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  1. Mims FM
    Nature, 1997 Nov 20;390(6657):222-3.
    PMID: 9384366 DOI: 10.1038/36715
    Matched MeSH terms: Smoke/adverse effects*
  2. Afroz R, Hassan MN, Ibrahim NA
    Environ Res, 2003 Jun;92(2):71-7.
    PMID: 12854685
    In the early days of abundant resources and minimal development pressures, little attention was paid to growing environmental concerns in Malaysia. The haze episodes in Southeast Asia in 1983, 1984, 1991, 1994, and 1997 imposed threats to the environmental management of Malaysia and increased awareness of the environment. As a consequence, the government established Malaysian Air Quality Guidelines, the Air Pollution Index, and the Haze Action Plan to improve air quality. Air quality monitoring is part of the initial strategy in the pollution prevention program in Malaysia. Review of air pollution in Malaysia is based on the reports of the air quality monitoring in several large cities in Malaysia, which cover air pollutants such as Carbon monoxide (CO), Sulphur Dioxide (SO2), Nitrogen Dioxide (NO2), Ozone (O3), and Suspended Particulate Matter (SPM). The results of the monitoring indicate that Suspended Particulate Matter (SPM) and Nitrogen Dioxide (NO2) are the predominant pollutants. Other pollutants such as CO, O(x), SO2, and Pb are also observed in several big cities in Malaysia. The air pollution comes mainly from land transportation, industrial emissions, and open burning sources. Among them, land transportation contributes the most to air pollution. This paper reviews the results of the ambient air quality monitoring and studies related to air pollution and health impacts.
    Matched MeSH terms: Smoke/adverse effects
  3. Awang MB, Jaafar AB, Abdullah AM, Ismail MB, Hassan MN, Abdullah R, et al.
    Respirology, 2000 Jun;5(2):183-96.
    PMID: 10894109
    OBJECTIVE: Observations have been made on the long-term trends of major air pollutants in Malaysia including nitrogen dioxide, carbon monoxide, the ozone and total suspended particulate matter (particularly PM10), and sulfur dioxide, emitted from industrial and urban areas from early 1970s until late 1998.

    METHODOLOGY: The data show that the status of atmospheric environment in Malaysia, in particular in highly industrialized areas such as Klang Valley, was determined both by local and transboundary emissions and could be described as haze and non-haze periods.

    RESULTS: During the non-haze periods, vehicular emissions accounted for more than 70% of the total emissions in the urban areas and have demonstrated two peaks in the diurnal variations of the aforementioned air pollutants, except ozone. The morning 'rush-hour' peak was mainly due to vehicle emissions, while the late evening peak was mainly attributed to meteorological conditions, particularly atmospheric stability and wind speed. Total suspended particulate matter was the main pollutant with its concentrations at few sites often exceeding the Recommended Malaysia Air Quality Guidelines. The levels of other pollutants were generally within the guidelines. Since 1980, six major haze episodes were officially reported in Malaysia: April 1983, August 1990, June 1991, October 1991, August to October 1994, and July to October 1997. The 1997 haze episode was the worst ever experienced by the country. Short-term observations using continuous monitoring systems during the haze episodes during these periods clearly showed that suspended particulate matter (PM10) was the main cause of haze and was transboundary in nature. Large forest fires in parts of Sumatra and Kalimantan during the haze period, clearly evident in satellite images, were identified as the probable key sources of the widespread heavy haze that extended across Southeast Asia from Indonesia to Singapore, Malaysia and Brunei. The results of several studies have also provided strong evidence that biomass burning is the dominating source of particulate matter. The severity and extent of 1997's haze pollution was unprecedented, affecting some 300 million people across the region. The amount of economic costs suffered by Southeast Asian countries during this environmental disaster was enormous and is yet to be fully determined. Among the important sectors severely affected were air and land transport, shipping, construction, tourism and agro-based industries. The economic cost of the haze-related damage to Malaysia presented in this study include short-term health costs, production losses, tourism-related losses and the cost of avertive action. Although the cost reported here is likely to be underestimated, they are nevertheless significant (roughly RM1 billion).

    CONCLUSIONS: The general air quality of Malaysia since 1970 has deteriorated. Studies have shown that should no effective countermeasures be introduced, the emissions of sulfur dioxide, nitrogen oxides, particulate matter, hydrocarbons and carbon monoxide in the year 2005 would increase by 1.4, 2.12, 1.47 and 2.27 times, respectively, from the 1992 levels.

    Matched MeSH terms: Smoke/adverse effects
  4. Azizi BH, Henry RL
    Int J Epidemiol, 1991 Mar;20(1):144-50.
    PMID: 2066213 DOI: 10.1093/ije/20.1.144
    The effects of indoor environmental factors on respiratory illness were studied in 15017-12 year old school children in Kuala Lumpur. Exposure to mosquito coil smoke for at least three nights a week was independently associated with asthma and persistent wheeze. Passive smoking, defined as sharing a bedroom with an adult smoker, was independently associated with a chest illness in the past year. No relationships were found between exposure to kerosene stoves, wood stoves, fumigation mat mosquito repellents or aerosol insecticides and respiratory illness. Host factors predictive of at least one respiratory outcome included family history of chest illness, history of allergy, male sex, hospitalization in the neonatal period and low paternal education. With 95% confidence, avoidance of regular exposure to mosquito coil smoke and passive smoking could reduce the prevalences of persistent wheeze, asthma and chest illness by up to 29%. Measurements of lung function confirmed the validity of questions pertaining to wheezing and asthma in the study questionnaire.
    Matched MeSH terms: Smoke/adverse effects
  5. Tai Li Min E, Abdullah B
    Ear Nose Throat J, 2020 Nov;99(9):NP103-NP104.
    PMID: 31184208 DOI: 10.1177/0145561319856576
    Matched MeSH terms: Smoke/adverse effects
  6. De Rubis G, Paudel KR, Yeung S, Mohamad S, Sudhakar S, Singh SK, et al.
    Pathol Res Pract, 2024 May;257:155295.
    PMID: 38603841 DOI: 10.1016/j.prp.2024.155295
    Tobacco smoking is a leading cause of preventable mortality, and it is the major contributor to diseases such as COPD and lung cancer. Cigarette smoke compromises the pulmonary antiviral immune response, increasing susceptibility to viral infections. There is currently no therapy that specifically addresses the problem of impaired antiviral response in cigarette smokers and COPD patients, highlighting the necessity to develop novel treatment strategies. 18-β-glycyrrhetinic acid (18-β-gly) is a phytoceutical derived from licorice with promising anti-inflammatory, antioxidant, and antiviral activities whose clinical application is hampered by poor solubility. This study explores the therapeutic potential of an advanced drug delivery system encapsulating 18-β-gly in poly lactic-co-glycolic acid (PLGA) nanoparticles in addressing the impaired antiviral immunity observed in smokers and COPD patients. Exposure of BCi-NS1.1 human bronchial epithelial cells to cigarette smoke extract (CSE) resulted in reduced expression of critical antiviral chemokines (IP-10, I-TAC, MIP-1α/1β), mimicking what happens in smokers and COPD patients. Treatment with 18-β-gly-PLGA nanoparticles partially restored the expression of these chemokines, demonstrating promising therapeutic impact. The nanoparticles increased IP-10, I-TAC, and MIP-1α/1β levels, exhibiting potential in attenuating the negative effects of cigarette smoke on the antiviral response. This study provides a novel approach to address the impaired antiviral immune response in vulnerable populations, offering a foundation for further investigations and potential therapeutic interventions. Further studies, including a comprehensive in vitro characterization and in vivo testing, are warranted to validate the therapeutic efficacy of 18-β-gly-PLGA nanoparticles in respiratory disorders associated with compromised antiviral immunity.
    Matched MeSH terms: Smoke/adverse effects
  7. Mohamed M, Sulaiman SA, Jaafar H
    PMID: 23983363
    The effect of cigarette smoke (CS) on histology of male accessory reproductive organs and the possible protective effect of honey supplementation in rats were investigated in this study. Rats received distilled water, honey, CS exposure or honey plus CS exposure. Honey (1.2 g/kg body weight/day) was administered by gavage and CS exposure (3 times per day) was done in a chamber for 13 weeks. CS exposure significantly increased relative weight of epididymis and ventral prostate. There were also significantly increased number of clear cells and epithelial height of cauda epididymis as well as severe interstitial oedema and decreased epithelial height of prostate gland. However, with the supplementation of honey, these histological changes were significantly reversed suggesting the protective effect of honey against the toxic effect of CS on male accessory reproductive organs in rats.
    Matched MeSH terms: Smoke/adverse effects
  8. Mott JA, Mannino DM, Alverson CJ, Kiyu A, Hashim J, Lee T, et al.
    Int J Hyg Environ Health, 2005;208(1-2):75-85.
    PMID: 15881981 DOI: 10.1016/j.ijheh.2005.01.018
    We investigated the cardiorespiratory health effects of smoke exposure from the 1997 Southeast Asian Forest Fires among persons who were hospitalized in the region of Kuching, Malaysia. We selected admissions to seven hospitals in the Kuching region from a database of all hospital admissions in the state of Sarawak during January 1, 1995 and December 31, 1998. For several cardiorespiratory disease classifications we used Holt-Winters time-series analyses to determine whether the total number of monthly hospitalizations during the forest fire period (August 1 to October 31, 1997), or post-fire period (November 1, 1997 to December 31, 1997) exceeded forecasted estimates established from a historical baseline period of January 1, 1995 to July 31, 1997. We also identified age-specific cohorts of persons whose members were admitted for specific cardiorespiratory problems during January 1 to July 31 of each year (1995--1997). We compared Kaplan-Meier survival curves of time to first readmission for the 1997 cohorts (exposed to the forest fire smoke) with the survival curves for the 1995 and 1996 cohorts (not exposed, pre-fire cohorts). The time-series analyses indicated that statistically significant fire-related increases were observed in respiratory hospitalizations, specifically those for chronic obstructive pulmonary disease (COPD) and asthma. The survival analyses indicated that persons over age 65 years with previous hospital admissions for any cause (chi2(1df) = 5.98, p = 0.015), any cardiorespiratory disease (chi2(1df) = 5.3, p = 0.02), any respiratory disease (chi2(1df) = 7.8, p = 0.005), or COPD (chi2(1df) = 3.9, p = 0.047), were significantly more likely to be rehospitalized during the follow-up period in 1997 than during the follow-up periods in the pre-fire years of 1995 or 1996. The survival functions of the exposed cohorts resumed similar trajectories to unexposed cohorts during the post-fire period of November 1, 1997 to December 31, 1998. Communities exposed to forest fire smoke during the Southeast Asian forest fires of 1997 experienced short-term increases in cardiorespiratory hospitalizations. When an air quality emergency is anticipated, persons over age 65 with histories of respiratory hospitalizations should be preidentified from existing hospitalization records and given priority access to interventions.
    Matched MeSH terms: Smoke/adverse effects*
  9. Teasdale JE, Hazell GG, Peachey AM, Sala-Newby GB, Hindmarch CC, McKay TR, et al.
    Sci Rep, 2017 Jan 06;7:39945.
    PMID: 28059114 DOI: 10.1038/srep39945
    Endothelial dysfunction caused by the combined action of disturbed flow, inflammatory mediators and oxidants derived from cigarette smoke is known to promote coronary atherosclerosis and increase the likelihood of myocardial infarctions and strokes. Conversely, laminar flow protects against endothelial dysfunction, at least in the initial phases of atherogenesis. We studied the effects of TNFα and cigarette smoke extract on human coronary artery endothelial cells under oscillatory, normal laminar and elevated laminar shear stress for a period of 72 hours. We found, firstly, that laminar flow fails to overcome the inflammatory effects of TNFα under these conditions but that cigarette smoke induces an anti-oxidant response that appears to reduce endothelial inflammation. Elevated laminar flow, TNFα and cigarette smoke extract synergise to induce expression of the transcriptional regulator activating transcription factor 3 (ATF3), which we show by adenovirus driven overexpression, decreases inflammatory gene expression independently of activation of nuclear factor-κB. Our results illustrate the importance of studying endothelial dysfunction in vitro over prolonged periods. They also identify ATF3 as an important protective factor against endothelial dysfunction. Modulation of ATF3 expression may represent a novel approach to modulate proinflammatory gene expression and open new therapeutic avenues to treat proinflammatory diseases.
    Matched MeSH terms: Smoke/adverse effects*
  10. Chen YB, Lan YW, Chen LG, Huang TT, Choo KB, Cheng WT, et al.
    Cell Stress Chaperones, 2015 Nov;20(6):979-89.
    PMID: 26243699 DOI: 10.1007/s12192-015-0627-7
    Chronic obstructive pulmonary disease (COPD) is a sustained blockage of the airways due to lung inflammation occurring with chronic bronchitis and/or emphysema. Progression of emphysema may be slowed by vascular endothelial growth factor A (VEGFA), which reduces apoptotic tissue depletion. Previously, authors of the present report demonstrated that cis-resveratrol (c-RSV)-induced heat-shock protein 70 (HSP70) promoter-regulated VEGFA expression promoted neovascularization of genetically modified mesenchymal stem cells (HSP-VEGFA-MSC) in a mouse model of ischemic disease. Here, this same stem cell line was evaluated for its protective capacity to alleviate elastase-induced pulmonary emphysema in mice. Results of this study showed that c-RSV-treatment of HSP-VEGFA-MSC exhibited synergy between HSP70 transcription activity and induced expression of anti-oxidant-related genes when challenged by cigarette smoke extracts. Eight weeks after jugular vein injection of HSP-VEGFA-MSC into mice with elastase-induced pulmonary emphysema followed by c-RSV treatment to induce transgene expression, significant improvement was observed in respiratory functions. Expression of VEGFA, endogenous nuclear factor erythroid 2-related factor (Nrf 2), and manganese superoxide dismutase (MnSOD) was significantly increased in the lung tissues of the c-RSV-treated mice. Histopathologic examination of treated mice revealed gradual but significant abatement of emphysema and restoration of airspace volume. In conclusion, the present investigation demonstrates that c-RSV-regulated VEGFA expression in HSP-VEGFA-MSC significantly improved the therapeutic effects on the treatment of COPD in the mouse, possibly avoiding side effects associated with constitutive VEGFA expression.
    Matched MeSH terms: Smoke/adverse effects
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