DNA damage associated with ultrastructural alterations in rat myocardium after loud noise exposure

Noise exposure causes changes at different levels in human organs, particularly the cardiovascular system, where it is responsible for increasing heart rate, peripheral vascular resistance, and blood pressure. In this study, we evaluated the effect of noise exposure on DNA integrity and ultrastructure of rat cardiomyocytes. The exposure to loud noise (100 dBA) for 12 hr caused a significant increase of DNA damage, accompanied by swelling of mitochondrial membranes, dilution of the matrix, and cristolysis. These alterations were concomitant with increased in situ noradrenaline levels and utilization. Genetic and ultrastructural alterations did not decrease 24 hr after the cessation of the stimulus. An elevated oxyradical generation, possibly related to altered sympathetic innervation, is hypothesized as responsible for the induction and persistence of noise-induced cellular damage.     

Could zinc prevent reproductive alterations caused by cigarette smoke in male rats?

The aim of the present study was to evaluate the effects of zinc on fertility through semen parameters, testosterone level and oxidative DNA damage to spermatozoa of rats exposed to cigarette smoke. Male Wistar rats (60 days old) were divided into four groups (n = 10 per group): control, cigarette-smoking (20 cigarettes per day), zinc (zinc chloride 20 mg kg?1 day?1) and zinc plus cigarette-smoking (zinc chloride 20 mg kg?1 day?1; 20 cigarettes per day). The treatment was applied for nine weeks and the following parameters were analysed: bodyweight, wet weights of the reproductive organs and the adrenal gland, plasma testosterone concentration, testicular function (seminal analysis and daily sperm production) and sperm DNA oxidative damage. The exposure to cigarette smoke decreased testosterone concentration, the percentage of normal morphology and the motility of spermatozoa. In addition, this exposure increased sperm DNA oxidative damage. Zinc treatment protected against the toxic damage that smoking caused to spermatozoa. This study showed a correlation between smoking and possible male infertility and subfertility, and also that the majority of smoking-induced changes in spermatozoa were prevented by zinc treatment. In conclusion, zinc, an antioxidant and stimulant of cell division, can be indicated as a promising treatment in men with infertility caused by the toxic components of cigarette smoke.     

饮水硼对大鼠肾上腺组织结构的影响

目的研究饮水添加不同水平硼对大鼠肾上腺的平均质量、器官指数及微细结构的影响。方法选用192只(28±2)天清洁级SD大鼠,分为对照组和40、80、160、320和640mg/L硼染毒组,每组32只,雌雄各半,染毒组饮水添加硼酸,对照组饮用蒸馏水,试验期60天。分别于试验的第30天和60天每组随机取鼠16只,雌雄各8只,解剖取肾上腺称重并取材,石蜡切片,HE染色及嗜铬细胞特染,显微观察与摄影。结果试验30天各染毒组雄鼠的肾上腺平均质量均显著或极显著低于对照组(P<0.05或P<0.01);试验60天640mg/L染毒组雄鼠的肾上腺器官指数显著高于对照组(P<0.05)。40mg/L染毒组肾上腺组织结构较对照组有明显改善,髓质细胞内嗜铬颗粒明显增多;80～640mg/L染毒组肾上腺可见不同程度病理组织学变化,病变程度随硼添加量增大而趋于严重;比较观察发现,肾上腺髓质细胞的损伤先于皮质出现,雄鼠的病变较雌鼠明显。结论饮水添加硼40mg/L对大鼠肾上腺的组织结构有较明显改善作用;添加80～640mg/L硼对肾上腺组织结构则有不同程度损伤,甚至有明显毒性作用。     

Noise exposures aboard catcher/processor fishing vessels

BACKGROUND: Commercial fishing workers have extended work shifts and potential for 24 hr exposures to high noise. However, exposures in this industry have not been adequately characterized. METHODS: Noise exposures aboard two catcher/processors (C/P) were assessed using dosimetry, sound-level mapping, and self-reported activities and hearing protection device (HPD) use. These data were combined to estimate work shift, non-work, and 24 hr overall exposure levels using several metrics. The length of time during which HPDs were worn was also used to calculate the effective protection received by crew members. RESULTS: Nearly all workers had work shift and 24 hr noise levels that exceeded the relevant limits. After HPD use was accounted for, half of the 24 hr exposures remained above relevant limits. Non-work-shift noise contributed nothing to 24 hr exposure levels. HPDs reduced the average exposure by about 10 dBA, but not all workers wore them consistently. CONCLUSIONS: The primary risk of hearing loss aboard the monitored vessels comes from work shift noise. Smaller vessels or vessels with different layouts may present more risk of hearing damage from non-work periods. Additional efforts are needed to increase use of HPDs or implement noise controls.     

Magnetic-field-induced DNA strand breaks in brain cells of the rat

In previous research, we found that rats acutely (2 hr) exposed to a 60-Hz sinusoidal magnetic field at intensities of 0.1-0.5 millitesla (mT) showed increases in DNA single- and double-strand breaks in their brain cells. Further research showed that these effects could be blocked by pretreating the rats with the free radical scavengers melatonin and N-tert-butyl-alpha-phenylnitrone, suggesting the involvement of free radicals. In the present study, effects of magnetic field exposure on brain cell DNA in the rat were further investigated. Exposure to a 60-Hz magnetic field at 0.01 mT for 24 hr caused a significant increase in DNA single- and double-strand breaks. Prolonging the exposure to 48 hr caused a larger increase. This indicates that the effect is cumulative. In addition, treatment with Trolox (a vitamin E analog) or 7-nitroindazole (a nitric oxide synthase inhibitor) blocked magnetic-field-induced DNA strand breaks. These data further support a role of free radicals on the effects of magnetic fields. Treatment with the iron chelator deferiprone also blocked the effects of magnetic fields on brain cell DNA, suggesting the involvement of iron. Acute magnetic field exposure increased apoptosis and necrosis of brain cells in the rat. We hypothesize that exposure to a 60-Hz magnetic field initiates an iron-mediated process (e.g., the Fenton reaction) that increases free radical formation in brain cells, leading to DNA strand breaks and cell death. This hypothesis could have an important implication for the possible health effects associated with exposure to extremely low-frequency magnetic fields in the public and occupational environments.     

大气可吸入颗粒物致HepG2细胞DNA损伤

目的 研究大气可吸入颗粒物 (PM10)致人肝细胞瘤细胞 (HepG2)DNA损伤及其可能机制.方法 单细胞凝胶电泳 (SCGE)试验检测细胞DNA链断裂;2',7'-二氢二氯荧光素 (DCFH)法测定细胞内活性氧水平;免疫组化方法测定8-羟脱氧鸟苷 (8-OHdG)在细胞内的表达水平;免疫细胞化学法检测细胞内核转录因子NF-κBp65蛋白表达水平.结果 大连市4个监测点PM10有机提取物致HepG2细胞DNA链断裂作用存在地点和季节差异;7.5～30μg/mLPM10有机提取物作用HepG2细胞1h后,尾DNA%增大,呈剂量依赖关系.HepG2细胞与7.5～30μg/mL的PM10有机提取物接触1h后,可引起细胞内ROS水平表达的明显增加;7.5～30μg/mL的PM10有机提取物作用于HepG2细胞3h后,细胞内8-OHdG水平的表达增强;HepG2细胞与30μg/mL的PM10有机提取物接触24h后,NF-κBp65蛋白表达水平明显增高.结论 PM10有机提取物可引起体外HepG2细胞DNA链断裂;DNA链断裂水平随不同季节和不同监测点而异;PM10引起DNA损伤的机制可能是细胞内ROS生成增多,8-OHdG表达增高及NF-κBp65蛋白表达水平升高而导致的氧化性DNA损伤.     

Chronic Oral Exposure to Bunker C Fuel Oil Causes Adrenal Insufficiency in Ranch Mink (<Emphasis Type="Italic">Mustela vison</Emphasis>)

Animals living in the near-shore marine environment are predisposed to contact with chemical contaminants through land- and ocean-based activities. The release of petroleum hydrocarbons into the marine environment is a stressor to this environment and its resident wildlife. The stress response to chemical threats is dependent on an intact hypothalamic-pituitary-adrenal axis, which also may be a target to the effects of these chemicals. Ranch mink (Mustela vison) were used as surrogates for sea otters (Enhydra lutris) to examine the development of adrenal hypertrophy after chronic, oral exposure to low concentrations of bunker C fuel oil. Animals were fed three different concentrations of fuel oil (48, 520, and 908 ppm) or mineral oil (control) for 60-62 days. At the end of the exposure, blood and fecal samples were collected and organs were weighed and examined microscopically. In all fuel oil groups, exposure resulted in adrenal hypertrophy, an adaptation suggestive of adrenal activation. However, concentrations of serum and fecal glucocorticoids and serum progesterone were not elevated over control values. Hematologic parameters and serum chemistries showed no changes consistent with increased adrenal activity. In addition, adrenal glands from animals fed the higher concentrations of fuel oil contained large numbers of heavily vacuolated cells. We conclude that petroleum hydrocarbons are inducing an adrenal insufficiency that leads to the adaptive enlargement of the gland. This would increase the susceptibility of fuel oil-exposed animals to the deleterious effects of other environmental stressors.     

出生前邻苯二甲酸二(2-乙基己基)酯暴露对子代大鼠血清皮质醇激素水平的影响

目的探讨出生前邻苯二甲酸二(2-乙基己基)酯(DEHP)暴露对大鼠肾上腺功能的潜在干扰作用。方法将32只健康SD孕鼠按体重随机分为溶剂对照组(玉米油)及2、10、50 mg/kg DEHP染毒组,每组8只。自孕14~19 d连续灌胃染毒,每日1次。子代大鼠于出生后第21天断乳,雌雄分笼饲养至70日龄,断头处死,取血及双侧肾上腺,计算肾上腺脏器系数,并采用Luminex液态芯片技术测定血清皮质醇水平。结果成年雌性仔鼠肾上腺脏器系数在各染毒组间有差异,与对照组相比,2 mg/kg染毒组的肾上腺重量及脏器系数较低,差异有统计学意义(P0.05);成年雄性仔鼠肾上腺脏器系数在各染毒组间差异均无统计学意义(P0.05)。与对照组相比,10、50 mg/kg染毒组的成年雌性仔鼠血清皮质醇水平较高,差异有统计学意义(P0.01);而2 mg/kg染毒组与对照组相比无明显差异(P0.05)。与对照组相比,10 mg/kg染毒组的成年雄性仔鼠血清皮质醇水平较高,差异有统计学意义(P0.01);而2、50 mg/kg染毒组与对照组相比无明显差异(P0.05)。结论出生前DEHP暴露可能干扰子代大鼠肾上腺功能。     

Road traffic noise and annoyance--an increasing environmental health problem

Traffic noise, which is steadily increasing, is considered to be an important environmental health problem. The aim of this study was to estimate the degree of annoyance and sleep disturbance related to road traffic noise in residential settings in an urban community. The study is based on a questionnaire on environmentally related health effects distributed to a stratified random sample of 1000 individuals, 19-80 years old, in a municipality with heavy traffic in the county of Stockholm. The response rate was 76%. The individual noise exposure was estimated using evaluated noise dispersion models and local noise assessments. Frequent annoyance was reported by 13% of subjects exposed to Leq 24 hr >50 dBA compared to 2% among those exposed to <50 dBA, resulting in a difference of 11% (95% Confidence Interval (CI) 7%, 15%). Sometimes or frequently occurring sleep disturbance was reported by 23% at Leq 24 hr >50 dBA and by 13% at levels <50 dBA, a difference of 11% (95% CI 4%, 18%). A positive exposure- response relation was indicated for annoyance as well as for sleep disturbances when classifying the individuals into four different exposure categories (< 45, 46- 50, 51-55 and >55 dBA Leq 24 hr). There was some habituation to noise for problems related to sleep but not for annoyance. The prevalence of both annoyance and sleep problems was higher when bedroom windows were facing streets. People living in apartments had more sleep problems compared to people living in detached or semi-detached houses. In conclusion traffic noise exposure, even at low levels, was associated with annoyance and sleep disturbance. Access to a quiet side seemed to be a major protective factor for noise related problems.     

Noise and solvent,alcohol and solvent: two dangerous interactions on auditory function

While noise exposure is the most significant contributor to occupational hearing loss, recent evidence points to solvents and their interactions as additional contributors to occupational deafness. Furthermore, due to the metabolic competitive inhibition between aromatic solvents and ethanol, the solvent toxicity can be even enhanced in certain circumstances. So, two dangerous interactions: noise and solvents, solvents and ethanol deserve to be taken into consideration in an exhaustive preventive policy. Based on the investigations reviewed in the present study, it appears that the combined effects of an exposure to noise and solvent exceed the summation of the damage produced by each agent alone. Such a statement can be also made for a combined exposure to solvent and ethanol. It is therefore important to bear in mind that noise effects can be exacerbated by non-acoustic agents. Thus, if our noise regulations have to be more effective, it is necessary to take into consideration the ototoxic effects of noise in a multifactorial environment.     

砷对雌性大鼠生殖内分泌影响的研究

目的研究砷对雌性大鼠血清中雌二醇、卵泡刺激素及黄体生成素、泌乳素水平及卵巢、肾上腺病理改变的影响。方法雌性大鼠经砷染毒10周后用放射免疫法测定血清中激素水平;光镜观察子宫和肾上腺的病理改变。结果除了黄体生成素各染毒组与对照组比较有统计学意义外,其余各组均无统计学意义;但卵巢及肾上腺有不同程度的病理改变。结论砷对雌性大鼠的内分泌激素黄体生成素是一个敏感指标,且对生殖系统有直接的损害作用。     

Effect of varying dietary fat levels on rat growth and oxidative DNA damage.

Dietary fat has previously been shown to have somewhat complicated relationships to levels of oxidative stress in rats. In this study, we examined the effects of five different dietary fat intakes on levels of oxidative DNA damage in rats. Animals fed diets containing 3%, 5%, 10%, or 15% corn oil had body weights that were similar after 20 weeks. Animals fed a 20% fat diet, however, had significantly higher mean body weight than any other group. Levels of 5-hydroxymethyl-2'-deoxyuridine, one marker of oxidative DNA damage, had different relationships to dietary fat in blood and mammary gland. In blood, levels increased with dietary fat levels, and the highest levels were observed with the 20% fat diet (65% higher levels than with the 3% fat diet). In mammary gland, a plateau-type effect was observed, with maximal levels of oxidative DNA damage being obtained using 10% fat (representing a 68% increase relative to the 3% fat diet). This could be a result of induction of compensatory mechanisms in response to a high-fat diet in mammary gland but not in the short-lived nucleated blood cells. Oxidative DNA damage levels in blood thus appear to be a marker of dietary fat intake. In mammary gland, however, levels of DNA damage are consistent with previously observed promotional effects of dietary fat on mammary gland tumorigenesis at lower levels of fat intake with little or no incremental promoting effects at higher levels of fat intake.     

Hypertension and Chronic Exposure to Noise

The effects of noise on various cardiovascular parameters are conflicting and uncertain. In the current study, the authors studied 52 workers who were employed in a bedframe factory who were chronically exposed to noise and who had poor hearing. An additional group of 65 workers who had jobs in the light-metal sector and another group of 64 office workers served as two control groups; none of the controls were exposed to noise, and none had hearing defects. Blood pressure was measured for each person in the supine and standing positions, and an electrocardiogram was also performed. Sound-level measurements were taken in the workplaces. Mean systolic and diastolic blood pressures and diastolic blood pressure distributions were significantly higher in the noise-exposed group than in both control groups. Among the three groups, there were significantly different frequencies of hypertension, drops in blood pressure, and electrocardiogram anomalies. Within the group of bedframe workers, those exposed to a personal daily level of exposure (i.e., equivalent continuous noise level for exposure to noise for each individual workers in an 8-hr shift) that exceeded 90 dBA had a higher mean diastolic blood pressure and a higher frequency of diastolic hypertension than workers exposed to a personal daily level of exposure of < 90 dBA. The findings suggested that (a) work performed by the bedframe group had some effects on the cardiovascular system, (b) noise is a cardiovascular risk factor, and (c) cardiovascular effects are relative to intensity and type of exposure. Vascular damage often accompanies auditory damage, but—depending on individual susceptibility—the cardiovascular system can respond in various ways.     

Hypertension and chronic exposure to noise

The effects of noise on various cardiovascular parameters are conflicting and uncertain. In the current study, the authors studied 52 workers who were employed in a bedframe factory who were chronically exposed to noise and who had poor hearing. An additional group of 65 workers who had jobs in the light-metal sector and another group of 64 office workers served as two control groups; none of the controls were exposed to noise, and none had hearing defects. Blood pressure was measured for each person in the supine and standing positions, and an electrocardiogram was also performed. Sound-level measurements were taken in the workplaces. Mean systolic and diastolic blood pressures and diastolic blood pressure distributions were significantly higher in the noise-exposed group than in both control groups. Among the three groups, there were significantly different frequencies of hypertension, drops in blood pressure, and electrocardiogram anomalies. Within the group of bedframe workers, those exposed to a personal daily level of exposure (i.e., equivalent continuous noise level for exposure to noise for each individual workers in an 8-hr shift) that exceeded 90 dBA had a higher mean diastolic blood pressure and a higher frequency of diastolic hypertension than workers exposed to a personal daily level of exposure of < 90 dBA. The findings suggested that (a) work performed by the bedframe group had some effects on the cardiovascular system, (b) noise is a cardiovascular risk factor, and (c) cardiovascular effects are relative to intensity and type of exposure. Vascular damage often accompanies auditory damage, but--depending on individual susceptibility--the cardiovascular system can respond in various ways.     

Occupational noise exposure and hearing protector use in Canadian lumber mills

Noise exposure is probably the most ubiquitous of all occupational hazards, and there is evidence for causal links between noise and both auditory and nonauditory health effects. Noise control at source is rarely considered, resulting in reliance on hearing protection devices to reduce exposure. A comprehensive noise survey of four lumber mills using a randomized sampling strategy was undertaken, resulting in 350 full-shift personal dosimetry measurements. Sound frequency spectrum data and information on hearing protector usage was collected. A determinants-of-exposure regression model for noise was developed. Mean (L(eq,8hr)) exposure level was 91.7 dBA, well above the exposure British Columbia (BC) limit of 85 dBA. Of 52 jobs for which more than a single observation was made, only 4 were below the exposure limit. Twenty-eight jobs had means over 90 dBA, and four jobs had means over 100 dBA. The sawmill and by-products departments of the lumber mills had the highest exposure to low frequency noise, while the planing and saw filing areas had the highest exposure to high frequency noise. Hearing protector use was greatest among those exposed above 95 dBA, and among those exposed between 85 and 95 dBA, self-reported use was 84% for 73% of the time. The determinants of exposure model had an R(2) of 0.52, and the within-participant correlation was 0.07. Key predictors in the final model were mill; enclosure and enclosure construction material; and certain departments, jobs, and noise sources. The study showed that workers in lumber mills are highly exposed to noise, and although the prevalence of the use of hearing protection is high, their use is unlikely to provide complete protection again noise-induced hearing loss at the observed exposures. Determinants of noise exposure modeling offers a good method for the quantitative estimation of noise exposure.     

Genotoxicity of acute and chronic gamma-irradiation on zebrafish cells and consequences for embryo development

The effects of radiation on biological systems have been studied for many years, and it is now accepted that direct damage to DNA from radiation is the triggering event leading to biological effects. In the present study, DNA damage induced by acute or chronic irradiation was compared at the cellular (zebrafish [Danio rerio] cell line ZF4) and developmental (embryo) levels. Zebrafish ZF4 cells and embryos (at 3 h postfertilization) were exposed within ranges of acute doses (0.3-2 Gy/d) or chronic dose rates (0.1-0.75 Gy/d). DNA damage was assessed by immunodetection of γ-H2AX and DNA-PK (DNA double-strand breaks) and the alkaline comet assay (DNA single-strand breaks). Zebrafish embryo development and DNA damage were examined after 120 h. At low doses, chronic irradiation induced more residual DNA damage than acute irradiation, but embryo development was normal. From 0.3 Gy, a hyper-radiosensitivity phenomenon compared to other species was shown for acute exposure with an increase of DNA damage, an impairment of hatching success, and larvae abnormalities. These results suggest a dose-dependent correlation between unrepaired DNA damage and abnormalities in embryo development, supporting the use of DNA repair proteins as predictive biomarkers of ionizing radiation exposure. This could have important implications for environmental protection.     

Risk of hypertension related to road traffic noise among reproductive-age women

Chronic noise exposure is associated with adverse pathophysiological effects, which may contribute to the progression of hypertension. However, evidence supporting its effect on women is still inconsistent. The aim of the study was to examine the hypertension risk related to road traffic noise in residential settings in an urban community amongst reproductive-aged women. Cross-sectional study data including 3,121 pregnant women, 20-45 years old, and a geographic information system (GIS) to assess the average road noise (LAeq 24 hr) for every subject at the current residential address were used. Effects on physician-diagnosed hypertension were estimated by logistic regression with adjustments for age, social status, marital status, education, alcohol consumption, ethnic group, parity, body mass index, chronic disease, and exposure duration. The prevalence of hypertension amongst women aged 20-45 years in the lowest exposure category was 13.1% in comparison to 13.6% and 18.1% amongst those exposed to the medium and the highest exposure category, respectively. After making adjustments for the selected variables, no exposure effects [Odds ratio (OR) ≈ 1.0] were noted in the medium exposure category [51-60 dB(A)]. However, a slight increase was noted in the highest exposure category [≥61 dB(A)), OR 1.36; 95% CI 0.86-2.15]. The effect was more pronounced amongst women aged 30-45 years and a positive exposure-response relation was indicated for hypertension: An effect was seen at noise levels 51-60 dB(A) (OR = 1.03; 95% CI 0.72-1.49) and at >61 dB(A) (OR = 1.94, 95% CI 1.01-3.72). The present study shows some evidence for an association between the residential road traffic noise and hypertension amongst reproductive-aged women, and an exposure-response relationship.     

The effects of nitrous oxide after exposure during middle and late gestation

Recent evidence has indicated that the anesthetic gas nitrous oxide (N2O) is teratogenic to rats if exposed during the organogenesis phase of gestation. Little is known, however, of the anatomical or functional consequences of exposures occurring later in gestation when the brain is developing. Timed pregnant Sprague-Dawley rats were exposed to 75% N2O/25% O2 using one of the following protocols: 24 hr exposures on gestational days 11-15 or 16-20; or 8 hr exposures on gestational days 9-13, 11-15, 14-15 or day 15 only. Both 24 hr exposure protocols significantly reduced fetal and maternal body weight, an effect not observed after the 8 hr exposures. No N2O exposure resulted in gross morphological or skeletal changes. Likewise, no significant effects on total protein and DNA levels in fetal liver and brain tissues could be found subsequent to 24 hr exposures on days 16-20; or on one, three or six days following an 8 hr exposure on day 15. Evaluations of postnatal growth and neurological development in pups prenatally exposed for 8 hr on days 14 and 15 revealed two noteworthy effects. Their rate of growth in body weight was greater with respect to controls between the ages of 14 and 21 days, especially in the males. Also, reflex suspension was reduced, significantly so in the females. In conclusion, unlike 24 hr exposures, multiple 8 hr exposures to nitrous oxide during the middle to late stages of gestation did not produce effects detectable with standard teratological measures. Subtle differences in growth rate and reflex suspension, however, indicated that normal development had been interrupted, but its clear distinction as a lasting effect requires additional measures of function.     

Effects of occupational noise exposure on 24-hour ambulatory vascular properties in male workers

BACKGROUND: Epidemiologic studies have demonstrated that occupational noise exposure is associated with hypertension, but the related mechanism in vascular structural changes is unclear. OBJECTIVE: This panel study aimed to investigate effects of occupational noise exposure on ambulatory vascular structural properties in male workers. METHODS: We recruited 20 volunteers and divided them into a high-noise-exposure group of 15 and a low-noise-exposure group of 5 based on environmental noise measurement in an automobile manufacturing company. We determined individual noise exposure and measured personal ambulatory vascular property parameters simultaneously during 24 hr. Linear mixed-effects regression models were used to estimate transient and sustained effects of noise exposure on vascular parameters by adjusting some confounders collected from self-administrated questionnaires and health checkups. RESULTS: The high-noise-exposed (85 +/- 8 dBA) workers had significantly higher systemic vascular resistance (SVR) than the low-noise-exposed workers (59 +/- 4 dBA) during work and sleep periods. Contrarily, low-noise-exposed workers had significantly higher brachial artery compliance (BAC), brachial artery distensibility (BAD), and systemic vascular compliance (SVC; marginal, p = 0.07) than high-noise-exposed workers during off-duty periods. We also found that high-noise-exposed workers had significantly lower BAC (1.38 +/- 0.55 %mL/mmHg) and BAD (1.29 +/- 0.51 %/mmHg), as well as lower SVC (0.24 +/- 0.10 mL/L/mmHg), but higher SVR (1.93 +/- 0.67 mL/L/min) compared with low-noise-exposed workers over a 24-hr period. CONCLUSIONS: Our findings suggest that in automobile workers, occupational noise exposure may have sustained, not transient, effects on vascular properties and also enhances the development of hypertension.