system. It showed that increased prevalence of respiratory disease (e.g. chronic bronchitis and asthma), and decreased lung function, immunity were associated with automobile exhaust. The carcinogenic potential from the exposure to automobile exhausts needs to be further explored because the carcinogenesis is multifactorial.

Animals↗

On the contribution of polycyclic aromatic hydrocarbons to the carcinogenic impact of automobile exhaust condensate evaluated by local application onto mouse skin.

The objective of this investigation was to identify the substances chiefly responsible for the carcinogenicity of automobile exhaust condensate using topical application onto the skin of mice. This was performed by comparing the carcinogenic effect of various fractions with that of an unseparated sample of automobile exhaust condensate, tested in 3 different doses. The probit and Weibull analysis of the result shows: (a) The condensate, emitted from a gasoline-driven automobile provokes local tumors after long-term application to the dorsal skin of mice. The tumor incidence demonstrates a clear cut dose-response relationship. (b) The fraction of polycyclic aromatic hydrocarbons (PAH) containing more than 3 rings accounts for about 84-91% of the total carcinogenicity of automobile exhaust condensate. This fraction represents only about 3.5% by wt of the condensate. (c) The content of benzo[a]pyrene (BaP) (0.414 mg/g) accounts for 6-7.6% of the total carcinogenicity of automobile exhaust condensate, 15 selected PAHs for about 41%. (d) Regarding the minor effect of the PAH-free fraction (about 83% by wt), no hints for a cocarcinogenic activity were observed.

Animals↗

Importance of automobile exhaust catalyst emissions for the deposition of platinum, palladium, and rhodium in the northern hemisphere.

An estimated 500 million vehicles worldwide are equipped with an exhaust catalyst that uses platinum group elements (PGE) as the main active components and thus contribute to global PGE emissions. Although PGE emitted from automobile exhaust catalysts were first believed to remain in the roadside environment, we propose here that fine PGE-containing particles in automobile exhaust have resulted in a widespread distribution of emitted PGE. Regional and long-range transport of PGE from automobile exhaust catalysts is supported by elevated PGE deposition in both a peat bog located 250 m from traffic and in central Greenland, respectively. Russian smelters were also found to contribute to PGE contamination in central Greenland. Deposition rates estimated for the roadside environment, the peat bog, and central Greenland were used to provide a first estimate of PGE deposition in the northern hemisphere. The results show that deposition of regionally or long-range transported PGE accounts for a large fraction of total PGE deposition, and PGE deposition in the roadside environment represents less than 5% of the total deposition. Transport at the regional and global scales represents an important component in the environmental cycle of emitted PGE and needs to be further studied to fully assess the environmental fate of PGE from automobile exhaust catalysts.

Aerosols↗

Study of lead exposure from automobile exhaust as a risk for nephrotoxicity among traffic policemen.

BACKGROUND: Traffic policemen are the most exposed population to lead (Pb) from automobile exhaust. There has been increasing concern about the possible harmful effects of Pb from automobile exhaust on health of traffic policemen. However, no such study was concerned with the impact of Pb exposure on renal function among them. Therefore, we aimed to study the effect of Pb exposure from automobile exhaust on renal integrity among traffic policemen. METHODS: Markers of tubular damage [urinary excretion of beta(2)-microglobulin (beta(2)M), N-acetyl-beta-D-glucosaminidase (NAG), alkaline phosphatase (ALP) and gamma-glutamyl transferase (gamma-GT)], a marker of glomerular injury (albuminuria), and markers of glomerular filtration [serum creatinine, serum beta(2)M and blood urea nitrogen (BUN)] were determined in 43 traffic policemen (Pb-exposed group) and 52 matched healthy persons (control group). Pb levels in blood, urine, hair and nails were determined in the two groups as exposure indices of Pb. RESULTS: The results obtained show that the Pb-exposed group had higher Pb levels in blood, urine, hair and nails than the controls. Among the Pb-exposed group, Pb levels in blood, hair and nails showed significant and positive correlations with the duration of exposure to Pb which is measured as the duration of employment. Among the studied markers of kidney damage, urinary excretion of NAG and albumin were significantly higher in the Pb-exposed group than in the controls. Urinary excretion of NAG was positively correlated with duration of exposure, blood Pb and nail Pb. Urinary albumin was positively correlated with duration of exposure, blood Pb and hair Pb. The other markers of kidney damage were neither elevated nor correlated with exposure indices of Pb. CONCLUSION: Traffic policemen are liable to Pb toxicity, and the determination of Pb in blood, hair and nails are good markers of such toxicity. In these exposure conditions, kidney damage is possible. Such damage is both tubular and glomerular in nature and can be documented by determination of the urinary excretion of NAG and albumin.

Acetylglucosaminidase↗

The health effects of automobile exhaust. VI. Relationship of respiratory symptoms and pulmonary function in tunnel and turnpike workers.

To examine the effect of automobile exhaust on respiratory symptoms and pulmonary function, the authors studied 175 tunnel and turnpike workers employed by the Massachusetts Turnpike Authority on two occasions 3 yr apart beginning in 1972. A standard respiratory symptom and illness questionnaire was administered, spirometry was performed, and proximal hair lead and blood lead content were measured as biologic indices of automobile exhaust exposure. One hundred nine (63%) workers were current cigarette smokers, 41 (23%) were exsmokers, and 24 (14%) had never smoked. Smoking was strongly related to respiratory symptoms of cough (P less than .001) and phlegm production (P less than .001), but not to wheezing (P = .41), breathlessness (P = .14), bronchial asthma (P = .13), or frequent chest colds (P = .14). When workers were stratified by smoking status, no effect could be seen between high automobile exhaust exposure as measured by a variety of parameters and all of the above respiratory symptoms and illnesses. The level of pulmonary function [forced expiratory volume in 1 sec (FEV1.0) and forced vital capacity (FVC)] was not related to past or current exhaust exposure in a cross-sectional analysis when we controlled for age, height, and cigarette consumption. In a prospective analysis of 84 of these workers, the observed changes in FEV1.0 and FVC over 3 yr were unrelated to exhaust exposure after controlling for age, height, cigarette consumption, and initial level of pulmonary function.

Adult↗

Chrysotile asbestos exposure associated with removal of automobile exhaust systems (ca. 1945-1975) by mechanics: results of a simulation study.

For decades, asbestos-containing gaskets were used in virtually every system that involved the transport of fluids or gases. Prior to the mid-1970s, some automobile exhaust systems contained asbestos gaskets either at flanges along the exhaust pipes or at the exhaust manifolds of the engine. A limited number of automobile mufflers were lined with asbestos paper. This paper describes a simulation study that characterized personal and bystander exposures to asbestos during the removal of automobile exhaust systems (ca. 1945-1975) containing asbestos gaskets. A total of 16 pre-1974 vehicles with old or original exhaust systems were studied. Of the 16 vehicles, 12 contained asbestos gaskets in the exhaust system and two vehicles had asbestos lining inside the muffler. A total of 82 samples (23 personal, 38 bystander, and 21 indoor background) were analyzed by Phase Contrast Microscopy (PCM) and 88 samples (25 personal, 41 bystander, and 22 indoor background) by Transmission Electron Microscopy (TEM). Only seven of 25 worker samples analyzed by TEM detected asbestos fibers and 18 were below the analytical sensitivity limit (mean 0.013 f/cc, range 0.001-0.074 f/cc). Applying the ratio of asbestos fibers:total fibers (including non-asbestos) as determined by TEM to the PCM results showed an average (1 h) adjusted PCM worker exposure of 0.018 f/cc (0.002-0.04 f/cc). The average (1 h) adjusted PCM airborne concentration for bystanders was 0.008 f/cc (range 0.0008-0.015 f/cc). Assuming a mechanic can replace four automobile single exhaust systems in 1 workday, the estimated 8-h time-weighted average (TWA) for a mechanic performing this work was 0.01 f/cc. Under a scenario where a mechanic might repeatedly conduct exhaust work, these results suggest that exposures to asbestos from work with automobile exhaust systems during the 1950s through the 1970s containing asbestos gaskets were substantially below 0.1 f/cc, the current PEL for chrysotile asbestos, and quite often were not detectable.

Air Pollutants, Occupational↗

Respiratory health associated with exposure to automobile exhaust. I. Results of cross-sectional studies in 1979, 1982, and 1983.

Three cross-sectional studies were conducted in an effort to investigate the effect of automobile exhaust on respiratory symptoms. Female adult subjects were selected from residents who lived near roadways that were subjected to very heavy traffic. A standard questionnaire was administered to approximately 5,000 people. Distances of the residences from the roadside were adopted as an index of exposure to automobile exhaust. The estimated odds ratios for chronic cough, chronic phlegm, chronic wheeze, shortness of breath, and chest cold with phlegm, relative to distance from the roadside--adjusted by age, smoking status, years at residence, occupation, and type of home heating-ranged from 0.76 to 2.75. The 95% confidence limits of the odds ratios for chronic cough and chronic phlegm excluded or approached 1.00 in each of the studies. This suggests that exposure to automobile exhaust may be associated with an increased risk of certain respiratory symptoms.

Adult↗

The tumor-producing effect of automobile exhaust condensate and fractions thereof. Part III: mathematical-statistical evaluation of the test results.

This paper deals with the mathematical-statistical evaluation of experiments devoted to the following problems: 1. To what extent is the carcinogenic potency of automobile exhaust gas condensate dependent on the dose? 2. What fractions (groups of substances) of the automobile exhaust gas condensate are mainly responsible for the carcinogenic potency? 3. To what extent can the potency be explained by fractions (or single substances)? In order to answer the above questions, the working group planned animal experiments (cf. Misfeld and Timm, 1973) and obtained, prepared, and fractionalized automobile exhaust gas condensate (Grimmer, 1978). The exhaust gas condensate and its fractions were dropped onto the skin of female CFLP mice (Brune et al., 1978). In view of the problems posed above, the aim of the mathematical-statistical evaluation was to establish the dose-response relations, to assess the combined effect, and to estimate the relative potency and the assumed potency. In particular, the hypothesis (basis for the separation process) that the potency of the entire exhaust gas condensate is mainly attributable to the fraction which contains the polycyclic aromatic hydrocarbons (nitromethane phase) was examined.

Animals↗

Methemoglobinemia induced by automobile exhaust fumes.

Although methemoglobinemia is an uncommon disorder, it should always be considered in the differential diagnosis of cyanosis. Major causes of acquired methemoglobinemia are nitrates, aniline, and analgesics, though rare cases have been reported to have been caused by automobile exhaust fumes. A 24-year-old man had inhaled a large amount of automobile exhaust fumes, intending to commit suicide. He had become unconscious, with dilated pupils and symptoms of cyanosis. Arterial hemoglobin oxygen saturation (Sp(O2)) was 86%, with a methemoglobin level of 44.3% and a carboxyhemoglobin level of 0%, while electrolytes, blood urea nitrogen, creatine, and glucose measurement results were normal. He was treated with methylene blue 250 mg (approximately 4 mg/kg) through a nasogastric tube. Four hours after the treatment, because the methemoglobin level was slightly above normal (2.2%), we added 180 mg of methylene blue. The results of final arterial blood gas analysis were a methemoglobin level of 0.4% and a carboxyhemoglobin level of 0.8%. He recovered uneventfully and returned home by himself the next day. To summarize, we successfully treated, with methylene blue given through a nasogastric tube, a young man who had developed severe methemoglobinemia from inhaling automobile exhaust fumes.

Adult↗

Detection of polycyclic aromatic hydrocarbon exposure from automobile exhaust fumes using urinary 1-hydroxypyrene level as an index.

UNLABELLED: Polycyclic aromatic hydrocarbons (PAHs) are hydrocarbon compounds which originate from incomplete combustion. In humans, PAHs are bioactivated to reactive metabolites which can bind covalently to DNA and subsequently initiate mutation and carcinogenesis. The measurement of PAHs exposure may be used as an index to classify a cancer risk group. The purpose of the present study was to measure the level of urinary 1-hydroxypyrene, a metabolite of PAHs, in subjects exposed to automobile exhaust fumes compared to non-exposed subjects. A urine sample was collected from each individual subject after the end of a working day and quantitated for 1-hydroxypyrene and creatinine by HPLC and spectrophotometric method, respectively. The results showed that average urinary 1-hydroxypyrene level in exposed subjects was significantly higher than non-exposed subjects (mean +/- SD of 0.0035 +/- 0.0032 and 0.0011 +/- 0.0010 micromol/l, respectively; P = 0.000). Average urinary creatinine level in exposed subjects was also significantly higher than non-exposed subjects (mean +/- SD of 0.01 +/- 0.005 and 0.008 +/- 0.006 mol/l, respectively; P = 0.040). The ratio of urinary 1-hydroxypyrene/mol creatinine level, of the exposed subjects was significantly higher than that of the non-exposed subjects (mean +/- SD of 0.37 +/- 0.28 and 0.19 +/- 0.22 micromol/mol creatinine, respectively; P = 0.002). CONCLUSION: Automobile exhaust fume exposed subjects have a higher risk to be exposed to PAHs than the non-exposed subjects. Urinary 1-hydroxypyrene level can be used as an index for an exposure of PAHs which have originated from automobile exhaust fumes and other sources as well.

Adult↗

Effect of automobile exhaust on the distribution of trace elements and its modulation following Fe, Cu, and Zn supplementation.

The effect of automobile exhaust on the distribution of trace elements with special reference to Pb and its modulation following Cu, Zn, and Fe supplementation, in mouse organs, has been studied using Energy Dispersive X-ray Fluorescence technique. Seven elements, namely K, Fe, Cu, Zn, Br, Rb, and Pb, were detected in all the organs. The maximum concentration of Pb was found in lungs followed by that in liver and kidney. The effect of automobile exhaust was found to be significant on the concentrations of Fe and Pb; their concentrations were found to increase in all the organs. However, the concentrations of Cu and Zn were found to be decreased significantly in the liver. In the animals given Fe, Cu, or Zn supplementation along with motor exhaust, the percentage change in the concentration of Pb in lungs was decreased, and that of Fe was increased significantly. In kidney, no significant change was observed for the animals given Cu and Zn, whereas for animals given Fe, the level of Pb decreased significantly. In liver, the reduction in the level of Zn in the exhaust-exposed animals was made up and the level of Pb was reduced following Zn supplementation. These results clearly indicate that Fe and Zn play an important role in Pb metabolism and tend to lower the absorption of Pb. The effect of Fe is more pronounced than that of Zn, whereas the effect of Cu seems to be insignificant.

Administration, Inhalation↗

Investigations on the carcinogenic burden by air pollution in man. XIV. Effects of automobile exhaust condensate on the Syrian golden hamster lung.

Syrian golden hamsters were intratracheally instilled with 5 or 2.5 mg/animal of automobile exhaust condensate at two weekly intervals. Moribund animals were fixed by intravascular perfusion. Samples of lobar and segmental bronchi, as well as of peripheral lung tissue, were taken for electron microscopical examination. In addition, all organs were examined histologically. After a survival time of 30 to 60 weeks all animals developed multiple pulmonary adenomas, thus indicating a marked carcinogenic effect of automobile exhaust condensate.

Adenoma↗

Determination of mutagenic activities in different fractions of automobile exhaust condensate by the Salmonella/oxygenase mutagenicity test system.

Automobile exhaust condensate of a passenger car (gasoline engine) was separated into fractions of 2-3 rings containing -, 4-7 rings containing polycyclic aromatic hydrocarbons (PAHs) and PAH-free fractions. All fractions were tested for mutagenicity by the Ames system. The highest dose-dependent increase in revertant colonies was found for the 4-7 ring PAH-fraction when tested with Salmonella typhimurium TA 98 and TA 100. These results are compatible with data obtained in in-vivo tests by previous investigations. The mutagenicity of these fractions in the absence of the oxygenase was negligible.

Animals↗

Rat and rabbit response (in relation to age) to inhalation of automobile exhaust fumes.

Rats of two age groups, of 119 and 163 g mean body weight, were exposed for three and thirty days, respectively, to automobile gases diluted with air. In addition, rabbits, of 1.88 kg mean body weight, were exposed for twenty-four days. The conditions of exposure were kept nearly constant as related to the concentration of CO in the chamber. The following determinations were performed: (1) Body weight measurements as evidence of growth of the animals; (2) The number of alveolar macrophages (AM) in the lung washings; (3) Damage to the integrity of the cytoplasmic membrane of AM; (4) Glucose-6-phosphate dehydrogenase activity (G6PD) in AM; (5) The acid-base balance in the capillary blood of the rabbits. The results of the 30-day exposure show that automobile exhaust gases significantly inhibit the growth of both age groups; with significant body weight losses in the older animals from the 16th day of exposure. The number of AM was elevated in both groups. The activity of G6PD increased in the AM of the younger animals and decreased in the AM of the older as compared with the controls. The number of dead AM was higher in the older than in the younger rats. After the three-day exposure, no significant difference was found in the number of AM washed from the lungs of both exposed groups, compared with the controls. However, G6PD activity and the number of viable AM in the older animals were decreased and the percent of dead phagocytes was significant. The opposite effect was seen in the younger group. Alterations of lung tissue structure in the exposed animals were apparent to the naked eye. Acid-base response showed metabolic and respiratory disturbances as evidenced by the decrease in carbon dioxide tension (PCo2), the rise of hemoglobin by the reduction of pH level and by the base excess (BE). The inhibition of the growth of the rabbits was noted. The intra- and extrapulmonary effect of automobile exhaust gases after inhalation was observed as a complex of disturbances of the fundamental metabolic processes in the organism. The gases affected the cells of lung defence-alveolar macrophages and their biosynthetic activity.

Acid-Base Equilibrium↗

Respiratory health associated with exposure to automobile exhaust. III. Results of a cross-sectional study in 1987, and repeated pulmonary function tests from 1987 to 1990.

We conducted an epidemiological study to investigate the association between exposure to automobile exhaust and respiratory health. We selected 3 zones from two geographically different areas in Tokyo on the basis of expected exposure levels: (1) within 20 m from the side of major roads with heavy traffic, (2) between 20 and 150 m from the side of the same road, and (3) a residential district of suburban Tokyo. The subjects of the study were female adults aged 30-59 y. A cross-sectional study of respiratory symptoms and repeated pulmonary function testing were also performed in each zone. The results suggested that exposure to automobile exhaust may be associated with respiratory symptoms. Nevertheless, repeated pulmonary function testing did not reveal any consistent differences. Investigators should conduct additional follow-up studies to investigate the decline of pulmonary functions with age.

Adult↗

What interaction does indoor nitrogen dioxide have on the effect of the automobile exhaust.

An attempt was made to investigate the effects of automobile exhaust to the people living alongside major traffic arterial in Tokyo. Several hundreds of housewives aged from 40 to 59 who lived more than 3 years were sampled both from the area A; within 20 m from road side, and from the area B which extended from 20 m to 150 m along the road next to the area A. ATS-DLD questionnaire was used to check the prevalence of respiratory symptom, its results was analysed with a deliberate consideration on smoking habits and using status of unvented kerosene space heater. Among each symptom prevalence, difference between the area A and the B was observed significantly in symptom rate related persistent cough and phlegm. These differences became much distinguished in non-smoking group and people not using unvented heater. For about one tenth of sample subject, joined the study of measurement of personal exposure to NO2 for 24 hr using NO2 filter badge. The average concentration of exposure depends largely on heater using status but does not on the study area, even though the atmospheric concentration of NO2 in the area A was higher than that of the area B. The difference of symptom prevalence between the study area becomes not significant compared with the group of using unvented heater. This means that, we suppose, the substantial higher symptom prevalence which observed in the area along the roadside is masked by repeated exposure to elevated indoor concentration of NO2 resulted from using kerosene space heater.

Climate↗