SHORT-TERM AND LONG-TERM EFFECTS OF AIR POLLUTION ON LUNG FUNCTION

Epidemiology ◽  
2004 ◽  
Vol 15 (4) ◽  
pp. S42 ◽  
Author(s):  
Heike Luttmann-Gibson ◽  
Douglas W. Dockery ◽  
Frank E. Speizer
Epidemiology ◽  
2008 ◽  
Vol 19 (5) ◽  
pp. 690-701 ◽  
Author(s):  
Thomas Götschi ◽  
Joachim Heinrich ◽  
Jordi Sunyer ◽  
Nino Künzli

2019 ◽  
Vol 76 (8) ◽  
pp. 583-591 ◽  
Author(s):  
Stefan Edginton ◽  
Dylan E O’Sullivan ◽  
Will King ◽  
M Diane Lougheed

The effect of acute and long-term exposures to outdoor particulate air pollution on lung function in healthy adults is not well established. The objective of this study was to conduct a systematic literature review and meta-analysis of studies that assessed the relationship of outdoor particulate air pollution and lung function in healthy adults. Studies that contained data on outdoor air particulate matter levels (PM10 or PM2.5) and forced expiratory volume in 1 s (FEV1) in healthy adults were eligible for inclusion. Effect estimates, in relation to long-term and acute exposures, were quantified separately using random effects models. A total of 27 effect estimates from 23 studies were included in this review. Acute exposures were typically assessed with PM2.5, while long-term exposures were predominantly represented by PM10. A 10 µg/m3 increase in short-term PM2.5 exposure (days) was associated with a −7.02 mL (95% CI −11.75 to –2.29) change in FEV1. A 10 µg/m3 difference in long-term PM10 exposure was associated with a −8.72 mL (95% CI −15.39 to –2.07) annual change in FEV1 and an absolute difference in FEV1 of −71.36 mL (95% CI −134.47 to –8.24). This study provides evidence that acute and long-term exposure to outdoor particulate air pollution are associated with decreased FEV1 in healthy adults. Residual confounding from other risk factors, such as smoking, may explain some of the effect for long-term exposures. More studies are required to determine the relationship of long-term exposure to PM2.5 and short-term exposure to PM10, which may have different biologic mechanisms.


Atmosphere ◽  
2020 ◽  
Vol 11 (12) ◽  
pp. 1274
Author(s):  
Frederick W. Lipfert

This paper considers timing issues in health-effect exposure and response studies. Short-term studies must consider delayed and cumulative responses; prior exposures, disease latency, and cumulative impacts are required for long-term studies. Lacking individual data, long-term air quality describes locations, as do greenspaces and traffic density, rather than exposures of residents. Indoor air pollution can bias long-term exposures and effect estimates but short-term effects also respond to infiltrated outdoor air. Daily air quality fluctuations may affect the frail elderly and are necessarily included in long-term averages; any true long-term effects must be given by differences between annual and daily effects. I found such differences to be negligible after adjusting for insufficient lag effects in time-series studies and neglect of prior exposures in long-term studies. Aging of subjects under study implies cumulative exposures, but based on age-specific mortality, I found relative risks decreasing with age, precluding cumulative effects. A new type of time-series study found daily mortality of previously frail subjects to be associated with various pollutants without exposure thresholds, but the role of air pollution in the onset of frailty remains an unexplored issue. The importance of short-term fluctuations has been underestimated and putative effects of long-term exposures have been overestimated.


Author(s):  
D.E. Loudy ◽  
J. Sprinkle-Cavallo ◽  
J.T. Yarrington ◽  
F.Y. Thompson ◽  
J.P. Gibson

Previous short term toxicological studies of one to two weeks duration have demonstrated that MDL 19,660 (5-(4-chlorophenyl)-2,4-dihydro-2,4-dimethyl-3Hl, 2,4-triazole-3-thione), an antidepressant drug, causes a dose-related thrombocytopenia in dogs. Platelet counts started to decline after two days of dosing with 30 mg/kg/day and continued to decrease to their lowest levels by 5-7 days. The loss in platelets was primarily of the small discoid subpopulation. In vitro studies have also indicated that MDL 19,660: does not spontaneously aggregate canine platelets and has moderate antiaggregating properties by inhibiting ADP-induced aggregation. The objectives of the present investigation of MDL 19,660 were to evaluate ultrastructurally long term effects on platelet internal architecture and changes in subpopulations of platelets and megakaryocytes.Nine male and nine female beagle dogs were divided equally into three groups and were administered orally 0, 15, or 30 mg/kg/day of MDL 19,660 for three months. Compared to a control platelet range of 353,000- 452,000/μl, a doserelated thrombocytopenia reached a maximum severity of an average of 135,000/μl for the 15 mg/kg/day dogs after two weeks and 81,000/μl for the 30 mg/kg/day dogs after one week.


Psibernetika ◽  
2018 ◽  
Vol 11 (1) ◽  
Author(s):  
Devina Calista ◽  
Garvin Garvin

<p><em>Child abuse by parents is common in households. The impact of violence on children will bring short-term effects and long-term effects that can be attributed to their various emotional, behavioral and social problems in the future; especially in late adolescence that will enter adulthood. Resilience factors increase the likelihood that adolescents who are victims of childhood violence recover from their past experiences</em><em>,</em><em> become more powerful individuals and have a better life. The purpose of this study was to determine the source of resilience in late adolescents who experienced violence from parents in their childhood. This research uses qualitative research methods with in-depth interviews as a method of data collection. The result shows that the three research participants have the aspects of "I Have", "I Am", and "I Can"; a participant has "I Can" aspects as a source of resilience, and one other subject has no source of resilience. The study concluded that parental affection and acceptance of the past experience have role to the three sources of resilience (I Have, I Am, and I Can)</em></p><p><em> </em></p><p><strong><em>Keyword : </em></strong><em>Resilience, adolescence, violence, parents</em></p>


2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Patrick D. M. C. Katoto ◽  
Amanda S. Brand ◽  
Buket Bakan ◽  
Paul Musa Obadia ◽  
Carsi Kuhangana ◽  
...  

Abstract Background Air pollution is one of the world’s leading mortality risk factors contributing to seven million deaths annually. COVID-19 pandemic has claimed about one million deaths in less than a year. However, it is unclear whether exposure to acute and chronic air pollution influences the COVID-19 epidemiologic curve. Methods We searched for relevant studies listed in six electronic databases between December 2019 and September 2020. We applied no language or publication status limits. Studies presented as original articles, studies that assessed risk, incidence, prevalence, or lethality of COVID-19 in relation with exposure to either short-term or long-term exposure to ambient air pollution were included. All patients regardless of age, sex and location diagnosed as having COVID-19 of any severity were taken into consideration. We synthesised results using harvest plots based on effect direction. Results Included studies were cross-sectional (n = 10), retrospective cohorts (n = 9), ecological (n = 6 of which two were time-series) and hypothesis (n = 1). Of these studies, 52 and 48% assessed the effect of short-term and long-term pollutant exposure, respectively and one evaluated both. Pollutants mostly studied were PM2.5 (64%), NO2 (50%), PM10 (43%) and O3 (29%) for acute effects and PM2.5 (85%), NO2 (39%) and O3 (23%) then PM10 (15%) for chronic effects. Most assessed COVID-19 outcomes were incidence and mortality rate. Acutely, pollutants independently associated with COVID-19 incidence and mortality were first PM2.5 then PM10, NO2 and O3 (only for incident cases). Chronically, similar relationships were found for PM2.5 and NO2. High overall risk of bias judgments (86 and 39% in short-term and long-term exposure studies, respectively) was predominantly due to a failure to adjust aggregated data for important confounders, and to a lesser extent because of a lack of comparative analysis. Conclusion The body of evidence indicates that both acute and chronic exposure to air pollution can affect COVID-19 epidemiology. The evidence is unclear for acute exposure due to a higher level of bias in existing studies as compared to moderate evidence with chronic exposure. Public health interventions that help minimize anthropogenic pollutant source and socio-economic injustice/disparities may reduce the planetary threat posed by both COVID-19 and air pollution pandemics.


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