Long-term exposure to gaseous air pollutants and cardio-respiratory mortality in Brisbane, Australia

Air pollution is ranked by the World Health Organisation as one of the top ten contributors to the global burden of disease and injury. Exposure to gaseous air pollutants, even at a low level, has been associated with cardiorespiratory diseases (Vedal, Brauer et al. 2003). Most recent epidemiological studies of air pollution have used time-series analyses to explore the relationship between daily mortality or morbidity and daily ambient air pollution concentrations based on the same day or previous days (Hajat, Armstrong et al. 2007). However, most of the previous studies have examined the association between air pollution and health outcomes using air pollution data from a single monitoring site or average values from a few monitoring sites to represent the whole population of the study area. In fact, for a metropolitan city, ambient air pollution levels may differ significantly among the different areas. There is increasing concern that the relationships between air pollution and mortality may vary with geographical area (Chen, Mengersen et al. 2007). Additionally, some studies have indicated that socio-economic status can act as a confounder when investigating the relation between geographical location and health (Scoggins, Kjellstrom et al. 2004). This study examined the spatial variation in the relationship between long-term exposure to gaseous air pollutants (including nitrogen dioxide (NO2), ozone (O3) and sulphur dioxide (SO2)), and cardiorespiratory mortality in Brisbane, Australia, during the period 1996 - 2004.

Long term exposure to asbestos satisfies test for causation

Background In Booth v Amaca Pty Ltd and Amaba Pty Ltd,1 the New South Wales Dust Diseases Tribunal awarded a retired motor mechanic $326 640 in damages for his malignant pleural mesothelioma allegedly caused by exposure to asbestos through working with the brake linings manufactured by the defendants. The evidence before the Tribunal was that the plaintiff had been exposed to asbestos prior to working as a mechanic from home renovations when he was a child and loading a truck as a youth. However, as a mechanic he had been exposed to asbestos in brake linings on which he worked from 1953 to 1983. Curtis DCJ held at [172] that the asbestos from the brake linings ‘materially contributed to [the plaintiff’s] contraction of mesothelioma’. This decision was based upon acceptance that the effect of exposure to asbestos on the development of mesothelioma was cumulative and rejection of theory that a single fibre of asbestos can cause the disease...

Effect of long-term exposure to endosulfan on blood cell count in Channa gachua

In the present investigation, live specimens of Channa gachua were exposed to sublethal concentrations, i.e., 0.0017 and 0.00087 ppm of endosulfan for a period of 60 days. After the completion of 60 days, red and white blood corpuscles were counted from control as well as experimental fishes.

Long-term exposure to extremely low-frequency magnetic fields impairs spatial recognition memory in mice

1. In the present study, we investigated the short- and long-term effects of extremely low-frequency (ELF) magnetic fields on spatial recognition memory in mice by using a two-trial recognition Y-maze that is based on the innate tendency of rodents to exp

Fragmentation of extracellular DNA by long-term exposure to radiation from uranium in aquatic environments

Persistent harmful scenarios associated with disposal of radioactive waste, high-background radiation areas and severe nuclear accidents are of great concern regarding consequences to both human health and the environment. Of particular concern is the extracellular DNA in aquatic environments contaminated by radiological substances. Strand breaks induced by radiation promote decrease in the transformation efficiency for extracellular DNA. The focus of this study is the quantification of DNA damage following long-term exposure (over one year) to low doses of natural uranium (an alpha particle emitter) to simulate natural conditions, since nothing is known about alpha radiation induced damage to extracellular DNA. A high-resolution Atomic Force Microscope was used to evaluate DNA fragments. Double-stranded plasmid pBS as a model for extracellular DNA was exposed to different amounts of natural uranium. It was demonstrated that low concentrations of U in water (50 to 150 ppm) produce appreciable numbers of double strand breaks, scaling with the square of the average doses. The importance of these findings for environment monitoring of radiological pollution is addressed.

Identification and quantification of phytochelatins in roots of rice to long-term exposure: evidence of individual role on arsenic accumulation and translocation

Rice has the predilection to take up arsenic in the form of methylated arsenic (o-As) and inorganic arsenic species (i-As). Plants defend themselves using i-As efflux systems and the production of phytochelatins (PCs) to complex i-As. Our study focused on the identification and quantification of phytochelatins by HPLC-ICP-MS/ESI-MS, relating them to the several variables linked to As exposure. GSH, 11 PCs, and As–PC complexes from the roots of six rice cultivars (Italica Carolina, Dom Sofid, 9524, Kitrana 508, YRL-1, and Lemont) exposed to low and high levels of i-As were compared with total, i-As, and o-As in roots, shoots, and grains. Only Dom Sofid, Kitrana 508, and 9524 were found to produce higher levels of PCs even when exposed to low levels of As. PCs were only correlated to i-As in the roots (r=0.884, P <0.001). However, significant negative correlations to As transfer factors (TF) roots–grains (r= –0.739, P <0.05) and shoots–grains (r= –0.541, P <0.05), suggested that these peptides help in trapping i-As but not o-As in the roots, reducing grains’ i-As. Italica Carolina reduced i-As in grains after high exposure, where some specific PCs had a special role in this reduction. In Lemont, exposure to elevated levels of i-As did not result in higher i-As levels in the grains and there were no significant increases in PCs or thiols. Finally, the high production of PCs in Kitrana 508 and Dom Sofid in response to high As treatment did not relate to a reduction of i-As in grains, suggesting that other mechanisms such as As–PC release and transport seems to be important in determining grain As in these cultivars.

Long-term exposure to high corticosterone levels attenuates serotonin responses in rat hippocampal CA1 neurons

Recent studies indicated that hyperactivity of the hypothalamo-pituitary-adrenal system is a considerable risk factor for the precipitation of affective disorders, most notably of major depression. The mechanism by which this hyperactivity eventually leads to clinical symptoms of depression is unknown. In the present animal study, we tested one possible mechanism, i.e., that long-term exposure to high corticosterone levels alters functional responses to serotonin in the hippocampus, an important area in the etiology of depression. Rats were injected daily for 3 weeks with a high dose of corticosterone; electrophysiological responses to serotonin were recorded intracellularly from CA1 pyramidal neurons in vitro. We observed that daily injections with corticosterone gradually attenuate the membrane hyperpolarization and resistance decrease mediated by serotonin-1A receptors. We next used single-cell antisense RNA amplification from identified CA1 pyramidal neurons to resolve whether the functional deficits in serotonin responsiveness are accompanied by decreased expression levels of the serotonin-1A receptor. It appeared that expression of serotonin-1A receptors in CA1 pyramidal cells is not altered; this result was supported by in situ hybridization. Expression of corticosteroid receptors in the same cells, particularly of the high-affinity mineralocorticoid receptor, was significantly reduced after long-term corticosterone treatment. The present findings indicate that prolonged elevation of the corticosteroid concentration, a possible causal factor for major depression in humans, gradually attenuates responsiveness to serotonin without necessarily decreasing serotonin-1A receptor mRNA levels in pyramidal neurons. These functional changes may occur by a posttranscriptional mechanism or by transcriptional regulation of genes other than the serotonin-1A receptor gene itself.

Teratologic effects of long-term exposure to diesel exhaust emissions (rabbits) /

"Contract no. 68-03-2652."

Risk of serious NSAID-related gastrointestinal events during long-term exposure: a systematic review

Objective: Exposure to non-steroidal anti-inflammatory drugs (NSAIDs) is associated wit increased risk of serious gastrointestinal (GI) events compared with non-exposure. We investigated whether that risk is sustained over time. Data sources: Cochrane Controlled Trials Register (to 2002); MEDLINE, EMBASE, Derwent Drug File and Current Contents (1999-2002); manual searching of reviews (1999-2002). Study selection: From 479 search results reviewed and 221 articles retrieved, seven studies of patients exposed to prescription non-selective NSAIDs for more than 6 months and reporting time-dependent serious GI event rates were selected for quantitative data synthesis. These were stratified into two groups by study design. Data extraction: Incidence of GI events and number of patients at specific time points were extracted. Data synthesis: Meta-regression analyses were performed. Change in risk was evaluated by testing whether the slope of the regression line declined over time. Four randomised controlled trials (RCTs) provided evaluable data from five NSAID arms (aspirin, naproxen, two ibuprofen arms, and diclofenac). When the RCT data were combined, a small significant decline in annualised risk was seen: -0.005% (95% Cl, -0.008% to -0.001%) per month. Sensitivity analyses were conducted because there was disparity within the RCT data. The pooled estimate from three cohort studies showed no significant decline in annualised risk over periods up to 2 years: -0.003% (95% Cl, -0.008% to 0.003%) per month. Conclusions: Small decreases in risk over time were observed; these were of negligible clinical importance. For patients who need long-term (> 6 months) treatment, precautionary measures should be considered to reduce the net probability of serious GI events over the anticipated treatment duration. The effect of intermittent versus regular daily therapy on long-term risk needs further investigation.